Abstract
In the present study we have examined the effect of the general anesthetic agent sodium pentobarbital (given i.p. to the intact animal) on the hemodynamic function of the isolated perfused heart and its response to treatments which affect calcium transsarcolemmal influx: extracellular calcium concentration and thyroid hormone. Perfused hearts (modified Langendorff system) isolated from anesthetized rats were found to respond differently to the two aforementioned effectors than hearts excised from non-anesthetized animals. Hearts of the two groups demonstrated a gradual increase in inotropic activity in response to step-wise increase in calcium concentration in the perfusion medium. However, cardiac contractility and the pattern of the response to the gradual increase in calcium concentration were different. At the lower Ca 2+ concentrations of 0.5 and 1.0 m m, inotropic activity (left ventricular systolic pressure (LVP) and + dP dt values) of hearts from anesthetized animals was significantly greater ( P < 0.05) than that of hearts from non-anesthetized animals: LVP values (mmHg, mean ± s.e.m.) in hearts from anesthetized an non-anesthetized rats were: at 0.5 m m Ca 2+, 19 ± 3 and 9 ± 2; and at 1.0 m m, 103 ± 12 and 76 ± 6, respectively. At the higher Ca 2+ concentrations, hearts from anesthetized animals demonstrated maximal LVP at 1.75 m m calcium (139 ± 9 mmHg), whereas the LVP values in hearts from non-anesthetized animals continued to increase throughout all the Ca 2+ concentrations employed. A similar pattern of response was observed for + dP dt values. Anesthesia did not influence heart rate, and the increase in medium Ca 2+ concentration from 0.5 to 1.0 m m resulted in a small increase in heart rate, to reach maximal values, by 13 ± 2% and 16 ± 2% in hearts from anesthetized and non-anesthetized animals. The thyroid hormone 3,5,3′-triiodothyronine (T3, 1 μ m) produced a rapid and transient increase in cardiac inotropic activity which was evident already within 15–30 s, increased progressively to reach maximum at about 15–20 min, and then declined gradually. The effect of T3 was much greater in hearts from non-anesthetized animals than in hearts from anesthetized rats; being at maximum 120 ± 30% and 55 ± 10% above control respectively. T3 had no effect on cardiac chronotropic activity. Taken together, we demonstrate here that perfused hearts isolated from anesthetized rats respond differently than hearts from non-anesthetized animals to calcium-influx-mediated activity. We, therefore, recommend that in similar and other short-term studies, the effect of anesthesia should be examined or better be avoided altogether.
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