JTCS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Shin Takabayashi
Koji Onoda
Hideto Shimpo
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yokoyama, K.
Right arrow Articles by Shimpo, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yokoyama, K.
Right arrow Articles by Shimpo, H.
Related Collections
Right arrow Cardiac - pharmacology
Right arrow Congenital - acyanotic
Right arrow Congenital - cyanotic
Right arrow Extracorporeal circulation

J Thorac Cardiovasc Surg 2009;137:730-735
© 2009 The American Association for Thoracic Surgery

Cardiopulmonary Support

Removal of prostaglandin E2 and increased intraoperative blood pressure during modified ultrafiltration in pediatric cardiac surgery

Kazuto Yokoyama, MDa, Shin Takabayashi, MD, PhDa,*, Takuya Komada, MD, PhDa, Koji Onoda, MD, PhDa, Yoshihide Mitani, MD, PhDb, Hideki Iwata, MEc, Hideto Shimpo, MD, PhDa

a Department of Thoracic and Cardiovascular Surgery, Mie University Graduate School of Medicine, Tsu, Japan
b Department of Pediatrics, Mie University Graduate School of Medicine, Tsu, Japan
c Medical Engineer Room, Mie University Graduate School of Medicine, Tsu, Japan

Received for publication March 25, 2008; revisions received August 1, 2008; accepted for publication September 4, 2008.

* Address for reprints: Shin Takabayashi, MD, PhD, Department of Thoracic and Cardiovascular Surgery, Mie University Graduate School of Medicine, 2-174, Edobashi, Tsu, Mie 514-8507, Japan. (Email: shin1111{at}clin.medic.mie-u.ac.jp).


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Objective: We investigated the relationship between serum prostaglandin E2 and intraoperative blood pressure in pediatric cardiac surgery with modified ultrafiltration.

Methods: In 35 consecutive patients (31.6 ± 26.8 months, 0.4–111 months, 10.9 ± 5.5 kg, 2.9–23.8 kg) who underwent cardiac surgery with modified ultrafiltration, we measured intraoperative serum prostaglandin E2 changes and effluent prostaglandin E2, assessed the relationship between serum prostaglandin E2 and intraoperative hemodynamic parameters, and performed subset analyses to compare patients with low (<10 kg, n = 18) and high (>10 kg, n = 10) weights.

Results: During cardiopulmonary bypass, systolic blood pressure decreased from 80.8 ± 15.2 to 60.5 ± 11.3 mm Hg (P = .00000002979) and serum prostaglandin E2 increased from 16.6 ± 8.7 to 58.8 ± 53.3 pg/mL (P = .002). During modified ultrafiltration, although central venous pressure and catecholamine dosage transited at the same levels, systolic blood pressure increased from 60.5 ± 11.3 to 83.4 ± 14.1 mm Hg (P = .00000002979) and serum prostaglandin E2 decreased from 58.8 ± 53.3 to 21.1 ± 11.6 pg/mL (P = .001), with negative correlation between serum prostaglandin E2 and systolic blood pressure (R = –0.392, P = .0000277723) and 15,700 ± 10,700 pg (1790 ± 2230 pg/kg) prostaglandin E2 removed during modified ultrafiltration. Decrease in serum prostaglandin E2 was significantly higher in low-weight patients (51.8 ± 58.4 pg/mL) than in high-weight patients (15.7 ± 30.1 pg/mL).

Conclusion: Removal of prostaglandin E2 is one reason for increased blood pressure during modified ultrafiltration, with the effect more marked in low-weight patients.

