Ventricular performance and biochemical alteration of regional ischemic myocardium after reperfusion in the pig.
Reperfusion of acutely ischemic myocardium may cause profound alterations in left ventricular wall performance and metabolism. This study evaluates regional left ventricular wall thickness, analyzes metabolic and biochemical alterations, and examines tissue hemorrhage during 15, 30, and 120 minutes of myocardial ischemia, each followed by 120 minutes of reperfusion. Reperfusion after 15 minutes of ischemia showed nearly normal ventricular wall thickening and motion, intact metabolic and biochemical function, and no tissue hemorrhage. However, reperfusion after 30 and 120 minutes of ischemia was associated with ventricular wall thickening and failure to resume systolic and diastolic wall motion. Furthermore, adverse metabolic and biochemical alterations and reperfusion zone hemorrhaging increased proportionally with the duration of ischemia. These findings suggest critical myocardial damage occurring between 15 and 30 minutes of ischemia in an animal model without preexisting coronary collateral circulation. The observed metabolic and biochemical changes are consistent with irreversible cell membrane defects, allowing calcium ion accumulation and thus adversely affecting diastolic relaxation and systolic thickening.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000209:etiology; D002118:Calcium / Q000378:metabolism; D003327:Coronary Disease / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism*; D003331:Coronary Vessels / Q000503:physiopathology; D004452:Echocardiography; D006352:Heart Ventricles / Q000503:physiopathology*; D008929:Mitochondria, Heart / Q000378:metabolism; D010085:Oxidative Phosphorylation; D010477:Perfusion; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D013552:Swine
D000255:Adenosine Triphosphate; D002118:Calcium