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1 Department of Medical Physiology and 2 Department of Anesthesiology, University of Tromsø, N-9037 Tromsø, Norway
This study was aimed at elucidating whether
ventricular hypothermia-induced dysfunction persisting after rewarming
the unsupported in situ dog heart could be characterized as a systolic,
diastolic, or combined disturbance. Core temperature of 8 mongrel dogs
was gradually lowered to 25°C and returned to 37°C over a
period of 328 min. Systolic function was described by maximum rate of
increase in left ventricular (LV) pressure
(dP/dtmax),
relative segment shortening (SS%), stroke volume (SV), and the
load-independent contractility index, preload recruitable stroke work
(PRSW). Diastolic function was described by the isovolumic relaxation
constant (
) and the LV wall stiffness constant
(Kp). Compared
with prehypothermic control, a significant decrease in LV functional
variables 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 mm1, and 78.5 ± 3.7 vs. 25.8 ± 1.6 ms. After rewarming, the significant depression of
LV 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 PRSW
52.1 ± 3.6 m · 102, whereas
the diastolic values of
Kp and returned to control. Thus hypothermia induced a significant depression
of both systolic and diastolic LV variables. After rewarming, diastolic
LV function was 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 than on sarcoplasmic
reticulum Ca2+
trapping dysfunction or interstitial fluid content, making
posthypothermic LV dysfunction a systolic perturbation.
resuscitation; hemodynamics; diastolic function; cold; temperature
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