Tracer kinetics analysis of the extracellular spaces in saline perfused hearts.

Background: Precise estimation of the cellular water content presupposes a correct definition of the water fraction in tissue extracellular space. Low molecular weight markers (LMM), such as sulphate ion and sucrose, are widely used to define extracellular space size despite indications that they penetrate the cell. In contrast, inulin, with molecular weight of about 5000, is commonly regarded as a cell impermeable extracellular marker.

Dependence of the cardiac contractile force on the coronary perfusion pressure: difference between the isovolumic hearts of rat and guinea pig.

We have compared the contractile responses of the isovolumic hearts of rat and guinea pig to a rise in the coronary perfusion pressure in the range 60-120 mmHg (Gregg's phenomenon). Left ventricular systolic pressure was lower in guinea pig hearts than in rat hearts at a low coronary perfusion pressure and increased markedly less at a higher perfusion pressure, despite a greater increase in coronary flow. The rise in left ventricular systolic pressure in the guinea pig hearts was entirely due to an increased left ventricular end-diastolic pressure, while left ventricular developed pressure did not increase.

Myocardial adaptation to long-term action of substances associated with decreased intensity of cardiac function.

The effect of prolonged treatment of rats with 6-n-propyl-2-thiouracil (PTU), verapamil, or propranolol on cardiac pump function and the properties of myofibrils and mitochondria was studied. After 6-8 weeks of treatment, the heart rate and maximal cardiac output of the isolated heart of rats treated with verapamil or propranolol were higher than those in the control group. The PTU treatment was followed by lower heart rate and maximal work.

[Protective effect of 2,3-butanedione monooxime on ischemic myocardium of rats].

Effects of 2,3-butanedione monoxime (BDM), an ATPase inhibitor, on ischemia-reperfusion myocardial injury were examined in isolated working rat hearts perfused in vitro. Following cardiac arrest induced by cardioplegic solution, global ischemia was produced for 30 min. In untreated hearts, reperfusion for 45 min resulted in an incomplete recovery of cardiac pump function.