[abstract] INCREASED CARDIAC CONTRACTILITY IN THE ATENOLOL TREATED RAT AT 5 BAR AMBIENT PRESSURE.

Abstract

Previous studies have demonstrated increased contractility in rat myocardium in the hyperbaric environment, in vitro as well as in vivo. This study was performed to evaluate whether cardiac p-adrenoceptors mediated this response. Two groups of rats were habituated to the pressure chamber for 2 weeks. A cardiac and arterial catheter was inserted the day before the experiment. Group 1 rats were treated with atenolol twice during a 75 min exposure at 1 bar. The first atenolol injection caused a 8% decrease in peak left ventricular pressure (LVP) , while heart rate (HR) , maximal left ventricular pressure increase (+dP/dt) and decrease (-dP/dt) fell by 17% -22%. The effect on arterial pressure was small and shortlasting. The second injection caused only a shortlasting effect on HR, LVP, +dP/dt and -dP/dt~ Group 2 rats were treated with the first atenolol injection at 1 bar with a cardiovascular response identical to group 1 rats. During compression to 5 bar (pO2 0.2 bar, pN2 4.8 bar) LVP, +dP/dt and -dP/dt increased stepwise in spite of the p-adrenoceptor blockade. No change in AP and only a small increase in HR were observed during compression. The second atenolol injection -at 5 bar -caused a cardiovascular response similiar to group 1 rats. We conclude that increased ambient pressure causes an increase in cardiac inotropy which can not be abolished by blocking of the p-adrenoceptor.