Protection of the small intestine from nonocclusive mesenteric ischemic injury due to cardiogenic shock |
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| Authors: | R W Bailey G B Bulkley S R Hamilton J B Morris U H Haglund |
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| Affiliation: | 1. Department of Clinical Infection Microbiology and Immunology, Institute of Infection and Global Health, Liverpool, UK;2. Department of Otolaryngology, Alder Hey Children''s Hospital, Liverpool, UK;3. Department of Otolaryngology, Royal Liverpool University Hospital, Liverpool, UK;4. Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK;5. Department of Women''s and Children''s Health, Institute of Translational Medicine, University of Liverpool, Liverpool, UK;6. Institute of Microbiology and Infection and School of Immunity and Infection, University of Birmingham, Birmingham, UK;1. Department of Anesthesiology, Louisiana State University Health Sciences Center, 1542 Tulane Avenue, New Orleans, LA 70112, USA;2. Department of Anesthesiology, David Geffen UCLA School of Medicine, 757 Westwood Plaza, Los Angeles, CA 90095, USA;1. Department of General Surgery A, La Rabta Hospital Tunis, Tunisia;2. Faculty of Medicine of Tunis, University Tunis El Manar, Tunis, Tunisia;3. Department of Radiology, La Rabta Hospital Tunis, Tunisia;4. Department of Anesthesiology, La Rabta Hospital Tunis, Tunisia;5. Carthagene International Hospital Center Tunis, Tunisia;1. Samsun Education and Research Hospital, Cardiology Department, Samsun, Turkey;2. Ordu University, Education and Research Hospital, Cardiology Department, Turkey;3. Ordu University, Education and Research Hospital, Radiology Department, Turkey |
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| Abstract: | ![]()
In a pericardial tamponade model of cardiogenic shock in pigs, we had previously shown that acute reductions in cardiac output produce severe mesenteric ischemia due to disproportionate splanchnic vasoconstriction. In this study, we extended the period of cardiogenic shock in order to investigate the pathogenesis of ischemic injury to the small intestinal wall. Four hours of tamponade produced sustained changes in splanchnic hemodynamics, similar to those observed in the prior short-term experiments. The resultant mesenteric ischemia caused necrotic lesions of the small intestine which were characteristic of those seen in nonocclusive mesenteric ischemia in human subjects. Prior alpha-adrenergic blockade failed to prevent either sustained mesenteric vasospasm or ischemic injury. In contrast, prior blockade of the renin-angiotensin axis, whether by nephrectomy or angiotensin-converting enzyme inhibition, blocked the splanchnic vasoconstriction, and thereby protected the small intestine from ischemic injury. The primary hemodynamic and pathologic features of this model of nonocclusive mesenteric ischemia appear to be mediated by the renin-angiotensin axis. |
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