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

This Article Full Text 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 Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Saldanha, C. Articles by Hearse, D. J. Search for Related Content PubMed PubMed Citation Articles by Saldanha, C. Articles by Hearse, D. J.

J Thorac Cardiovasc Surg 1994;108:279-290
© 1994 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Cardioplegia and vascular injuryDissociation of the effects of ischemia from those of the cardioplegic solution

London, United Kingdom

Supported by The Special Trustees for St. Thomas' Hospital.

Received for publication Aug. 5, 1993. Accepted for publication Feb. 4, 1994. Address for reprints: Clyde Saldanha, FRCS (Ed), Department of Cardiothoracic Surgery, St. Bartholomew's Hospital, London EC1A 7BE, United Kingdom.

Abstract

Although cardioplegic solutions successfully protect myocardial contractile cells against ischemic injury, their effect on the vasculature remains controversial. To address this we used a vascular bed preparation (isolated rat mesentery) that permits the study of vascular function without the coincident changes in contractile status that affect vascular tone (and hence the assessment of vascular function in isolated hearts). Smooth muscle cell contraction was assessed by measurement of the vasoconstrictor response to phenylephrine, and relaxation was assessed by measurement of the vasodilator responses to sodium nitroprusside and the endothelium-dependent relaxant adenosine triphosphate. After characterization of basal vascular function, mesenteries were subjected to normothermic ischemia for 60, 90, 120, 150, and 180 minutes (n = 12 for each time period; 6 preparations were subjected to ischemia alone and 6 to ischemia preceded by a 3-minute infusion of the St. Thomas' Hospital cardioplegic solution). The tissue was then reperfused for 20 minutes and vascular function reassessed. Ischemia alone caused progressive time-dependent deterioration in vasoconstrictor responses (99% ± 13%, 90% ± 10%, 63% ± 6%, 51% ± 10%, and 27% ± 4%), endothelium-independent vasodilation (93% ± 3%, 86% ± 2%, 78% ± 5%, 61% ± 5%, and 38% ± 9%), and endothelium-dependent vasodilation (93% ± 3%, 96% ± 2%, 94% ± 2%, 87% ± 7%, and 62% ± 11%). There were similar time-dependent deteriorations in mesenteries subjected to ischemia coupled with cardioplegic solution that were not significantly different from any of the ischemia-alone groups when matched for ischemic times. Thus, for example, after 180 minutes of ischemia alone, the vasoconstrictor response was 18% ± 3%, endothelium-independent vasodilation was 44% ± 7%, and endothelium-dependent vasodilation was 40% ± 9%. The results demonstrate that under the conditions of this experiment, the St. Thomas' Hospital cardioplegic solution neither protects nor injures the vasculature during an episode of ischemia and reperfusion. However, in studies with 150 minutes of normothermic ischemia, multiple infusions of cardioplegic solution (given every 30 minutes during ischemia) resulted in protection of smooth muscle and endothelial function. Thus, after multiple infusions, vasoconstriction to phenylephrine was 74% ± 4%, vasodilation to nitroprusside was 81% ± 6%, and vasodilation to adenosine triphosphate was 89% ± 5%. In conclusion, when the St. Thomas' Hospital cardioplegic solution is used as a single infusion and coupled with ischemia, the solution fails to protect smooth muscle and endothelial function against ischemic injury, but some protection is obtained when the solution is infused intermittently throughout the ischemic period. (J THORAC CARDIOVASC SURG 1994;108:279-90)

This article has been cited by other articles:

				Q. Yang and G.-W. He Effect of Cardioplegic and Organ Preservation Solutions and Their Components on Coronary Endothelium-Derived Relaxing Factors Ann. Thorac. Surg., August 1, 2005; 80(2): 757 - 767. [Abstract] [Full Text] [PDF]

				Q. Yang, R.-Z. Zhang, A. P. C. Yim, and G.-W. He Effect of 11,12-epoxyeicosatrienoic acid as an additive to st. thomas' cardioplegia and university of wisconsin solutions on endothelium-derived hyperpolarizing factor-mediated function in coronary microarteries: influence of temperature and time Ann. Thorac. Surg., November 1, 2003; 76(5): 1623 - 1630. [Abstract] [Full Text] [PDF]

				F. Alamanni, A. Parolari, R. Visigalli, O. Bussolati, P. Rubini, R. Sala, L. Bonati, G. C. Gazzola, P. Biglioli, and V. Dall'Asta Endothelial cell injury induced by preservation solutions: a confocal microscopy study Ann. Thorac. Surg., May 1, 2002; 73(5): 1606 - 1614. [Abstract] [Full Text] [PDF]

				A. Parolari, P. Rubini, A. Cannata, L. Bonati, F. Alamanni, E. Tremoli, and P. Biglioli Endothelial damage during myocardial preservation and storage Ann. Thorac. Surg., February 1, 2002; 73(2): 682 - 690. [Abstract] [Full Text] [PDF]

				D. Curro, G. Bombardieri, C. Barilaro, P. Di Francesco, C. Varano, G. Possati, and C. Pragliola Time Dependence of Endothelium-Mediated Vasodilation by Intermittent Antegrade Warm Blood Cardioplegia Ann. Thorac. Surg., November 1, 1997; 64(5): 1354 - 1359. [Abstract] [Full Text]