Why the study?
Does catecholamine depletion alter the inotropic response to ouabain in isolated rat and guinea-pig hearts?
Does catecholamine depletion alter the inotropic response to ouabain in isolated rat and guinea-pig hearts?
Catecholamine depletion abolishes the inotropic response to ouabain in isolated rat hearts, likely mediated by increased initial left ventricular pressure, but this effect is not seen in guinea pigs.
Catecholamine depletion abolishes ouabain inotropy in rat hearts; leaves open relevance to other species or clinical digitalis use.
The effect of catecholamine-depleting pretreatments, reserpine, and 6-hydroxydopamine (6-OH-DA) on left ventricular pressure (LVP) and the inotropic response to graded doses of ouabain (up to 300 μg/0.05 ml) was studied in isolated perfused rat and guinea-pig hearts. In rats, reserpine and 6-OH-DA depleted myocardial catecholamine content (p <0.001), increased initial LVP (p < 0.05), and virtually abolished the inotropic response to ouabain (p < 0.01). The individual maximal inotropic response to ouabain was negatively correlated with the initial LVP (r = −0.47), and this relationship was significant. In guinea pigs, reserpine and 6-OH-DA significantly depleted the cardiac content of catecholamine, but did not increase initial LVP and did not reduce the inotropic response to the highest dose of ouabain. It is concluded that in isolated rat hearts, these catecholamine-depleting pretreatments nearly abolish the inotropic response to ouabain, and this effect appears to be mediated mainly through an increase in initial LVP. The reason why catecholamine depletion failed to increase initial LVP in guinea pigs remains unexplained.
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Tremblay et al. (1975) studied this question.
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