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ABSTRACT Changes in arterial blood pressure have been shown to alter epicardial ST segment elevations, and have been advocated to minimize infarct size and “salvage” ischemic myocardium. The effect of such changes on the regional function of ischemic myocardium has not been established. To investigate this, we studied the effect of increased afterload on the systolic wall thickening and myocardial perfusion of ischemic ventricular myocardium. In 20 open‐chest dogs, an echocardiographic transducer was fixed to the exposed right ventricle and directed to record the motion of the left ventricular posterior wall. Posterior ischemia was created by occlusion of the circumflex coronary, so that the ultrasound beam registered the motion of acutely ischemic myocardium. The ratio of end‐systolic to end‐diastolic posterior wall thickness (PTs/PTd) was greater than 1 (i.e. systolic thickening) before, and less than 1 (systolic thinning) after, posterior ischemia. Mean arterial pressure was then increased by infusion of methoxamine (Mx) or norepinephrine (NE) or by aortic constriction (CN). PTs/PTd improved from 0.89± 0.03 to 1.10± 0.06 (p<0.05) with CN. Perfusion of the ischemic areas, assessed with 8μ radioactive labled microspheres, showed a corresponding improvement; with MX ischemic myocardial perfusion improved from 32.4±6.2 to 59.6±13.8 ml/100g/min (p<05) and with CN perfusion rose from 30.2±9.3 to 43.8±10.3 ml/100g/min (p<0.5). Thus, increase in afterload improved both the perfusion and regional function of acutely ischemic myocardium.
Kerber et al. (1979) studied this question.