HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Michael Argenziano Asim F. Choudhri Eric A. Rose Mehmet C. Oz Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Argenziano, M. Articles by Oz, M. C. Search for Related Content PubMed PubMed Citation Articles by Argenziano, M. Articles by Oz, M. C.

J Thorac Cardiovasc Surg 1998;116:973-980
© 1998 Mosby, Inc.

SURGERY FOR ADULT CARDIOVASCULAR DISEASE

MANAGEMENT OF VASODILATORY SHOCK AFTER CARDIAC SURGERY: IDENTIFICATION OF PREDISPOSING FACTORS AND USE OF A NOVEL PRESSOR AGENT

From the Departments of Surgery and Medicine, Columbia University College of Physicians and Surgeons, New York.

Read at the Seventy-eighth Annual Meeting of The American Association for Thoracic Surgery, Boston, Mass, May 3-6, 1998.

Received for publication May 8, 1998. Revisions requested June 30, 1998; revisions received July 20, 1998. Accepted for publication Aug 10, 1998. Address for reprints: Dr Oz and Dr Landry, Division of Cardiothoracic Surgery, Milstein Hospital, Room 7-435, 177 Ft Washington Ave, New York, NY 10032.

	Abstract

Top Abstract Introduction Methods Results Discussion Appendix: Discussion References

 
Background:Cardiopulmonary bypass can be associated with vasodilatory hypotension requiring pressor support. We have previously found arginine vasopressin to be a remarkably effective pressor in a variety of vasodilatory shock states. We investigated the incidence and clinical predictors of vasodilatory shock in a general population of cardiac surgical patients and the effects of low-dose arginine vasopressin as treatment of this syndrome in patients with heart failure.
Methods: Patients undergoing cardiopulmonary bypass (n = 145) were studied prospectively. Preoperative ejection fraction, medications, and perioperative hemodynamics were recorded, and postbypass serum arginine vasopressin levels were measured. Vasodilatory shock was defined as a mean arterial pressure lower than 70 mm Hg, a cardiac index greater than 2.5 L/min/m², and norepinephrine dependence. Predictors of vasodilatory shock were investigated by logistic regression analysis. The hemodynamic responses of patients who received arginine vasopressin infusions for vasodilatory shock after cardiopulmonary bypass for left ventricular assist device placement or heart transplantation were analyzed retrospectively.
Results: Eleven of 145 general cardiac surgery patients (8%) met criteria for postbypass vasodilatory shock. By multivariate analysis, an ejection fraction lower than 0.35 and angiotensin-converting enzyme inhibitor use were independent predictors of postbypass vasodilatory shock (relative risks of 9.1 and 11.9, respectively). Vasodilatory shock was associated with inappropriately low serum arginine vasopressin concentrations (12.0 ± 6.6 pg/mL). Retrospective analysis found 40 patients with postbypass vasodilatory shock who received low-dose arginine vasopressin infusions, resulting in increased mean arterial pressure and decreased norepinephrine requirements.
Conclusions: Low ejection fraction and angiotensin-converting enzyme inhibitor use are risk factors for postbypass vasodilatory shock, and this syndrome is associated with vasopressin deficiency. In patients exhibiting this syndrome after high-risk cardiac operations, replacement of arginine vasopressin increases blood pressure and reduces catecholamine pressor requirements.

	Introduction

Top Abstract Introduction Methods Results Discussion Appendix: Discussion References

 
Cardiopulmonary bypass (CPB) can be complicated by a systemic inflammatory response characterized by profound vasodilation. ¹ This vasodilatory shock syndrome, which is especially noted after extended CPB, ² is attributed to endothelial injury ³ and the release of cytokines and other inflammatory mediators. ⁴ Pressor catecholamines are commonly administered to support systemic arterial pressure in these cases, ⁵ but their effectiveness is limited by frequent catecholamine resistance ⁶ and by significant toxic effects at high doses. ⁷ Alternative pressor agents could therefore be useful.

Arginine vasopressin (AVP) has little vasoconstrictive effect in hemodynamically normal subjects ⁸ but is an effective pressor in states associated with arterial hypotension. ^9,10 We previously observed a hypersensitivity to the pressor effects of AVP in vasodilatory septic shock, ¹¹ and we recently reported a similar sensitivity in patients with vasodilatory shock after placement of left ventricular assist devices (LVADs). ¹² In most cases AVP levels on weaning from CPB were inappropriately low for the degree of arterial hypotension, and this finding contrasted with the elevated levels usually found after CPB. ¹³ On the basis of this experience, we have used AVP extensively to treat patients with vasodilatory shock after CPB for LVAD placement and for heart transplantation (OHT). The general incidence of vasodilatory hypotension and the concordance with AVP deficiency remains to be defined, as does the therapeutic role of AVP in the management of this syndrome.

