Heart failure impairs vasomotor functions of the mesenteric bed after cardiopulmonary bypass

cc1002 CCJ Meeting abstract Heart failure impairs vasomotor functions of the mesenteric bed after cardiopulmonary bypass Szabó G Andrási TB Zima E Soós P Sack F-U Tanzeem A Hagl S Juhász-Nagy S

Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany

Department of Cardiovascular Surgery, Semmelweis University, Budapest, Hungary

Critical Care 3rd International Symposium on the Pathophysiology of Cardiopulmonary Bypass. Myocardial cell damage and myocardial protection Meeting abstracts 3rd International Symposium on the Pathophysiology of Cardiopulmonary Bypass. Myocardial cell damage and myocardial protection Aachen, Germany

16 December 2000

1364-8535 2001 5 Suppl B P9 10.1186/cc1002 12 2 2001 6 3 2001 2001 BioMed Central Ltd cc-5-2-105-p09

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.