Abstract

We examined the effect of hypothermia and rewarming on myocardial function and calcium control in Langendorff-perfused hearts from rat and guinea pig. Both rat and guinea pig hearts demonstrated a rise in myocardial calcium ([Ca]total) in response to hypothermic perfusion (40 min, 10°C), which was accompanied by an increase in left ventricular end diastolic pressure (LVEDP). The elevation in [Ca]totalwas severalfold higher in guinea pig than in rat hearts, reaching 12.9 ± 0.8 and 3.1 ± 0.6 μmol·g dry wt−1, respectively. The rise in LVEDP, however, was comparable in the two species: 62.5 ± 2.5 (guinea pig) and 52.5 ± 5.1 mm Hg (rat). Following rewarming, [Ca]totalremained elevated in guinea pig, whereas a moderate decline in [Ca]totalwas observed in the rat (13.6 ± 1.9 and 2.2 ± 0.3 μmol·g dry wt−1, respectively). Posthypothermic values of LVEDP were also significantly higher in guinea pig compared to rat hearts (42.5 ± 6.8 vs 20.5 ± 5.1 mm Hg,P< 0.027). Furthermore, whereas rat hearts demonstrated a 78 ± 7% recovery of left ventricular developed pressure, there was only a 15 ± 7% recovery in guinea pig hearts. Measurements of tissue levels of high energy phosphates and glycogen utilization indicated a higher metabolic requirement in guinea pig than in rat hearts in order to oppose the hypothermia-induced calcium load. Thus, we conclude that isolated guinea pig hearts are more sensitive to a hypothermic insult than rat hearts.

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