Experimental myocardial infarction. 14. Accelerated myocardial stiffening related to coronary reperfusion following ischemia.
In six dogs with surgically opened chests, segmental mechanical function was determined by measuring segment length using mercury-in-Silastic gauges attached to the epicardial surface of the left ventricular wall. Following coronary arterial occlusion the amplitude of the resulting paradoxical systolic bulge was quantitated in terms of "muscle lengths", defined as the ratio of the amplitude of the segment length over the end-diastolic segment length (EDSL). From an excursion of 0.176 +/- 0.029 muscle lengths at six hours of ischemia, the amplitude of the bulge decreased abruptly to 0.125 +/- 0.024 muscle lengths after 15 minutes of coronary reperfusion (P less than 0.05) but maintained paradoxical expansion in systole. Segmental "effective stiffness", calculated at the same periods of time from end-diastolic pressure-length relationships during transient pressure loading of the left ventricle, showed a reciprocal change, increasing from 1.416 +/- 0.161 to 2.051 +/- 0.238 mm Hg/% deltaEDSL (P less than 0.05). These data indicate that the degree of paradoxical bulging of an ischemic segment is affected by its pressure-length characteristics (distensibility) and that a rapid decrease both in the amplitude of the bulge and in distensibility occurs during reperfusion. The mechanism is uncertain but may relate to either myocardial edema or myofibrillar contracture.
D000818:Animals; D001011:Aorta; D003250:Constriction; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D004285:Dogs; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000209:etiology / Q000503:physiopathology*