Left ventricular dysfunction following rewarming from experimental hypothermia |
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Authors: | Tveita, Torkjel Ytrehus, Kirsti Myhre, Eivind S.P. Hevroy, Olav |
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Abstract: | This study was aimed at elucidating whetherventricular hypothermia-induced dysfunction persisting after rewarmingthe unsupported in situ dog heart could be characterized as a systolic,diastolic, or combined disturbance. Core temperature of 8 mongrel dogswas gradually lowered to 25°C and returned to 37°C over aperiod of 328 min. Systolic function was described by maximum rate ofincrease in left ventricular (LV) pressure(dP/dtmax),relative segment shortening (SS%), stroke volume (SV), and theload-independent contractility index, preload recruitable stroke work(PRSW). Diastolic function was described by the isovolumic relaxationconstant ( ) and the LV wall stiffness constant(Kp). Comparedwith prehypothermic control, a significant decrease in LV functionalvariables was measured at 25°C:dP/dtmax 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 ml, PRSW 90.5 ± 7.7 vs. 29.1 ± 5.9 J/m · 10 2,Kp 0.78 ± 0.10 vs. 0.28 ± 0.03 mm 1, and 78.5 ± 3.7 vs. 25.8 ± 1.6 ms. After rewarming, the significant depression ofLV systolic variables observed at 25°C persisted: dP/dtmax 1,241 ± 108 mmHg/s, SS% 10.2 ± 0.8 J, SV 7.3 ± 0.4 ml, and PRSW52.1 ± 3.6 m · 10 2, whereasthe diastolic values ofKp and returned to control. Thus hypothermia induced a significant depressionof both systolic and diastolic LV variables. After rewarming, diastolicLV function was restored, in contrast to the persistently depressed LVsystolic function. These observations indicate that cooling inducesmore long-lasting effects on the excitation-contraction coupling and the actin-myosin interaction than on sarcoplasmicreticulum Ca2+trapping dysfunction or interstitial fluid content, makingposthypothermic LV dysfunction a systolic perturbation. |
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