MECHANISMS OF INCREASED MYOCARDIAL-CONTRACTILITY WITH HYPERTONIC SALINE SOLUTIONS IN ISOLATED BLOOD-PERFUSED RABBIT HEARTS

Hypertonic saline improves organ perfusion and animal survival during hemorrhagic shock because it expands plasma volume and increases tissu e oxygenation Because both decreased and increased myocardial performa nce have been reported with hypertonic saline, the effects of hyperosm olarity and the mechanism accounting for it were investigated in isola ted blood-perfused rabbit hearts. Coronary blood flow (CBF), myocardia l contractility, relaxation, and oxygen consumption were measured duri ng administration of blood perfusates containing 140-180 mmol sodium c oncentrations ([Na+]). Ln two other series of experiments, the role of Na+-Ca2+ exchange in the inotropic effect of hyperosmolarity (160 mmo l sodium concentration) and hypertonicity (sucrose) were also investig ated. Hypertonic [Na+] induced a significant increase in contractility and relaxation, combined with a coronary vasodilation. Myocardial oxy gen consumption (MVO(2)) increased at all hypertonic [Na+] without sig nificant change in coronary venous oxygen tension (PVO2) and content ( CVO2). Amiloride (0.3 mmol) inhibited the improved contractility obser ved with 160 mmol sodium. Similar Na+-Ca2+ exchanger blockade did not inhibit the inotropic effect of sucrose. These results confirm the pos itive inotropic effect of hypertonic [Na+]. The inhibition of this imp rovement by amiloride suggests that calcium influx through the sarcole mna could be the major mechanism of this effect.