|
|
||||||||
J Thorac Cardiovasc Surg 2001;122:1011-1018
© 2001 The American Association for Thoracic Surgery
Cardiopulmonary Support and Physiology (CSP) |
From the Department of Thoracic and Cardiovascular Surgerya and Institute of Experimental Surgery,b Heinrich-Heine-University, Düsseldorf, Germany.
Received for publication Aug 23, 2000. Revisions requested Nov 29, 2000; revisions received Jan 2, 2001. Accepted for publication Feb 12, 2001. Address for reprints: Gerhard A. Kalweit, MD, Department of Thoracic and Cardiovascular Surgery, Heinrich-Heine-University, Moorenstraße 5, D-40225 Düsseldorf, Germany.
Abstract
Objective: Microvascular incompetence after ischemia and reperfusion may compromise the normal postischemic coronary perfusion and additionally jeopardize the recovery of the myocytes. We investigated whether such a form of acute endothelial dysfunction occurs in the routine operative setting despite the use of protective measures. For this purpose, we measured pressure-flow relations in the coronary vasculature during heart operations before and after ischemia and after reperfusion and their reaction to the nitric oxide donor nitroglycerin.
Methods: Forty-eight patients with a low risk profile scheduled for routine coronary artery bypass surgery were included. During normothermic extracorporeal circulation, the fibrillating heart was completely excluded from bypass by clamping of the ascending aorta and snaring of the caval veins. It was relieved of blood by opening the right atrium and venting the left atrium and ventricle to avoid distention. The coronary vessels were perfused under controlled flow, and the perfusion pressures were monitored. This protocol was performed in 24 patients before and immediately after ischemia and after a reperfusion period.
Results: Compared with the preischemic control, vascular resistance was decreased by 17% (P < .003) immediately after ischemia but increased again by 46% (P < .0001) during an average of 25 minutes of reperfusion and, even more important, by 23% (P < .028) in comparison with the preischemic values. In two groups of 12 patients, nitroglycerin was added to the perfusate either in a dosage of 3 µg · kg · min1 or as a bolus injection of 2 mg. Low-dose nitroglycerin did not reduce the elevated postreperfusion resistances significantly, but bolus injection did (P < .0002). Coronary vessel resistance increased during reperfusion in particular in patients with a history of hypertension.
Conclusion: Coronary vasoconstriction during postischemic reperfusion is regularly present in the routine operative setting in cardiac surgery, despite myocardial protection measures. The amount of vasoconstriction varies considerably and is particularly increased in patients with hypertension. The nitric oxide donor nitroglycerin can normalize the elevated resistances, but only in high dosages. This demonstrates a preserved ability of vascular smooth muscle to relax. The phenomenon had no sequelae in our low-risk patients having elective operations. However, it may gain significance in the case of severe left heart hypertrophy and in patients at risk with both a postoperative low-output syndrome and reduced mean arterial pressures during reperfusion.
This article has been cited by other articles:
![]() |
F. Eefting, B. Rensing, J. Wigman, W. J. Pannekoek, W. M. Liu, M. J. Cramer, D. J Lips, and P. A Doevendans Role of apoptosis in reperfusion injury Cardiovasc Res, February 15, 2004; 61(3): 414 - 426. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. L. Weiner, P. L. Hibberd, P. Betit, A. B. Cooper, C. A. Botelho, and C. Brugnara Preliminary Assessment of Inhaled Nitric Oxide for Acute Vaso-occlusive Crisis in Pediatric Patients With Sickle Cell Disease JAMA, March 5, 2003; 289(9): 1136 - 1142. [Abstract] [Full Text] [PDF] |
||||
| 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 |