Influence of mild hypothermia on myocardial contractility and circulatory function

Myocardial contractility depends on temperature. We investigated the influe nce of mild hypothermia (37-31 degreesC) on isometric twitch force, sarcopl asmic reticulum (SR) Ca2+-content and intracellular Ca2+-transients in vent ricular muscle strips from human and porcine myocardium, and on in vivo hem odynamic parameters in pigs. In vitro experiments: muscle strips from 5 non failing human and 8 pig hearts. Electrical stimulation (1 Hz), simultaneous recording of isometric force and rapid cooling contractures (RCCs) as an i ndicator of SR Ca2+-content, or intracellular Ca2+-transients (aequorin met hod). In vivo experiments: 8 pigs were monitored with Millar-Tip (left vent ricle) and Swan-Ganz catheter (pulmonary artery). Hemodynamic parameters we re assessed at baseline conditions (37 degreesC), and after stepwise coolin g on cardiopulmonary bypass to 35, 33 and 31 degreesC. Hypothermia increase d isometric twitch force significantly by 91 +/- 16 % in human and by 50 +/ - 9 % in pig myocardium (31 vs. 37 degreesC; p < 0.05, respectively). RCCs or aequorin light emission did not change significantly. In anesthetized pi gs, mild hypothermia resulted in an increase in hemodynamic parameters of m yocardial contractility. While heart rate decreased from 111 <plus/minus> 3 to 73 +/- 1 min(-1), cardiac output increased from 2.4 +/- 0.1 to 3.1 +/- 0.3 l/min, and stroke volume increased from 21 +/- 1 to 41 +/- 3 ml. +dP/dt (max) increased by 25 +/- 8 % (37 vs. 31 OC; p < 0.05 for all values). Syst emic and pulmonary vascular resistance did not change significantly during cooling. Mild hypothermia exerts significant positive inotropic effects in human and porcine myocardium without increasing intracellular Ca2+-transien ts or SR Ca2+-content. These effects translate into improved hemodynamic pa rameters of left ventricular function.