We therefore undertook this analysis with 2 objectives. First, we sought to prospectively establish in a general cardiac surgical population the incidence of vasodilatory shock and the characteristics of this syndrome, including presence of AVP deficiency and other predisposing factors. Second, we retrospectively evaluated our clinical experience with the use of AVP in the management of vasodilatory hypotension after CPB.

	Methods

Top Abstract Introduction Methods Results Discussion Appendix: Discussion References

 
Study patients and protocols.
The prospective study group consisted of 102 men and 43 women with a mean age of 61 years. After they provided informed consent, subjects undergoing elective cardiac surgery were enrolled and were selected for shock during the first 30 minutes after CPB weaning on the basis of hypotension (mean arterial pressure <70 mm Hg) requiring norepinephrine administration for at least 3 hours. Serum samples were collected for AVP assay from these patients 5 minutes after weaning from CPB, and perioperative hemodynamic parameters and exogenous pressor requirements were prospectively recorded. Subjects were further classified as having cardiogenic shock (cardiac index <2.5 L/min/m²) or vasodilatory shock (cardiac index >2.5 L/min/m²).

Next a retrospective analysis of LVAD and OHT clinical databases was performed to find the cases of patients who had received AVP for the treatment of vasodilatory hypotension during a 30-month period. Inclusion criteria for this analysis included post-CPB vasodilatory hypotension (requirement for exogenous norepinephrine to maintain mean arterial pressure >70 mm Hg and cardiac index >2.5 L/min/m²) and the administration of AVP. Fourteen LVAD recipients and 26 OHT recipients met these criteria and received AVP infusions at a rate of 0.1 U/min. The study group consisted of 32 men and 8 women, with a mean age of 49.5 years.

Demographic and hemodynamic data for these 40 patients were obtained for the perioperative period and during the postoperative intensive care unit stay. The generally applied protocol for AVP administration was as follows: on identification of vasodilatory hypotension and an increasing exogenous pressor requirement, patients received AVP (Pitressin; Parke-Davis, Morris Plains, NJ) intravenously at a rate of 0.1 U/min. Subsequently catecholamine and then AVP infusions were tapered to maintain mean arterial pressure above 70 mm Hg. When hemodynamic improvement allowed discontinuation of catecholamine agents, the AVP infusion rate was progressively decreased to 0.02 U/min and then discontinued.

Vasopressin assay.
Plasma AVP levels were measured by radioimmunoassay according to published protocols. ¹³

Analysis of data.
Hemodynamic and clinical data are reported as mean ± SD. Continuous variables were analyzed with the paired and unpaired Student t test and analysis of variance. The ² and Fisher exact tests were applied to discrete variables. Univariable and multivariable logistic regression analyses were used to determine the relative contribution of a variety of demographic and clinical factors to the development of vasodilatory hypotension. For the multivariable regression analysis, variables from the univariate analysis were allowed to enter at the P < .25 level.

	Results

Top Abstract Introduction Methods Results Discussion Appendix: Discussion References

 
Incidence and clinical predictors of postbypass vasodilatory shock and relationship with plasma arginine vasopressin levels.
Of 145 patients studied prospectively, 20 (14%) met criteria for post-CPB hypotension, with 11 cases (8%) meeting criteria for vasodilatory shock. This low incidence contrasts with the 42% observed in our earlier study of LVAD recipients. ¹² Univariate regression analysis of this data set examined the variables listed in Table I and found low ejection fraction (<35%, P < .0001) and the preoperative use of angiotensin-converting enzyme (ACE) inhibitors (P < .0001) and diuretics (P = .02) to be predictors of post-CPB vasodilatory shock. A multivariable logistic regression analysis analyzed a number of factors (ejection fraction, preoperative diuretics, digoxin, ACE inhibitors, b-blockers, and calcium-channel blockers), and found low ejection fraction (P = .003) and the use of ACE inhibitors (P = .001) to be independent predictors of increased risk of post-CPB vasodilatory shock. The relative risks of post-CPB vasodilatory shock, as described by odds ratios, were 9.1 (confidence interval 2.1-38.8) for low ejection fraction and 11.9 (confidence interval 2.7-53.1) for use of ACE inhibitors. Demographics for this group and for the 11 patients with vasodilatory shock are summarized in Table I.

The mean post-CPB AVP level in patients with cardiogenic shock was 29.3 ± 15.0 pg/mL, compared with 12.0 ± 6.6 pg/mL in patients with vasodilatory shock (P = .004), suggesting that AVP deficiency contributes to the development of vasodilatory shock. The hemodynamics and AVP levels in these 2 populations are listed in Table II, and the distribution of serum AVP values is depicted in Fig 1.

View larger version (12K): [in this window] [in a new window]   Fig. 1. Distribution of AVP levels in cardiogenic and vasodilatory shock.

