Key result
In conscious dogs with constant heart rate, carotid chemoreceptor stimulation increased left ventricular dP/dt by 21%, a greater positive inotropic effect than the 13% increase observed with carotid baroreceptor unloading.
Why the study?
Does carotid chemoreceptor stimulation increase myocardial contractility more than carotid baroreceptor unloading in conscious dogs?
Does carotid chemoreceptor stimulation increase myocardial contractility more than carotid baroreceptor unloading in conscious dogs?
Answers are grounded in this paper and cite their sources.
In conscious dogs, carotid chemoreceptor stimulation induces a clear positive inotropic effect that is greater than that of carotid baroreceptor unloading for an equal elevation in arterial pressure.
The effects of carotid chemoreceptor stimulation with intracarotid injections of either nicotine, 0.2 mug/kg, or cyanide, 2 mug/kg, were compared with the effects of bilateral carotid occlusion on left ventricular (LV) pressure, dP/dt, and diameter in conscious dogs instrumented with ultrasonic diameter gauges and miniature pressure gauges. With heart rate maintained constant, carotid chemoreceptor stimulation increased mean arterial pressure by 27+/-3%, LV and diastolic diameter by 4+/-0.9% and LV dP/dt by 21+/-2%. With ventilation controlled during succinylcholine infusion, carotid chemoreceptor stimulation increased mean arterial pressure by 43+/-2% and dP/dt by 37+/-5%, values significantly greater, P < 0.01, than were observed in dogs with spontaneous ventilation. Similarly, in dogs with spontaneous ventilation after vagotomy, carotid chemoreceptor stimulation also increased dP/dt by a greater amount, i.e., by 48+/-9%. The increases in LV end diastolic diameter were not affected significantly by either cholinergic blockade with atropine or beta adrenergic blockade with propranolol. Although cholinergic blockade did not affect the inotropic or pressor responses significantly, beta adrenergic blockade attenuated the pressor response and essentially abolished the inotropic response. Bilateral carotid occlusion increased mean arterial pressure and LV end diastolic diameter by similar amounts to those observed with chemoreceptor stimulation, but increased dP/dt significantly less, P < 0.02, i.e., by 13+/-2%. As was observed with chemoreceptor stimulation, inotropic responses were not affected significantly by cholinergic blockade, but were essentially abolished by beta adrenergic blockade. Thus, in the conscious dog with heart rate constant, carotid chemoreceptor stimulation induces a clear positive inotropic effect, which is greater in the absence of the attenuating influences of pulmonary inflation reflexes, and for an equal elevation in arterial pressure appears to exert a greater increase in myocardial contractility than does carotid baro-receptor unloading.
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Vatner et al. (1978) studied Healthy conscious dogs (animal model) (n=19). Carotid chemoreceptor stimulation (intracarotid nicotine or cyanide) vs. Bilateral carotid occlusion (baroreceptor unloading) was evaluated on Left ventricular dP/dt (myocardial contractility) (p=<0.02). In conscious dogs with constant heart rate, carotid chemoreceptor stimulation increased left ventricular dP/dt by 21%, a greater positive inotropic effect than the 13% increase observed with carotid baroreceptor unloading.
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