EFFECTS OF FATTY-ACIDS ON MYOCARDIAL CALCIUM CONTROL DURING HYPOTHERMIC PERFUSION

Although hypothermia is regarded as providing protection of the myocar dium during cardiac operations, rapid cooling of the myocardium in the nonarrested state may have detrimental effects on the function of the myocardial cell membrane as a permeability barrier. We therefore meas ured total cellular calcium in isolated working rat hearts, receiving either glucose (11.1 mmol/L) or glucose plus palmitate (1.2 mmol/L), b efore, during, and after a 40-minute hypothermic arrest (10 degrees C, Langendorff perfusion). In both groups a rise in total cellular calci um, measured by Ca-45(2+) technique, was observed during hypothermia, followed by a decline on rewarming. However, the rise in total cellula r calcium during hypothermia was significantly (p < 0.05) higher in he arts perfused with palmitate (from 1.0 +/- 0.2 to 3.5 +/- 0.2 nmol/mg dry weight) compared with that in glucose-perfused hearts (from 1.1 +/ - 0.13 to 2.6 +/- 0.2 nmol/mg dry weight). Palmitate-perfused, but not glucose-perfused, hearts showed arrhythmias and delayed pressure deve lopment 1 to 2 minutes after rewarming. In addition cardiac output of these hearts was significantly lower (p < 0.025) than that of glucose- perfused hearts 5 to 10 minutes after rewarming. These data show that hypothermia per se causes a net calcium uptake in isolated rat hearts and that this effect is aggravated by high concentrations of fatty aci ds. Thus the impaired recovery of myocardial function in palmitate-per fused hearts can possibly be related to a distorted calcium handling.