Left ventricular dysfunction following rewarming from experimental hypothermia

This study was aimed at elucidating whether ventricular hypothermia-induced dysfunction persisting after rewarming the unsupported in situ dog heart c ould be characterized as a systolic, diastolic, or combined disturbance. Co re temperature of 8 mongrel dogs was gradually lowered to 25 degrees C and returned to 37 degrees C over a period of 328 min. Systolic function was de scribed by maximum rate of increase in left ventricular (LV) pressure (dP/d t(max)), relative segment shortening (SS%), stroke volume (SV), and the loa d-independent contractility index, preload recruitable stroke work (PRSW). Diastolic function was described by the isovolumic relaxation constant (tau ) and the LV wall stiffness constant (K-p). Compared with prehypothermic co ntrol, a significant decrease in LV functional variables was measured at 25 degrees C: dP/dt(max) 2,180 +/- 158 vs. 760 +/- 78 mmHg/s, SS% 20.1 +/- 1. 2 vs. 13.3 +/- 1.0%, SV 11.7 +/- 0.7 vs. 8.5 +/- 0.7 mi, PRSW 90.5 +/- 7.7 vs. 29.1 +/- 5.9 J/m.10(-2), K-p 0.78 +/- 0.10 vs. 0.28 +/- 0.03 mm(-1), an d tau 78.5 +/- 3.7 vs. 25.8 +/- 1.6 ms. After rewarming, the significant de pression of LV systolic variables observed at 25 degrees C persisted: dP/dt (max) 1,241 +/- 108 mmHg/s, SS% 10.2 +/- 0.8 J, SV 7.3 +/- 0.4 mi, and PRSW 52.1 +/- 3.6 m.10(-2), whereas the diastolic values of K-p and tau returne d to control. Thus hypothermia induced a significant depression of both sys tolic and diastolic LV variables. After rewarming, diastolic LV function wa s restored, in contrast to the persistently depressed LV systolic function. These observations indicate that cooling induces more long-lasting effects on the excitation-contraction coupling and the actin-myosin interaction th an on sarcoplasmic reticulum Ca2+ trapping dysfunction or interstitial flui d content, making posthypothermic LV dysfunction a systolic perturbation.