View larger version (39K): [in this window] [in a new window]   Fig. 2. Relationship between degree of baseline hypotension and increase in mean arterial pressure (MAP) after AVP infusion in 40 LVAD and OHT recipients.

View larger version (38K): [in this window] [in a new window]   Fig. 3. Relationship between degree of baseline hypotension and increase in systemic vascular resistance (SVR) after AVP infusion in 40 LVAD and OHT recipients. MAP, Mean arterial pressure.

View larger version (34K): [in this window] [in a new window]   Fig. 4. Relationship between degree of baseline hypotension and decrease in norepinephrine (NE) requirements after AVP infusion in 40 LVAD and OHT recipients. MAP, Mean arterial pressure.

	Discussion

Top Abstract Introduction Methods Results Discussion Appendix: Discussion References

In our study of 145 cardiac surgical patients, the incidence of vasodilatory shock in the early post-CPB period was 8%, although this syndrome was significantly more common (27%) among patients with low ejection fraction. In a previous communication we reported that this syndrome developed in 42% of patients undergoing LVAD insertion for end-stage heart failure during a 1-year period. Perhaps not surprisingly, multivariate analyses of our study population found low ejection fraction and use of ACE inhibitors to be independent predictors of vasodilatory shock. Among the 11 patients with post-CPB vasodilatory shock, most had AVP levels that, although within the normal osmoregulatory range for healthy normotensive subjects (5-15 pg/mL), ²⁰ were inappropriately low for the degree of arterial hypotension that was present (15 pg/mL).

The mechanisms contributing to AVP deficiency in this syndrome are a matter of speculation. Hyponatremia can blunt the AVP response to baroreflex-mediated stimuli, ²¹ but serum sodium levels were normal (136.2 ± 1.7 mEq/L) in our patients. Similarly, activation of atrial stretch receptors is known to inhibit AVP release through vagal afferent pathways, ²² but central venous pressure was not elevated (12.0 ± 1.2 mm Hg) during the period of hypotension in our patients. Nonetheless, potential neurohumoral effects of preoperative elevations in cardiac filling pressures cannot be excluded. Atrial natriuretic peptide (ANP) could be responsible for AVP deficiency because it is also known to inhibit AVP secretion, and the serum levels of ANP are often increased after CPB. ²³ Finally, autonomic dysfunction could contribute because it is associated with AVP deficiency and has been documented in patients with heart failure. ²⁴

The dose of AVP administered to our patients undergoing LVAD implantation and OHT, 0.1 U/min, is between a fourth and a ninth that administered to patients with cirrhosis for the control of bleeding esophageal varices. This dose provides a steady-state plasma concentration of at least 150 pg/mL, ²⁵ comparable to levels previously reported after CPB. LVAD and OHT recipients with vasodilatory shock proved to be extremely sensitive to this dose of AVP, with rapid hemodynamic responses even in the absence of a loading dose. In several cases the AVP dose was decreased to 0.01 U/min, which was sufficient to maintain blood pressure without catecholamine pressors. This dose corresponds to a plasma concentration of less than 40 pg/mL²⁵ (similar to AVP levels observed in our patients in cardiogenic shock) and could therefore constitute physiologic replacement.

The mechanisms by which AVP acts as a pressor in patients resistant to catecholamines are not clear, but a number of intriguing possibilities exist. Vasodilatory shock after CPB is likely due to pathologic activation of several vasodilator mechanisms. The interleukin 1 level is elevated in inflammatory states and ANP is increased after CPB, and both promote vasodilation through increased levels of intracellular cyclic guanosine monophosphate. ^26,27 Also, adenosine triphosphate–activated potassium channels of vascular smooth muscle are activated by tissue hypoxia and hypoperfusion (and presumably by CPB), and this activation causes vasodilation by inducing cellular hyperpolarization and inhibiting voltage-gated calcium channels. ²⁸ Both catecholamines and AVP effect vasoconstriction by increasing intracellular calcium levels in vascular smooth muscle through activation of voltage-gated calcium channels, and the activation of vasodilator pathways could impair this calcium-dependent mechanism. In contrast to catecholamines, however, AVP also inhibits the production of cyclic guanosine monophosphate by interleukin 1 and by ANP ^29,30 and inhibits the adenosine triphosphate–activated potassium channels of vascular smooth muscle. ²⁸ Thus the efficacy of AVP as a pressor in a variety of clinical scenarios in which catecholamines are ineffective may rest on its ability to specifically counteract pathologically activated vasodilatory mechanisms. This hypothesis may also explain the restoration of catecholamine sensitivity that we have frequently observed after AVP administration.

