Changes in mesenteric vascular reactivity and inflammatory response after cardiopulmonary bypass in a rat model
| Autor: | Jean Paul Bessou, Fabien Doguet, Pierre-Yves Litzler, François Bouchart, Marie-France Hellot, A Tabley, Christian Thuillez, Vincent Richard, Fabienne Tamion |
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| Rok vydání: | 2004 |
| Předmět: |
Male
Nitroprusside Pulmonary and Respiratory Medicine Hemodynamics In Vitro Techniques Nitroarginine law.invention Phenylephrine Ileum law Mesenteric Vascular Occlusion medicine Cardiopulmonary bypass Animals Vasoconstrictor Agents Splanchnic Circulation Rats Wistar Mesenteric arteries Cardiopulmonary Bypass Tumor Necrosis Factor-alpha business.industry medicine.disease Acetylcholine Systemic Inflammatory Response Syndrome Mesenteric Arteries Rats Vasodilation Arterioles medicine.anatomical_structure Vasoconstriction Mesenteric ischemia Anesthesia Circulatory system Surgery Cardiology and Cardiovascular Medicine business Myograph medicine.drug Blood vessel |
| Zdroj: | The Annals of Thoracic Surgery. 77:2130-2137 |
| ISSN: | 0003-4975 |
| Popis: | 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 TNFα. 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 TNFα. Conclusions CPB was responsible for mesenteric endothelial dysfunction and direct increase in the contractile response to α1-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. |
| Databáze: | OpenAIRE |
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