Abbreviations and Acronyms BP = blood pressure; CPB = cardiopulmonary bypass; CVP = central venous pressure; DD = dopamine dosage; HR = heart rate; MUF = modified ultrafiltration; PGE2 = prostaglandin E2


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Modified ultrafiltration (MUF) was developed as a method to reduce the adverse effects of cardiopulmonary bypass (CPB) in pediatric patients.1Go In pediatric cardiac surgery with CPB, MUF has been reported not only to reduce total body water and decrease pulmonary vascular resistance but also to increase blood pressure (BP).2Go The mechanism for the increase in BP during MUF, however, remains unclear. The removal of interleukins 6 and 83Go and endothelin 14Go during MUF was reported in previous studies; however, these changes could not explain the increase in BP during a short period of MUF. In this study, we hypothesized that a major cause of the increase in BP is removal of some vasodilator by MUF. We therefore investigated the effects of MUF on the relationship between the serum prostaglandin E2 (PGE2) level that is activated through exposure of blood to artificial material during CPB and intraoperative BP in pediatric cardiac surgery.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
In this study, we assessed 35 consecutive patients who underwent pediatric cardiac surgery with CPB and MUF from October 2005 to September 2007. Informed consent to measure the serum PGE2 level and the PGE2 level in the MUF discharge had been obtained from the parents. The age, weight, and operative procedure data are shown in Table 1 . Exclusion criterion was body weight greater than 25 kg to ensure investigation of a pediatric population.


View this table:
[in this window]
[in a new window]

  		Table 1 Patient profiles
 
For pediatric cardiac surgery, we generally use four kinds of CPB circuit adapted for different body weights. In this study, CPB was performed with an SS circuit (priming volume 350 mL/circuit; Senko Medical Co, Ltd, Osaka, Japan; artificial lung baby-RX; Terumo Corporation, Tokyo, Japan) for body weights smaller than 7 kg, an S circuit (priming volume 500 mL/circuit; Senko; artificial lung D-902 Lilliput II; Dideco SpA, Mirandola, Italy) for body weights between 7 and 20 kg, and an M circuit (priming volume 700 mL/circuit; Senko; artificial lung CAPIOX RX-15; Terumo) for body weights greater than 20 kg. The CPB flow was maintained at 2.8 L/(m2/min) during cardiac arrest, and an {alpha}-blocker (chlorpromazine) was administered several times to a total dosage of 2 to 4 mg/kg. Initial blood priming was performed when the predicted hematocrit during CPB was lower than 15%, which was the criterion in a previous study.5Go Blood transfusion during CPB was performed to ensure a hematocrit greater than 30% at the end of the CPB. Cardiac arrest was obtained by crystalloid cardioplegia with added albumin. The CPB time, aortic crossclamp time, and amount of intraoperative blood transfusion are also shown in Table 1.

MUF was performed with a hemoconcentrator (CF04; JMS Co, Ltd, Hiroshima, Japan) connected to the CPB circuit in all cases. After CPB, we performed MUF through aortic and inferior venous caval cannulas with the same routes used for CPB. The blood was taken from the body through the aortic cannulas and hemofiltered. The remaining blood in the CPB reservoir and the hemofiltered blood were returned to the body through the inferior venous caval cannula. The MUF flow was 10 mL/(kg/min), and the time was 15 minutes. Diluted ultrafiltration with 1000 mL crystalloid solution was performed concomitantly during the CPB.

Many chemomediators are increased by an inflammatory reaction during pediatric heart surgery with CPB, and these chemomediators could act as vasodilators. A kallikrein–kinin system is one of the inflammatory systems, and prostaglandin E2 (PGE2) is one of the substances produced through activation of the kallikrein–kinin system during CPB (Figure 1 ). PGE2 has a low molecular weight and thus is removed through the membrane of the filter. We therefore measured the serum PGE2 level at the following four times (n = 28): before (before CPB) and after (end CPB) the CPB, after the MUF (end MUF), and after the operation (postoperative). Changes in systolic BP measured by an arterial line, central venous pressure (CVP) measured by a central venous catheter, heart rate (HR), and dopamine dosage (DD) were assessed from anesthesia records at the same four times as the measurement of the serum PGE2 level. Additionally, to confirm that PGE2 had been removed to MUF discharge, the PGE2 level in the discharge and the total PGE2 removed into the discharge during MUF were also investigated (n = 12).


Figure 1
View larger version (8K):
[in this window]
[in a new window]

  		Figure 1. Kallikrein–kinin system and prostaglandin E2.