We found in our prospective study that vasodilatory shock after CPB is associated with AVP deficiency and that this syndrome is more common among patients with low ejection fraction and those receiving ACE inhibitors. We also retrospectively observed, in a large number of patients undergoing LVAD implantation and OHT, that AVP is an effective pressor in the setting of post-CPB vasodilation, significantly increasing mean arterial pressure while reducing the requirement for catecholamine pressor agents. All patients in vasodilatory shock responded to AVP administration, and the magnitude of the hemodynamic response was proportional to the severity of hypotension at the time of infusion initiation. Our results are preliminary, and a large-scale controlled trial of AVP for the treatment of vasodilatory shock after CPB will be required to determine the risks and benefits associated with the use of this novel agent in the management of cardiac surgical patients.

	Appendix: Discussion

Top Abstract Introduction Methods Results Discussion Appendix: Discussion References

 
Dr Richard D. Weisel (Toronto, Ontario, Canada). The problem is important. We have all seen patients who are profoundly hypotensive after operation, but we seldom know why and our treatment is far from adequate. As you do, we give them pressor agents, and we are always afraid that the arterial grafts are going to go into spasm. Occasionally they do. This is a major concern.

You have previously published information about patients undergoing LVAD implantation and OHT. I think we can understand why these patients are perhaps a little bit different. Both populations have unique features that are going to make them more susceptible to this. Could you perhaps pick out for us, though, the patients who are not LVAD or OHT recipients and see whether in fact the same process is going on in these other patients—particularly those undergoing coronary bypass, who comprise the majority of the elective cardiac surgical patients?

How many patients undergoing general cardiac surgery actually had vasodilatory shock, and how many of those had low AVP levels? Did all patients with vasodilatory shock respond the same, whether or not their AVP levels were low to begin with? I wonder whether you could clarify this for me.

Otherwise I think that it is a great idea. If we can get specific information, we will probably have a more specific therapy for this disturbing complication after heart operations.

Dr Argenziano. Although we first noticed this phenomenon in LVAD recipients and then directed our attention to OHT recipients, we have also asked ourselves the question, "Is this a relevant syndrome in general cardiac surgery?" That question is really what prompted the prospective trial that we presented here today.

In this prospective trial of 145 patients there were only 4 LVAD and 5 OHT recipients. We performed a separate statistical analysis in which we pulled those patients out. Even after removing the LVAD and OHT recipients from that population of 145, we found the same statistical significance with respect to ejection fraction and ACE inhibitor therapy as predictors of this syndrome.

With respect to the number of patients in whom the syndrome developed, there were actually 11 patients in whom vasodilatory shock occurred among the 145 at whom we looked prospectively. Only 1 of those was an OHT recipient and 2 were LVAD recipients. So, after removal of the LVAD and OHT recipients there were 8 patients among 136 in whom this complication developed. Thus vasodilatory shock is a complication that occurred in 6% or 7% of the general cardiac surgical patients whom we studied, excluding the patients undergoing LVAD implantation and OHT. AVP levels were obtained for all these patients and, as I described in my presentation, the AVP levels were inappropriately low in all but 1 of the patients who had vasodilatory shock. All the levels were below 20 pg/mL except 1 that was about 23 pg/mL.

The AVP levels that we expect in patients who are profoundly hypotensive are in the 40 to 50 pg/mL range, and they range as high as 100 pg/mL in some reports. All our patients who were in profound vasodilatory shock therefore had grossly deficient secretion of AVP.

With respect to whether all patients responded similarly to AVP, we tried to analyze this by separating patients into 3 groups according to the degree of hypotension. All patients responded, but some responded more than others. If the mean arterial pressure is 65 mm Hg and AVP is administered, the pressure rises to 80 mm Hg. If the mean arterial pressure is 45 mm Hg and AVP is administered, the pressure rises to 80 mm Hg. So you might say, "Why give AVP to patients whose mean arterial pressure is 65 mm Hg?" That is a good point. You may not want to give it to those patients. You may instead want to give those patients a little norepinephrine. You should know, however, that in our opinion this hormone seems to act as a replacement therapy for some deficiency, rather than as an exogenous pressor. We do not titrate it to increasing doses. We do not give more AVP when we want a higher blood pressure. We just give a single dose, and it seems to be effective in most cases.

Dr Karl H. Krieger (New York, NY). These are really compelling data. In your current practice, if you have a patient at high risk, for example a patient with poor ejection fraction who has been receiving ACE inhibitors and diuretics, might you give AVP prophylactically? Is there any contraindication to giving AVP; have you had any problems with it?

Dr Argenziano. That is a good question. Certainly, as you might imagine, AVP is now stocked in both our intensive care units and operating rooms. We use it quite frequently. We have not yet, however, given it prophylactically to patients who are not hypotensive. We have reserved it for patients with demonstrated need. It must be remembered that we are using AVP to treat vasodilatory shock. Most patients in hemodynamically unstable condition before a cardiac operation are not in vasodilatory shock but rather in cardiogenic shock, in which the vascular tone is actually quite high. We would not expect AVP to have an effect in those cases, because it is not an inotrope but rather a pure vasoconstrictor. We generally reserve AVP for patients in whom vasodilatory shock develops after CPB, but we certainly have used it in a few cases in which this syndrome developed before the operation.

