부산대학교 도서관

Components of excitation-contraction (EC)-coupling were compared at 37[degrees]C and 22[degrees]C to determine whether hypothermia altered the gain of EC coupling in guinea pig ventricular myocytes. [Ca.sup.2+] concentration (fura-2) and cell shortening (edge detector) were measured simultaneously. Hypothermia increased fractional shortening (8.3 [+ or -] 1.7 vs. 2.6 [+ or -] 0.3% at 37[degrees]C), [Ca.sup.2+] transients (157 [+ or -] 33 vs. 35 [+ or -] 5 nM at 37[degrees]C), and diastolic [Ca.sup.2+] (100 [+ or -] 9 vs. 60 [+ or -] 6 nM at 37[degrees]C) in field-stimulated myocytes (2 Hz). In experiments with high-resistance microelectrodes, the increase in contractions and [Ca.sup.2+] transients was accompanied by a twofold increase in action potential duration (APD). When voltage-clamp steps eliminated changes in APD, cooling still increased contractions and [Ca.sup.2+] transients. Hypothermia increased sarcoplasmic reticulum (SR) [Ca.sup.2+] stores (83 [+ or -] 17 at 37[degrees]C to 212 [+ or -] 50 nM, assessed with caffeine) and increased fractional SR [Ca.sup.2+] release twofold. In contrast, peak [Ca.sup.2+] current was much smaller at 22[degrees]C than at 37[degrees]C (1.3 [+ or -] 0.4 and 3.5 [+ or -] 0.7 pA/pF, respectively). In cells dialyzed with sodium-free pipette solutions to inhibit [Ca.sup.2+] influx via reverse-mode [Na.sup.+]/[Ca.sup.2+] exchange, hypothermia still increased contractions, [Ca.sup.2+] transients, SR stores, and fractional release but decreased the amplitude of [Ca.sup.2+] current. The rate of SR [Ca.sup.2+] release per unit [Ca.sup.2+] current, a measure of EC-coupling gain, was increased sixfold by hypothermia. This increase in gain occurred regardless of whether cells were dialyzed with sodium-free solutions. Thus an increase in EC-coupling gain contributes importantly to positive inotropic effects of hypothermia in the heart. positive inotropy; calcium transient; contraction; calcium current; sarcoplasmic reticulum calcium stores