 
Correlation analyses between the serum PGE2 level and BP, CVP, HR, and DD and between BP and CVP, HR, and DD were performed. Because the adverse effects of CPB are increased in low-weight patients,6-10Go we divided the patients into two groups by body weight: less than 10 kg (group L, n = 18) and greater than 10 kg (group H, n = 10). Subset analyses between the two groups were performed.

After collection, blood samples were centrifuged at 3000 rpm for 5 minutes. Plasma was then separated and stored at –70°C until analysis. Discharge samples were treated in the same way as blood samples. The PGE2 level was measured with a commercially available radioimmunoassay kit (PerkinElmer Life and Analytical Sciences, Inc, Waltham, Mass).

Comparisons between two values were performed with unpaired 2-tailed t tests for the means of normally distributed variables and Wilcoxon rank sum tests for skewed data. Correlation coefficients were used to assess the correlations between BP and vasodilator level. A correlation coefficient R between –0.30 and 0.30 was considered to indicate a poor correlation. All the statistical analyses were performed with the statistical software package SPSS 12.0 J (SPSS Inc, Chicago, Ill) software for Windows (Microsoft Corporation, Redmond, Wash). All data are expressed as mean ± SD.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
The HR increased during CPB from 126 ± 18 beats/min before CPB to 149 ± 24 beats/min at end CPB (P = .0000356305), and no significant differences were observed after end MUF CPB (146 ± 21 beats/min postoperative 149 ± 24 beats/min). The CVP showed no significant changes during the procedure (7.8 ± 2.1 mm Hg before CPB, 9.1 ± 3.5 mm Hg at end CPB, 9.4 ± 4.1 mm Hg at end MUF, and 10.3 ± 3.6 mm Hg postoperative). The DD increased from 0.5 ± 1.6 µg/(kg/min) before CPB to 6.5 ± 2.3 µg/(kg/min) at end CPB (P = .0000000000000000008262). No significant differences, however, were observed after CPB (end MUF 6.3 ± 2.1 µg/[kg/min], postoperative 6.0 ± 1.9 µg/[kg/min].

The systolic BP decreased during CPB from 80.8 ± 15.2 mm Hg before CPB to 60.5 ± 11.3 mm Hg at end CPB (P = .00000002979). During MUF, however, systolic BP increased significantly to 83.4 ± 14.1 mm Hg at end MUF (P = .000000002802). After that, no significant difference was observed between end MUF and postoperative (84.0 ± 14.5 mm Hg) values (Figure 2 ).


Figure 2
View larger version (10K):
[in this window]
[in a new window]

  		Figure 2. Change in systolic blood pressure during operation. Asterisk indicates P < .01. MUF, Modified ultrafiltration; CPB, cardiopulmonary bypass; Postop, after operation.

 
The serum PGE2 level increased during CPB from 16.6 ± 8.7 pg/mL before CPB to 58.8 ± 53.3 pg/mL at end CPB (P = .002). During MUF, however, the serum PGE2 level decreased significantly to 21.1 ± 11.6 pg/mL at end MUF (P = .001); it also showed a tendency to be lower at the postoperative point (15.4 ± 9.7 pg/mL, P = .06) than at end MUF (Figure 3 ). The transitional pattern seen Figure 3 (serum PGE2) is much like a reversal of the transitional pattern seen in Figure 2 (systolic BP).


Figure 3
View larger version (10K):
[in this window]
[in a new window]

  		Figure 3. Change in serum prostaglandin E2 level during operation. Asterisk indicates P < .01. MUF, Modified ultrafiltration; CPB, cardiopulmonary bypass; Postop, after operation.

 
The mean amount of the discharge from MUF, the PGE2 level in the MUF discharge, total PGE2 in the MUF discharge, and PGE2 in MUF discharge per body weight are shown in Table 2 . During MUF, a large quantity of PGE2 was removed to the MUF discharge by ultrafiltration.