	References

Top Abstract Introduction Methods Results Discussion Appendix: Discussion References

 

1. Mills SA. Cerebral injury and cardiac operations. Ann Thorac Surg 1993;56(5 suppl):S86-91.
   
2. Kirklin JK. Prospects for understanding and eliminating the deleterious effects of cardiopulmonary bypass. Ann Thorac Surg 1991;51:529-31. [Medline]
   
3. Brigham KL. Mechanisms of lung injury. Eur Respir Rev 1992;2:867-72.
   
4. Hoshikawa-Fujimura AY, Auler JO Jr, Da Rocha TR, Brandizzi LI, Pascual JM, Chamone DA, et al. PAF-acether, superoxide anion and beta-glucuronidase as parameters of polymorphonuclear cell activation associated with cardiac surgery and cardiopulmonary bypass. Braz J Med Biol Res 1989;22:1077-82. [Medline]
   
5. Meadows D, Edwards JD, Wilkins RG, Nightingale P. Reversal of intractable septic shock with norepinephrine therapy. Crit Care Med 1988;16:663-6. [Medline]
   
6. Chernow B, Roth BL. Pharmacologic manipulation of the peripheral vasculature in shock: clinical and experimental approaches. Circ Shock 1986;18:141-55. [Medline]
   
7. Powers FM, Pifarre R, Thomas JX Jr. Ventricular dysfunction in norepinephrine-induced cardiomyopathy. Circ Shock 1994;43:122-9. [Medline]
   
8. Grollman A, Geiling EM. The cardiovascular and metabolic reactions of man to the intramuscular injection of posterior pituitary liquid (pituitrin), pitressin, and pitocin. J Pharmacol Exp Ther 1932;46:447-60. [Abstract/Free Full Text]
   
9. Aisenbrey GA, Handelman WA, Arnold P, Manning M, Schrier RW. Vascular effects of arginine vasopressin during fluid deprivation in the rat. J Clin Invest 1981;67:961-8.
   
10. Schwartz J, Reid IA. Effect of vasopressin blockade on blood pressure regulation during hemorrhage in conscious dogs. Endocrinology 1981;108:1778-80.
    
11. Landry DW, Levin HR, Gallant EM, Ashton RC Jr, Seo S, D'Alessandro DA, et al. Vasopressin deficiency in vasodilatory septic shock. Crit Care Med 1997;25:1279-82. [Medline]
    
12. Argenziano M, Choudhri AF, Moazami N, Levin H, Landry DW, Oz MC. A prospective randomized trial of arginine vasopressin in the treatment of vasodilatory shock after left ventricular assist device placement. Circulation 1997;96(suppl 2):II286-90.
    
13. Feddersen K, Aurell M, Delin K, Haggendal J, Aren C, Radegran K. Effects of cardiopulmonary bypass and prostacyclin on plasma catecholamines, angiotensin II and arginine vasopressin. Acta Anaesthesiol Scand 1985;29:224-30. [Medline]
    
14. Tan CK, Glisson SN, El-Etr AA, Ramakrishnaiah KB. Levels of circulating norepinephrine and epinephrine before, during and after cardiopulmonary bypass in man. J Thorac Cardiovasc Surg 1976;71:928-31. [Abstract]
    
15. Agnoletti G, Scotti C, Panzali AF, Ceconi C, Curello S, Alfieri O, et al. Plasma levels of atrial natriuretic factor (ANF) and urinary excretion on ANF, arginine vasopressin and catecholamines in children with congenital heart disease: effect of cardiac surgery. Eur J Cardiothorac Surg 1993;7:533-9. [Abstract]
    
16. Kuan P, Messenger JC, Ellestad MH. Transient central diabetes insipidus after aortocoronary bypass operations. Am J Cardiol 1983;52:1181-3. [Medline]
    
17. Robinson RO, Pagliero KM. Polyuria after cardiac surgery. BMJ 1970;3:265-6.
    
18. Egener TH, Comunale ME, Leckie RS. The use of a somatostatin analog in the treatment of refractory hypotension after cardiopulmonary bypass. J Cardiothorac Vasc Anesth 1992;6:458-60. [Medline]
    
19. Thaker U, Geary V, Chalmers P, Sheikh F. Low systemic vascular resistance during cardiac surgery: case reports, brief review, and management with angiotensin II. J Cardiothorac Anesth 1990;4:360-3. [Medline]
    
20. Woods WG, Forsling ML, LeQuesne LP. Plasma arginine vasopressin levels and arterial pressure during open heart surgery. Br J Surg 1989;76:29-32. [Medline]
    
21. Jones CW, Pickering BT. Comparison of the effects of water deprivation and sodium chloride imbibition on the hormone content of the neurohypophysis of the rat. J Physiol 1969;203:449-58. [Abstract/Free Full Text]
    
22. Zucker IH, Gorman AJ, Cornish KG, Huffman LJ, Gilmore JP. Influence of left ventricular receptor stimulation om plasma vasopressin in conscious dogs. Am J Physiol 1983;245:R792-9.
    
