The effect of molsidomine on intramyocardial pressure and regional myocardial blood flow in the canine ischemic myocardium.

Molsidomine was administered intraduodenally to anesthetized dogs which were instrumented for measurements of aortic and left ventricular (LV) pressures, coronary perfusion pressure, intramyocardial pressure in the subendocardium, and subendocardial and subepicardial myocardial blood flow in the ischemic and non-ischemic regions. The dogs were divided into two groups: group M (n = 9) was administered molsidomine (0.2 mg/kg), group S (n = 10), saline only. Maximum LV systolic pressure decline was 20% in group M and 3% in group S (p less than 0.05). Maximum LV end-diastolic pressure decline was 63% and 35% in groups M and S, respectively (p less than 0.05). There was no difference between mean aortic pressure and coronary perfusion pressure between the two groups. The subepicardial blood flow in the ischemic region was decreased (-23% in group M vs 5% in group S; p less than 0.05), but subendocardial blood flow in the ischemic region increased only slightly in group M. The ratio of subendocardial to subepicardial blood flow increased at 15 and 30 min after administration of molsidomine in the ischemic area (67% in group M vs -10% in group S; p less than 0.05), but did not show any change in the non-ischemic region. Intramyocardial pressure at systole did not show any change but it decreased at end-diastole, (-32% in group M vs -7% in group S; p less than 0.05). Thus molsidomine redistributed the myocardial blood flow from the subepicardium to the subendocardium and from the non-ischemic to the ischemic region. This redistribution was associated with a reduction in both LV end-diastolic pressure and intramyocardial pressure at end-diastole.