View this table:
[in this window]
[in a new window]

  		Table 2 Prostaglandin E2 in the modified ultrafiltration discharge
 
In correlation analyses, there was a significant negative correlation between serum PGE2 level and systolic BP (R = –0.392, y = –0.1801x + 79.7, P < .001; Figure 4 ). Although analyses between other parameters were performed, there were no correlations between serum PGE2 level and diastolic BP, CVP, HR, and DD or between BP (systolic and diastolic) and CVP, HR, and DD. During MUF, the serum PGE2 level was lower and the systolic BP was higher in almost all patients (Figure 5 ).


Figure 4
View larger version (11K):
[in this window]
[in a new window]

  		Figure 4. Correlation between serum prostaglandin E2 level and systolic blood pressure during operation. There was negative correlation between serum prostaglandin E2 level and systolic blood pressure (R = –0.392, y = –0.1801x + 79.7, P < .01).

 

Figure 5
View larger version (17K):
[in this window]
[in a new window]

  		Figure 5. Changes in serum prostaglandin E2 levels and systolic blood pressure during modified ultrafiltration (MUF). In almost all cases, serum prostaglandin E2 level decreased and systolic BP increased during modified ultrafiltration.

 
In subset analyses, the blood transfusion per body weight (67.7 ± 42.8 mL/kg in group L vs 21.2 ± 29.3 mL/kg in group H), the priming volume per body weight (58.8 ± 17.1 mL/kg in group L vs 35.2 ± 7.0 mL/kg in group H), and the area of CPB circuit per body weight (0.35 ± 0.11 m2/kg in group L vs 0.22 ± 0.05 m2/kg in group H) were all significantly larger in group L than in group H (P < .001).

In each group, systolic BP decreased during CPB, from 73.9 ± 10.7 mm Hg in group L and 89.7 ± 15.8 mm Hg in group H before CPB to 57.5 ± 12.1 mm Hg in group L and 64.6 ± 9.3 mm Hg in group H at end CPB (P = .0000836278984 in group L and .00000603 in group H), and systolic BP in group H was higher than in group L before CPB (P = .002). During MUF, systolic BP in each group increased, to 82.4 ± 12.3 mm Hg in group L and 85.2 ± 15.9 mm Hg in group H at end MUF; values were thereafter maintained at the same level to the postoperative measurement (87.1 ± 17.0 mm Hg in group L and 81.9 ± 11.6 mm Hg in group H).

In group L, the serum PGE2 level increased significantly during CPB from 16.7 ± 8.6 before CPB to 72.8 ± 58.1 pg/mL at end CPB (P = .000758); in group H, however, there was no significant difference between values of 15.6 ± 9.2 pg/mL before CPB and 32.5 ± 30.8 pg/mL at end CPB. At end CPB, the serum PGE2 level was significantly higher in group L than in group H (P = .02). In group L, the serum PGE2 level decreased significantly during MUF to 23.9 ± 12.5 pg/mL at end MUF (P = .04); in group H, however, this value was not significantly lower at end MUF (16.2 ± 7.6 pg/mL). After that, no significant differences were observed between end MUF and postoperative values (17.1 ± 11.0 pg/mL in group L and 12.4 ± 5.9 pg/mL in group H).

In correlation analyses, although there was a significant negative correlation between serum PGE2 level and systolic BP in group L (R = –0.433, P < .001, y = –0.191x + 82.3), there was no significant correlation in group H. The decrease in serum PGE2 during MUF was larger in group L than in group H (51.8 ± 58.4 pg/mL in group L vs 15.7 ± 30.1 pg/mL in group H, P = .04), and the amount of PGE2 in the MUF discharge per body weight was also larger in group L than in group H (3020 ± 2550 pg/kg in group L vs 930 ± 420 pg/kg in group H, P = .1) (Figure 6 ).


Figure 6
View larger version (12K):
[in this window]
[in a new window]

  		Figure 6. Subset analysis by body weight. Asterisk indicates P < .01. Group L, Patients with body weight <10 kg; Group H, patients with body weight >10 kg; MUF, modified ultrafiltration; N.S., not significant; CPB, cardiopulmonary bypass; Postop, after operation.

