This article is part of the supplement: 3rd International Symposium on the Pathophysiology of Cardiopulmonary Bypass. Myocardial cell damage and myocardial protection
Heart failure impairs vasomotor functions of the mesenteric bed after cardiopulmonary bypass
1 Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany
2 Department of Cardiovascular Surgery, Semmelweis University, Budapest, Hungary
Critical Care 2001, 5(Suppl B):P9 doi:10.1186/cc1002
The electronic version of this article is the complete one and can be found online at: http://ccforum.com/content/5/SB/P9
| Received: | 12 February 2001 |
| Published: | 6 March 2001 |
© 2001 BioMed Central Ltd
Introduction
Mesenteric dysfunction is a rare but severe complication after open heart surgery, which may be aggravated by coexistent heart failure. The aim of the study was to investigate the effects of cardiopulmonary bypass (CPB) on intestinal vascular endothelial and smooth muscle function in a canine model of heart failure.
Method
Volume overload heart failure was induced by arteriovenous shunt in six dogs; five healthy animals served as controls. Heart rate, mean arterial pressure (MAP), mesenteric blood flow and mesenteric vascular resistance (MVR) were measured before and after 90 min of CPB. Reactive hyperaemic response and the response to acetylcholine and sodium nitroprusside are expressed as percentage change in MVR.
Results
Before CPB, baseline haemodynamics (MAP: 125 ± 5 versus 117 ± 10 mmHg; MVR: 0.96 ± 0.03 versus 0.99 ± 0.17 mmHg × min/ml), reactive hyperemia (-53 ± 5 versus -53 ± 2%), and response to acetylcholine (-41 ± 3 versus -55 ± 6%) and sodium nitroprusside (-68 ± 4 versus -56 ± 4%) did not differ significantly. Ninety minutes after CPB, there was a similar significant drop in MAP in both groups (60 ± 17 and 51 ± 6 mmHg, respectively; P < 0.05 versus baseline). After CPB, reactive hyperaemia (-16 ± 5 versus -36 ± 15%; P < 0.05) and response to acetylcholine (-22 ± 9 versus -42 ± 9%; P < 0.05) and to sodium nitroprusside (-14 ± 4 versus -50 ± 7%; P < 0.002) exhibited a more pronounced decrease in the heart failure than in the control group.
Conclusion
The development of heart failure per se does not attenuate mesenteric vasomotor function. However, CPB induces a more pronounced impairment of mesenteric endothelium-dependent and -independent vasodilatory response in animals with heart failure. This phenomenon may have an impact on the higher incidence of mesenteric complications in cardiac patients with manifest heart failure.