Experimental myocardial ischemia and infarction Production of diffuse myocardial lesions in unanesthetized calves

To produce a chronic, ischemic heart failure preparation of controllable severity, plastic microspheres (6 to 14 μ in diameter) were injected into the left main coronary artery of unanesthetized calves. Two dose levels were used (4 and 5 mg/kg, Groups I and II, respectively). Hemodynamic and electrocardiographic changes were not observed during the microsphere infusion. Arterial-coronary sinus lactate differences shifted from positive control values (mean +5.3 mg/ 100 ml) to negative during and throughout the injection (mean −6.4 mg/100 ml). Significant hemodynamic abnormalities at rest (Group II only) were first noted on postinfusion day 1, and unaccompanied by subsequent significant physiologic recovery. These included an increase in left ventricular end-diastolic pressure (+18 to 21 mm Hg), reduction in stroke volume (−32 percent), cardiac output (−25 percent), dP/dt (−22 percent), mean ejection rate (−18 percent) and left ventricular ejection time, and a prolongation of preejection period. Cardiac response to angiotensin-induced stress was impaired in both test groups. Mean heart weight and left ventricular wall thickness increased by 65 and 45 percent, respectively, in both groups. Histopathologic examination demonstrated microinfarcts widely distributed throughout the myocardium supplied by the left coronary artery at various stages of healing, sometimes in the same heart, with typical time-dependent morphologic characteristics. The myocardial fibers were hypertrophied. In addition, atypical areas were found on glycogen selective staining.

The results suggest that the extent of microcirculatory ischemia and infarction determines the degree of myocardial impairment at rest and during stress irrespective of compensatory hypertrophy.