Effect of hemorrhagic shock on the performance, O2-consumption, and ultrastructure of isolated rat hearts.
Rat hearts were isolated from control animals anesthetized and sham treated for 2.5 hours and following 2.5 hours of hemorrhagic hypotension and they were perfused by modified Langendorff technique. Hearts isolated following hemorrhagic hypotension exhibited increased coronary resistance, depressed left ventricular mechanical performance, and significantly increased sensitivity to threefold elevation of perfusate Ca2+ (from 1.3 to 3.9 mM). Electron microscopic examination showed increased permeability of the plasma membrane for lanthanum, zonal lesions of contractile filaments, damage of mitochondria, and dilation of T-tubules and sarcoplasmic reticulum. Experimental results indicate that myocardial damage is of hypoxic/ischemic origin during the procedure used as a model for shock. Mechanical failure of postoligemic hearts may be caused by the combination of zonal lesions of the myofilaments, damage of energy production, and impairment of cellular calcium metabolism.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D004734:Energy Metabolism; D005260:Female; D007811:Lanthanum; D009206:Myocardium / Q000648:ultrastructure*; D010101:Oxygen Consumption; D010424:Pentobarbital / Q000494:pharmacology; D010477:Perfusion; D051381:Rats; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D013997:Time Factors; D014655:Vascular Resistance
D007811:Lanthanum; D010424:Pentobarbital; D002118:Calcium