Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1131-1137 |
| Number of pages | 7 |
| Journal | Journal of Applied Physiology |
| Volume | 84 |
| Issue number | 4 |
| State | Published - Apr 1 1998 |
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All Science Journal Classification (ASJC) codes
- Physiology
- Physiology (medical)
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Mechanisms of ventilatory inhibition by exogenous dopamine in cats. / Loos, N.; Haouzi, Philippe; Marchal, F.
In: Journal of Applied Physiology, Vol. 84, No. 4, 01.04.1998, p. 1131-1137.Research output: Contribution to journal › Article
TY - JOUR
T1 - Mechanisms of ventilatory inhibition by exogenous dopamine in cats
AU - Loos, N.
AU - Haouzi, Philippe
AU - Marchal, F.
PY - 1998/4/1
Y1 - 1998/4/1
N2 - 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.
AB - 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=0031953959&partnerID=8YFLogxK
M3 - Article
C2 - 9516175
AN - SCOPUS:0031953959
VL - 84
SP - 1131
EP - 1137
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 8750-7587
IS - 4
ER -