It has been shown that simultaneous administration of norepinephrine (10mug/kg/min) and drotaverine (200 mug/kg/min) does induce interstitial myocardial edema which tends to increase left ventricular diastolic stiffness. These results suggest that in myocardial ischaemia temporary increase of left ventricular diastolic stiffness may be caused by interstitial edema.

The cardiovascular effects of glibenclamide, gliclazide and carbutamide were studied on myocardial contractile force, cardiac output, mean arterial pressure and heart rate in 43 intact, 14 pancreatectomized and 18 adrenalectomized dogs. It is shown that a positive inotropic and hypertensive effect of hypoglycaemic sulphonylureas develops without the mediation of glucagon, insulin or adrenaline. Contrary to the other investigated sulphonylureas, glibenclamide reduced myocardial contractile force and arterial blood pressure.

Coronary blood flow, left ventricular diastolic stiffness, ventricular water content and ventricular thiocyanate space were investigated in empty fibrillating and empty beating dog hearts during cardiopulmonary bypass. In empty fibrillating hearts coronary blood flow was considerably enhanced even at levels of normal perfusion pressure. A close correlation was demonstrated between enhanced coronary flow, left ventricular diastolic stiffness, tissue water content and thiocyanate space.

Changes in myocardial water content, left ventricular diastolic stiffness, cardiac performance, coronary blood flow, myocardial contractile force, rate of change of myocardial force, and peak acceleration of the aortic volume flow were examined in twenty-five dogs during glucose-induced hyperosmolality before and after pancreatectomy, the latter with and without insulin treatment. Glucose-induced hyperosmolality accounted for myocardial dehydration, increased diastolic stiffness and consequent decrease of left ventricular performance only in the absence of insulin, while coronary blood flow, myocardial contractile force, rate of change of myocardial force and peak acceleration of the aortic volume flow increased independently from the presence or absence of insulin during the glucose-induced hyperosmolality. These findings suggest that the frequent development of heart failure in hyperosmolar diabetic coma could partly be explained by myocardial dehydration and by the consequent decrease in left ventricular compliance and performance.