Intravenous injection of dopamine (DA) has consistently been shown to depress minute ventilation (V̇E). Whereas at low dosage (≤10 μg/kg) this effect may be accounted for by inhibition of the carotid sinus nerve chemosensory discharge (CSNCD), other mechanisms appear to be involved with large dosage (≤50 μg/kg). The purpose of this study was to elucidate the mechanisms of DA-induced V̇E depression. The effects of intravenous injection of DA doses ranging from 1 to 200 μg/kg were studied in 18 anesthetized cats. DA was injected during air and O2 breathing, after α- adrenergic blockade by phenoxybenzamine and after baro- and chemodenervation. V̇E and CSNCD were also simultaneously recorded on four occasions. In contrast to that with use of low-dose DA, V̇E depression induced by high- dose DA was dissociated from CSNCD, persisted during 100% O2 breathing, and was significantly correlated with the rise in arterial blood pressure. Although blunted, V̇E depression was still present after complete chemo- and barodenervation but was suppressed by blocking of the concomitant vasoconstriction with phenoxybenzamine. It is concluded that reflexes of circulatory origin contribute to the V̇E depression induced by large-dose DA, in addition to its effects on arterial chemoreceptors. The contribution of baroreceptor stimulation and peripheral vasoconstriction is discussed.
All Science Journal Classification (ASJC) codes
- Physiology (medical)