 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
MUF has been reported to have several clinical benefits: increasing intraoperative BP,11,12Go reducing the incidence of pleural or pericardial effusion, and shortening hospital stay13Go and duration of ventilatory support.14Go With regard to the reason that MUF induces these clinical improvements, two major contrasting effects can be suggested, "concentration" or "removal" of some factor or factors in the blood. For example, increases in the hematocrit, fibrinogen, or total plasma protein15,16Go during MUF would be brought about by concentration, whereas decreases in interleukin 6 or 8 or in tumor necrosis factor {alpha}3 would occur through removal.

Although it has been suggested that the increase in BP during MUF might result in part from improvements in myocardial contractility associated with a reduction in myocardial water content,2Go the precise mechanism for any increase in BP remains unclear. During MUF, the removal of serum PGE2 could decrease cardiac index in response to an increase in cardiac afterload. Although systolic BP increased during MUF in this study, we did not examine whether cardiac index increased. A previous study, however, showed that ventricular systolic function improved during MUF as a result of reduced myocardial edema.17Go We suppose that increased cardiac index would be brought by improved ventricular function despite increased afterload caused by removal of PGE2 during MUF. An earlier study of ours showed that systolic BP was not correlated with increased hematocrit after MUF, and there was also no correlation between the percentage increases in systolic BP and hematocrit, suggesting that the rise in hematocrit was unlikely to be responsible for the increased BP after MUF.11Go To investigate the major reason for the increase in BP during MUF, in this study we therefore paid attention to another effect, the removal of a major vasodilator.

PGE2 production is stimulated by the kallikrein–kinin system,18Go which is activated through the exposure of blood to artificial materials during CPB.19,20Go Additionally, PGE2 is a major intrinsic vasodilator, and a relationship has been reported between increased serum PGE2 levels and decreased BP in patients with intraoperative hypotension under conditions of CPB21Go and hemodialysis.22Go As in a previous report of coronary artery bypass grafting with CPB in adult patients,23Go our study found that the serum PGE2 level increased and systolic BP decreased significantly during CPB in pediatric patients. In contrast, during MUF, the serum PGE2 level decreased and systolic BP increased significantly. Additionally, with respect to the relationship between serum PGE2 level and systolic BP, there was a significant negative correlation.

During MUF, we used the JMS CF04 membrane for ultrafiltration; this has a screening coefficient that allows the passage of 90% of molecules 5000 Da in molecular size and 50% of molecules 10,000 Da in molecular size. PGE2 (352 Da in molecular size) will theoretically be removed almost entirely through the membrane during ultrafiltration. The serum PGE2 level in our study, however, remained above the reference range even after MUF. Possible explanations for this are that PGE2 production may be increased under rewarming of body temperature during MUF24Go and that limited MUF flow can not ultrafilter all the body's blood.

