In experimental ischemic dog heart with coronary-constriction, no increase of coronary blood flow, Max dP/dt or MVO2 with no change of
kinin in arterial blood were exhibited. Following sympathetic nerve stimulation, remarkable increases of
kinin in coronary sinus blood were observed with a significant elevation of left ventricular end-diastolic pressure and an augmented production of
lactate from the heart as well as an ischemic change of ECG-ST. Infusion of
kinin into the left main coronary artery resulted in no change in the mean systemic blood pressure, coronary blood flow, coronary vascular resistance, cardiac function, myocardial metabolism or ECG-ST in the control and coronary-constricted groups. These data suggest that
kinin was released significantly from the ischemic heart, however, such a level of
kinin has no significant effect on coronary circulation or myocardial metabolism. In
ischemia-reperfusion rabbit hearts, no significant influence of the
ACE inhibitors,
captopril and
ramiprilat, were observed. Species differences may be responsible for the beneficial role of
ACE inhibitors in the limitation of
infarct size in the dog hearts, possessing collateral flow, that are not seen in the rabbit heart with poor collateral flow.