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Ann Thorac Surg 2004;77:2130-2137
© 2004 The Society of Thoracic Surgeons

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Original article: cardiovascular

Changes in mesenteric vascular reactivity and inflammatory response after cardiopulmonary bypass in a rat model

^a Department of Thoracic and Cardiovascular Surgery, Rouen University Hospital, Rouen, France
^b Inserm 9920, Rouen University Medical School, Rouen, France
^c Department of Biostatistics, Rouen University Hospital, Rouen, France

Accepted for publication October 8, 2003.

^* Address reprint requests to Dr Doguet, Department of Thoracic and Cardiovascular Surgery, Charles Nicolle Hospital, 1 rue de Germont, 76031 Rouen Cedex, France
e-mail: chirurgie.thoracique.cardio-vasculaire{at}chu-rouen.fr

BACKGROUND: Mesenteric ischemia and acidosis leading to intestinal ischemia has been observed during cardiopulmonary bypass (CPB) despite normal flow in the mesenteric vessels. The aim of this study was to assess mesenteric endothelium-dependent reactivity and vasoconstrictor responses of small mesenteric arteries in a rat model of CPB without aortic cross-clamping.

METHODS: After femoral cannulation a partial 90 minutes CPB was performed with hemodynamics and blood gas parameters monitoring. Blood samples and segments of small mesenteric arteries were obtained in rats sacrificed 2.5 hours (CPBH2.5) or 6 hours (CPBH6) after femoral cannulation. Sham surgery (sham H2.5, sham H6) was performed with femoral cannulation only. Segments of small mesenteric arteries were placed in a myograph in order to assess the contractile response to phenylephrine (with or without NO synthase inhibitor) or the endothelium-dependent relaxation to acetylcholine. Systemic inflammation was evaluated by measuring plasma concentrations of TNF. Pulmonary and intestinal infiltration of activated leukocytes was assessed by immunohistochemistry.

RESULTS: CPB induced increased contractile response to phenylephrine which persisted after blockade of NO synthesis as well as transient impairment of endothelium-dependent relaxations. CPB also led to early and marked release of TNF.

CONCLUSIONS: CPB was responsible for mesenteric endothelial dysfunction and direct increase in the contractile response to 1-adrenergic agonist with increased systemic inflammatory response. This phenomenon might contribute to an increase in the risk of mesenteric ischemic events during cardiac surgery especially when vasopressor agents are used.

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