23. Sehested J, Wacker B, Forssmann WG. Natriuresis after cardiopulmonary bypass: relationship to urodilatin, atrial natriuretic factor, antidiuretic hormone, and aldosterone. J Thorac Cardiovasc Surg 1997;114:666-71. [Abstract/Free Full Text]
    
24. Zerbe RL, Henry DP, Robertson GL. Vasopressin response to orthostatic hypotension: etiologic and clinical implications. Am J Med 1983;74:265-71. [Medline]
    
25. Mohring J, Glanzer K, Maciel JA Jr, Dusing R, Kramer HJ, Arbogast R, et al. Greatly enhanced pressor response to antidiuretic hormone in patients with impaired cardiovascular reflexes due to idiopathic orthostatic hypotension. J Cardiovasc Pharmacol 1980;2:367-76. [Medline]
    
26. Beasley D, Cohen RA, Levinsky NG. Interleukin-1 inhibits contraction of vascular smooth muscle. J Clin Invest 1989;83:331-5.
    
27. Winquist RJ, Faison EP, Waldman SA, Schwartz K, Murad F, Rapoport RM. Atrial natriuretic factor elicits an endothelium-independent relaxation and activates particulate guanylate cyclase in vascular smooth muscle. Proc Natl Acad Sci U S A 1984;81:7661-4. [Abstract/Free Full Text]
    
28. Wakatsuki T, Nakaya Y, Inoue I. Vasopressin modulates K-channel activities of cultured smooth muscle cells from porcine coronary artery. Am J Physiol 1992;283(suppl):H491-6.
    
29. Kusano E, Tian S, Umino T, Tetsuka T, Ando Y, Asano Y. Arginine vasopressin inhibits interleukin-1-beta–stimulated nitric oxide and cyclic guanosine monophosphate production via the V1 receptor in cultured rat vascular smooth muscle cells. J Hypertens 1997;15:627-32. [Medline]
    
30. Nambi P, Whitman M, Gessner G, Aiyar N, Crooke ST. Vasopressin-mediated inhibition of atrial natriuretic factor–stimulated cGMP accumulation in an established smooth muscle cell line. Proc Natl Acad Sci U S A 1986;83:8492-5. [Abstract/Free Full Text]
    

This article has been cited by other articles:

				A. Miceli, R. Capoun, C. Fino, P. Narayan, A. J. Bryan, G. D. Angelini, and M. Caputo Effects of Angiotensin-Converting Enzyme Inhibitor Therapy on Clinical Outcome in Patients Undergoing Coronary Artery Bypass Grafting J. Am. Coll. Cardiol., November 3, 2009; 54(19): 1778 - 1784. [Abstract] [Full Text] [PDF]

				M. A. Levin, H.-M. Lin, J. G. Castillo, D. H. Adams, D. L. Reich, and G. W. Fischer Early On-Cardiopulmonary Bypass Hypotension and Other Factors Associated With Vasoplegic Syndrome Circulation, October 27, 2009; 120(17): 1664 - 1671. [Abstract] [Full Text] [PDF]

				A. Haase-Fielitz, M. Haase, R. Bellomo, G. Lambert, G. Matalanis, D. Story, L. Doolan, B. Buxton, G. Gutteridge, F. C. Luft, et al. Decreased Catecholamine Degradation Associates with Shock and Kidney Injury after Cardiac Surgery J. Am. Soc. Nephrol., June 1, 2009; 20(6): 1393 - 1403. [Abstract] [Full Text] [PDF]

				Z. Cao, Y. Gao, and G. Tao Vasoplegic Syndrome During Liver Transplantation Anesth. Analg., June 1, 2009; 108(6): 1941 - 1943. [Abstract] [Full Text] [PDF]

				X. Sun, L. Zhang, P. C. Hill, R. Lowery, A. T. Lee, R. E. Molyneaux, P. J. Corso, and S. W. Boyce Is incidence of postoperative vasoplegic syndrome different between off-pump and on-pump coronary artery bypass grafting surgery? Eur. J. Cardiothorac. Surg., October 1, 2008; 34(4): 820 - 825. [Abstract] [Full Text] [PDF]

				U. Benedetto, S. Sciarretta, A. Roscitano, B. Fiorani, S. Refice, E. Angeloni, and R. Sinatra Preoperative Angiotensin-Converting Enzyme Inhibitors and Acute Kidney Injury After Coronary Artery Bypass Grafting Ann. Thorac. Surg., October 1, 2008; 86(4): 1160 - 1165. [Abstract] [Full Text] [PDF]