In this study, a large amount of PGE2, 15700 ± 10700 pg (1790 ± 2230 pg/kg) was removed by discharge during MUF, while at the same time systolic BP increased. In the light of these results, there is strong evidence that one reason for the decrease in serum PGE2 is removal by MUF. The predicted total amount of PGE2 decreased during MUF, however, was as follows: 10.9 (mean body weight in kilograms) x 80 (mean circulated blood in mL/kg) x (58.8 – 21.1 [mean serum PGE2 level during MUF in pg/mL]) = 32,874 pg. Therefore about 50% of the predicted total amount of PGE2 would have been expected to be removed through the ultrafiltration membrane during MUF in this study. The rest of the decrease in PGE2 during MUF would have to be due to inactivation or removal by other means, such as short-term inactivation by enzymatic action25Go in the lungs,26Go excretion to urine,27Go and adsorption onto the membrane of the ultrafiltration or artificial CPB circuit, as with cytokine removal by a polymethymethacrylate membrane hemofilter.28Go Although in our method of MUF (performed with blood derived from the aorta and returned into the inferior vena cava) the pulmonary to systemic perfusion ratio theoretically could become higher during MUF than after MUF, which might bring about greater lung inactivation of serum PGE2, we unfortunately have no data on this. Furthermore, we did not measure preoperative PGE2 level in this study. A previous study of evaluating the serum PGE2 level, however, showed that mean serum PGE2 level before oral PGE2 administration was 45 ± 33 pg/mL in infants 27 ± 9.0 days old with pulmonary atresia and patent ductus arteriosus,29Go and mean serum PGE2 level during the first 2 days after birth was 12.4 ± 6.8 pg/mL in patients with patent ductus arteriosus.30Go To investigate the effect of the difference in morphology, we performed another subset analysis of the patients with univentricular morphology (n = 6) and biventricular morphology (n = 22). The results showed that the increase in serum PGE2 level and the decrease in systolic BP during CPB tended to be lower in the patients with univentricular morphology than in those with biventricular morphology. We suspect that the reason for the tendency for serum PGE2 to be lower in the patients with univentricular morphology may be increased pulmonary blood flow from collateral arteries developed as a result of preoperative cyanosis. Further investigation to clarify the mechanism of the decrease in serum PGE2 level during MUF is therefore warranted.

It has been reported that large priming volumes produce deleterious hemodynamic effects and postoperative cardiopulmonary dysfunction.6,7Go In our subset analysis by body weight, the amount of blood transfused per body weight, priming volume per body weight, and area of CPB circuit per body weight were larger in group L patients (<10 kg) than in group H patients. Previous studies have demonstrated that increased priming volume8,9Go or blood product transfusion10Go enhances inflammatory response to CPB. It was suggested that the greater invasiveness of using CPB in low-weight patients would result in an increased serum PGE2 level from the greater production of PGE2 that in turn produces a greater decrease in BP. Interestingly, the decrease of serum PGE2 during MUF was larger in group L than in group H; this because the increased serum PGE2 levels of the smaller patients decreased to the same level as those of the other patients after MUF. These results suggest that the effect of PGE2 removal by MUF on increased serum PGE2 levels would be greater in low-weight patients.

Several limitations of this study should be noted. This study was not randomized and did not have a control group, because it is our policy that MUF should be performed for all pediatric patients undergoing cardiac surgery with CPB and that the benefits of MUF must be provided to all these patients. In this study, the circuits, priming volumes, morphology, pulmonary to systemic perfusion ratio, age, and weight were not standardized, because the number of patients was not large enough. There were the problems of the relatively small size of the study with a diverse range of anomalies and widely range of age and weight. This was a pilot study to define the effectiveness of the MUF and to examine the removal and reduction in PGE2 during MUF; standardization of these factors should therefore be performed in the future. Although statistical significance was obtained, the SD of serum PGE2 at the end of CPB became large, because various types of patients with various ages, body weights, and diagnoses (many pathologies, with univentricular as well as biventricular physiology) were included in our study. An uncontrolled bias may have been induced, because CPB circuits change according to the body surface area of the patient. In this study, the circuits, priming volumes, morphology, and pulmonary to systemic perfusion ratio were not standardized, because the number of patients was not large enough. Although BP is regulated by various vasoactive substances, only PGE2 was measured in our study, and we did not assess whether the cardiac index might be improved during MUF because of a reduction in cardiac edema.

