Myocardial performance in splanchnic arterial occlusion shock

• Published in: The Journal of surgical research Vol. 15; no. 6; pp. 417 - 428
• Main Authors: Hinshaw, L.B., Archer, L.T., Black, M.R., Greenfield, L.J.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.01.1973
• Subjects: Animals; Aorta; Blood Pressure; Carbon Dioxide - blood; Coronary Vessels; Dogs; Extracorporeal Circulation; Heart - physiopathology; Heart Rate; Heart Ventricles - physiopathology; Ischemia; Mesenteric Arteries; Mesenteric Vascular Occlusion - physiopathology; Mesentery - blood supply; Myocardium - metabolism; Oxygen - blood; Oxygen Consumption; Perfusion; Pressure; Regional Blood Flow; Vascular Resistance
• ISSN: 0022-4804; 1095-8673
• DOI: 10.1016/0022-4804(73)90113-3

The adverse combined effects of mesenteric ischemia and the subsequently precipitated lethal shock after restoration of mesenteric blood flow have implicated direct or indirect roles of the heart in the pathogenesis of shock. The present experiments were carried out to assay the role of the heart in splanchnic arterial occlusion (SAO) shock. Studies were designed to evaluate the combined effects of SAO shock and diminished coronary perfusion pressure on the performance of a stressed heart. Experiments were carried out on isolated hearts exchanging blood with an intact dog subjected to 2 hr of splanchnic arterial occlusion. Release of the occlusion did not result in any measurable detrimental effect on the heart: LVEDP and cardiac power were maintained in the normal range at mean aortic pressures (afterloads) between 34 and 125 mm Hg at all times during the postocclusion period. dP/dt was elevated, possibly as a result of increased coronary blood flow and decreased coronary vascular resistance. Myocardial oxidative metabolic characteristics were unchanged from control preocclusion values. Normal myocardial function was observed after the release of a lethal period of splanchnic arterial occlusion during both early and terminal periods of shock. Results, though not revealing the cause of SAO shock, suggest that diminished cardiac performance resulting from the actions of blood-borne substances released from the ischemic splanchnic region is not a significant factor in the development of systemic hypotension and death.