				C. B. Overgaard and V. Dzavik Inotropes and Vasopressors: Review of Physiology and Clinical Use in Cardiovascular Disease Circulation, September 2, 2008; 118(10): 1047 - 1056. [Full Text] [PDF]

				J. A. Russell, K. R. Walley, J. Singer, A. C. Gordon, P. C. Hebert, D. J. Cooper, C. L. Holmes, S. Mehta, J. T. Granton, M. M. Storms, et al. Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock N. Engl. J. Med., February 28, 2008; 358(9): 877 - 887. [Abstract] [Full Text] [PDF]

				J. H. Levy, K. A. Tanaka, and J. M. Bailey Cardiac Surgical Pharmacology Card. Surg. Adult, January 1, 2008; 3(2008): 77 - 110. [Full Text]

				E. Tayama, T. Ueda, T. Shojima, K. Akasu, T. Oda, S. Fukunaga, H. Akashi, and S. Aoyagi Arginine vasopressin is an ideal drug after cardiac surgery for the management of low systemic vascular resistant hypotension concomitant with pulmonary hypertension Interactive CardioVascular and Thoracic Surgery, December 1, 2007; 6(6): 715 - 719. [Abstract] [Full Text] [PDF]

				M. Egi, R. Bellomo, C. Langenberg, M. Haase, A. Haase, L. Doolan, G. Matalanis, S. Seevenayagam, and B. Buxton Selecting a Vasopressor Drug for Vasoplegic Shock After Adult Cardiac Surgery: A Systematic Literature Review Ann. Thorac. Surg., February 1, 2007; 83(2): 715 - 723. [Abstract] [Full Text] [PDF]

				Y. J. Oh, J. H. Lee, S. B. Nam, J. K. Shim, J. H. Song, and Y. L. Kwak Effects of chronic angiotensin II receptor antagonist and angiotensin-converting enzyme inhibitor treatments on neurohormonal levels and haemodynamics during cardiopulmonary bypass Br. J. Anaesth., December 1, 2006; 97(6): 792 - 798. [Abstract] [Full Text] [PDF]

				G. Shanmugam Vasoplegic syndrome--the role of methylene blue Eur. J. Cardiothorac. Surg., November 1, 2005; 28(5): 705 - 710. [Abstract] [Full Text] [PDF]

				M. P Devbhandari, S. K Balasubramanian, M. Codispoti, O. C Nzewi, and S. U Prasad Preoperative Angiotensin-Converting Enzyme Inhibition Can Cause Severe Post CPB Vasodilation Current UK Opinion Asian Cardiovasc Thorac Ann, December 1, 2004; 12(4): 346 - 349. [Abstract] [Full Text] [PDF]

				P. C. Dyke II and J. D. Tobias Vasopressin: Applications in Clinical Practice J Intensive Care Med, July 1, 2004; 19(4): 220 - 228. [Abstract] [PDF]

				J. G. Byrne, M. Leacche, S. Paul, T. Mihaljevic, J. D. Rawn, S. K. Shernan, G. H. Mudge, and L. W. Stevenson Risk factors and outcomes for 'vasoplegia syndrome' following cardiac transplantation Eur. J. Cardiothorac. Surg., March 1, 2004; 25(3): 327 - 332. [Abstract] [Full Text] [PDF]

				R. L. Levin, M. A. Degrange, G. F. Bruno, C. D. Del Mazo, D. J. Taborda, J. J. Griotti, and F. J. Boullon Methylene blue reduces mortality and morbidity in vasoplegic patients after cardiac surgery Ann. Thorac. Surg., February 1, 2004; 77(2): 496 - 499. [Abstract] [Full Text] [PDF]

				D. L. Ngaage Off-pump coronary artery bypass grafting: the myth, the logic and the science Eur. J. Cardiothorac. Surg., October 1, 2003; 24(4): 557 - 570. [Abstract] [Full Text] [PDF]

				M. Poullis, M. Shackcloth, P. R. B. Evora, and F. Viaro Catastrophic Cardiovascular Adverse Reactions to Protamine Chest, July 1, 2003; 124(1): 411 - 412. [Full Text] [PDF]

				R. G. Leyh, T. Kofidis, M. Struber, S. Fischer, K. Knobloch, B. Wachsmann, C. Hagl, A. R. Simon, and A. Haverich Methylene blue: The drug of choice for catecholamine-refractory vasoplegia after cardiopulmonary bypass? J. Thorac. Cardiovasc. Surg., June 1, 2003; 125(6): 1426 - 1431. [Abstract] [Full Text] [PDF]

				P. Motta, E. Mossad, and R. Savage Right Ventricular Exclusion Surgery for Arrhythmogenic Right Ventricular Dysplasia with Cardiomyopathy Anesth. Analg., June 1, 2003; 96(6): 1598 - 1602. [Abstract] [Full Text] [PDF]

				M. W. Dunser, A. J. Mayr, H. Ulmer, H. Knotzer, G. Sumann, W. Pajk, B. Friesenecker, and W. R. Hasibeder Arginine Vasopressin in Advanced Vasodilatory Shock: A Prospective, Randomized, Controlled Study Circulation, May 13, 2003; 107(18): 2313 - 2319. [Abstract] [Full Text] [PDF]

				D. L.S. Morales, M. J. Garrido, J. D. Madigan, D. N. Helman, J. Faber, M. R. Williams, D. W. Landry, and M. C. Oz A double-blind randomized trial: prophylactic vasopressin reduces hypotension after cardiopulmonary bypass Ann. Thorac. Surg., March 1, 2003; 75(3): 926 - 930. [Abstract] [Full Text] [PDF]

				W. J. Gomes, M. R. Erlichman, M. L. Batista-Filho, M. Knobel, D. R. Almeida, A. C. Carvalho, R. Catani, and E. Buffolo Vasoplegic syndrome after off-pump coronary artery bypass surgery Eur. J. Cardiothorac. Surg., February 1, 2003; 23(2): 165 - 169. [Abstract] [Full Text] [PDF]

				J. M. Bailey, K. A. Tanaka, and J. H. Levy Cardiac Surgical Pharmacology Card. Surg. Adult, January 1, 2003; 2(2003): 85 - 118. [Full Text]

				T. N. Albright, M. A. Zimmerman, and C. H. Selzman Vasopressin in the Cardiac Surgery Intensive Care Unit Am. J. Crit. Care., July 1, 2002; 11(4): 326 - 330. [Abstract] [Full Text] [PDF]

				J. H. Levy, J. M. Bailey, and G. M. Deeb Intravenous milrinone in cardiac surgery Ann. Thorac. Surg., January 1, 2002; 73(1): 325 - 330. [Abstract] [Full Text] [PDF]

				A. Tsuda, K. A. Tanaka, C. Huraux, F. Szlam, N. Sato, K. Yamaguchi, and J. H. Levy The In Vitro Reversal of Histamine-Induced Vasodilation in the Human Internal Mammary Artery Anesth. Analg., December 1, 2001; 93(6): 1453 - 1459. [Abstract] [Full Text] [PDF]

				A. C. Schoolwerth, D. A. Sica, B. J. Ballermann, and C. S. Wilcox Renal Considerations in Angiotensin Converting Enzyme Inhibitor Therapy: A Statement for Healthcare Professionals From the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association Circulation, October 16, 2001; 104(16): 1985 - 1991. [Full Text] [PDF]

				A. Albage, J. van der Linden, L. Bengtsson, D. Lindblom, G. Kenneback, and H. Berglund Elevations in antidiuretic hormone and aldosterone as possible causes of fluid retention in the Maze procedure Ann. Thorac. Surg., July 1, 2001; 72(1): 58 - 64. [Abstract] [Full Text] [PDF]

				A. Mekontso-Dessap, R. Houel, C. Soustelle, M. Kirsch, D. Thebert, and D. Y. Loisance Risk factors for post-cardiopulmonary bypass vasoplegia in patients with preserved left ventricular function Ann. Thorac. Surg., May 1, 2001; 71(5): 1428 - 1432. [Abstract] [Full Text] [PDF]

				D. P. Taggart, M. Dipp, S. Mussa, and P. C. G. Nye Phenoxybenzamine prevents spasm in radial artery conduits for coronary artery bypass grafting J. Thorac. Cardiovasc. Surg., October 1, 2000; 120(4): 815 - 817. [Full Text] [PDF]

				M. P. Talbot, I. Tremblay, A. Y. Denault, and S. Belisle Vasopressin for refractory hypotension during cardiopulmonary bypass J. Thorac. Cardiovasc. Surg., August 1, 2000; 120(2): 401 - 402. [Full Text] [PDF]

				M. Poullis Vasodilatation after cardiac surgery J. Thorac. Cardiovasc. Surg., April 1, 2000; 119(4): 857 - 857. [Full Text]

				D. L.S. Morales, D. Gregg, D. N. Helman, M. R. Williams, Y. Naka, D. W. Landry, and M. C. Oz Arginine vasopressin in the treatment of 50 patients with postcardiotomy vasodilatory shock Ann. Thorac. Surg., January 1, 2000; 69(1): 102 - 106. [Abstract] [Full Text] [PDF]

				Vasopressin: A Novel Agent for Postoperative Vasodilatory Shock Journal Watch Cardiology, January 15, 1999; 1999(115): 6 - 6. [Full Text]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Michael Argenziano Asim F. Choudhri Eric A. Rose Mehmet C. Oz Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Argenziano, M. Articles by Oz, M. C. Search for Related Content PubMed PubMed Citation Articles by Argenziano, M. Articles by Oz, M. C.