In conclusion, serum PGE2 level decreased and systolic BP increased during MUF, with no change in the CVP and DD. There was a negative correlation between intraoperative serum PGE2 levels and systolic BP. A large quantity of PGE2 was filtered out during MUF, resulting in a decrease in serum PGE2. These results suggested that the decrease in serum PGE2 levels caused by removal of PGE2 is one of the reasons for the increase in BP seen during MUF. PGE2 removal by MUF is more effective in low-weight patients and may counteract the more marked increase in serum PGE2 levels caused by CPB in these patients.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Naik SK, Knight A, Elliott M. A prospective randomized study of a modified technique of ultrafiltration during pediatric open-heart surgery. Circulation 1991;84:422-431.
  2. Elliott MJ. Ultrafiltration and modified ultrafiltration in pediatric open heart operations. Ann Thorac Surg 1993;56:1518-1522.[Medline]
  3. Grünenfelder J, Zünd G, Schoeberlein A, Maly FE, Schurr U, Guntli S, et al. Modified ultrafiltration lowers adhesion molecule and cytokine levels after cardiopulmonary bypass without clinical relevance in adults. Eur J Cardiothorac Surg 2000;17:77-83.[Abstract/Free Full Text]
  4. Huang H, Yao T, Wang W, Zhu D, Zhang W, Chen H, et al. Continuous ultrafiltration attenuates the pulmonary injury that follows open heart surgery with cardiopulmonary bypass. Ann Thorac Surg 2003;76:136-140.[Abstract/Free Full Text]
  5. Ando M, Takahashi Y, Suzuki N. Open heart surgery for small children without homologous blood transfusion by using remote pump head system. Ann Thorac Surg 2004;78:1717-1722.[Abstract/Free Full Text]
  6. Lau CL, Posther KE, Stephenson GR, Lodge A, Lawson JH, Darling EM, et al. Mini-circuit cardiopulmonary bypass with vacuum assisted venous drainage: feasibility of an asanguineous prime in the neonate. Perfusion 1999;14:389-396.[Abstract/Free Full Text]
  7. Wabeke E, Elstrodt JM, Mook PH, Gathier S, Wildevuur CR. Clear prime for infant cardiopulmonary bypass: a miniaturized circuit. J Cardiovasc Surg 1988;29:117-122.[Medline]
  8. Miyaji K, Miyamoto T, Kohira S, Nakashima K, Inoue N, Sato H, et al. Miniaturized cardiopulmonary bypass system in neonates and small infants. Interact Cardiovasc Thorac Surg 2008;7:75-79.[Abstract/Free Full Text]
  9. Jansen PG, te Velthuis H, Bulder ER, Paulus R, Scheltinga MR, Eijsman L, et al. Reduction in prime volume attenuates the hyperdynamic response after cardiopulmonary bypass. Ann Thorac Surg 1995;60:544-550.[Abstract/Free Full Text]
  10. Karamlou T, Schultz JM, Silliman C, Sandquist C, You J, Shen I, et al. Using a miniaturized circuit and an asanguineous prime to reduce neutrophil-mediated organ dysfunction following infant cardiopulmonary bypass. Ann Thorac Surg 2005;80:6-14.[Abstract/Free Full Text]
  11. Takabayashi S, Shimpo H, Yokoyama K. Relationship between increased blood pressure and hematocrit during modified ultrafiltration for pediatric open heart surgery. Gen Thorac Cardiovasc Surg 2007;55:12-18.[Medline]
  12. Kiziltepe U, Uysalel A, Corapcioglu T, Dalva K, Akan H, Akalin H. Effects of combined conventional and modified ultrafiltration in adult patients. Ann Thorac Surg 2001;71:684-693.[Abstract/Free Full Text]
  13. Koutlas TC, Gaynor JW, Nicolson SC, Steven JM, Wernovsky G, Spray TL. Modified ultrafiltration reduces postoperative morbidity after cavopulmonary connection. Ann Thorac Surg 1997;64:37-43.[Abstract/Free Full Text]
  14. Bando K, Turrentine MW, Vijay P, Sharp TG, Sekine Y, Lalone BJ, et al. Effect of modified ultrafiltration in high-risk patients undergoing operations for congenital heart disease. Ann Thorac Surg 1998;66:821-828.[Abstract/Free Full Text]
  15. Friesen RH, Campbell DN, Clarke DR, Tornabene MA. Modified ultrafiltration attenuates dilutional coagulopathy in pediatric open heart operations. Ann Thorac Surg 1997;64:1787-1789.[Abstract/Free Full Text]
  16. Ootaki Y, Yamaguchi M, Oshima Y, Yoshimura N, Oka S. Effects of modified ultrafiltration on coagulation factors in pediatric cardiac surgery. Surg Today 2002;32:203-206.[Medline]
  17. Davies MJ, Nguyen K, Gaynor JW, Elliott MJ. Modified ultrafiltration improves left ventricular systolic function in infants after cardiopulmonary bypass. J Thorac Cardiovasc Surg 1998;115:361-370.[Abstract/Free Full Text]
  18. Colman RW, Schmaier AH. Contact system: a vascular biology modulator with anticoagulant, profibrinolytic, antiadhesive, and proinflammatory attributes. Blood 1997;90:3819-3843.[Free Full Text]
  19. Campbell DJ, Dixon B, Kladis A, Kemme M, Santamaria JD. Activation of the kallikrein-kinin system by cardiopulmonary bypass in humans. Am J Physiol Regul Integr Comp Physiol 2001;281:R1059-R1070.[Abstract/Free Full Text]
  20. Downing SW, Edmunds Jr. LH. Release of vasoactive substances during cardiopulmonary bypass. Ann Thorac Surg 1992;54:1236-1243.[Abstract/Free Full Text]
  21. Takewa Y, Seki T, Tatsumi E, Taenaka Y, Takano H. Prostaglandin synthesis inhibitor improves hypotension during normothermic cardiopulmonary bypass. ASAIO J 2001;47:673-676.[Medline]
  22. Schultze G, Maiga M, Neumayer HH, Wagner K, Keller F, Molzahn M, et al. Prostaglandin E2 promotes hypotension on low-sodium hemodialysis. Nephron 1984;37:250-256.[Medline]
  23. Lavee J, Naveh N, Dinbar I, Shinfeld A, Goor DA. Prostacyclin and prostaglandin E2 mediate reduction of increased mean arterial pressure during cardiopulmonary bypass by aspiration of shed pulmonary venous blood. J Thorac Cardiovasc Surg 1990;100:546-551.[Abstract]
  24. Ohata T, Sawa Y, Kadoba K, Masai T, Ichikawa H, Matsuda H. Effect of cardiopulmonary bypass under tepid temperature on inflammatory reactions. Ann Thorac Surg 1997;64:124-128.[Abstract/Free Full Text]
  25. Piper PJ, Vane JR, Wyllie JH. Inactivation of prostaglandins by the lungs. Nature 1970;225:600-604.[Medline]
  26. Ferreira SH, Vane JR. Prostaglandins: their disappearance from and release into the circulation. Nature 1967;216:868-873.[Medline]
  27. Ignatowska-Switalska H, Januszewicz P. Urinary prostaglandins E2 and F2{alpha} in healthy newborns, infants, children, and adults. Prostaglandins Med 1980;5:289-296.[Medline]
  28. Hirasawa H, Oda S, Matsuda K. Continuous hemodiafiltration with cytokine-adsorbing hemofilter in the treatment of severe sepsis and septic shock. Contrib Nephrol 2007;156:365-370.[Medline]
  29. Silove ED, Coe JY, Shiu MF, Brunt JD, Page AJ, Singh SP, et al. Oral prostaglandin E2 in ductus-dependent pulmonary circulation. Circulation 1981;63:682-688.[Abstract/Free Full Text]
  30. Clyman RI, Brett C, Mauray F. Circulating prostaglandin E2 concentrations and incidence of patent ductus arteriosus in preterm infants with respiratory distress syndrome. Pediatrics 1980;66:725-729.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 PerfusionHome page
S. Wang, D. Palanzo, and A. Undar
Current ultrafiltration techniques before, during and after pediatric cardiopulmonary bypass procedures
Perfusion, September 1, 2012; 27(5): 438 - 446.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Shin Takabayashi
Koji Onoda
Hideto Shimpo
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yokoyama, K.
Right arrow Articles by Shimpo, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yokoyama, K.
Right arrow Articles by Shimpo, H.
Related Collections
Right arrow Cardiac - pharmacology
Right arrow Congenital - acyanotic
Right arrow Congenital - cyanotic
Right arrow Extracorporeal circulation

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS