VOLATILE ANESTHETIC ACTIONS ON NOREPINEPHRINE-INDUCED CONTRACTION OF SMALL SPLANCHNIC RESISTANCE ARTERIES

Citation
T. Akata et al., VOLATILE ANESTHETIC ACTIONS ON NOREPINEPHRINE-INDUCED CONTRACTION OF SMALL SPLANCHNIC RESISTANCE ARTERIES, Canadian journal of anaesthesia, 42(11), 1995, pp. 1040-1050
Citations number
62
Categorie Soggetti
Anesthesiology
ISSN journal
0832610X
Volume
42
Issue
11
Year of publication
1995
Pages
1040 - 1050
Database
ISI
SICI code
0832-610X(1995)42:11<1040:VAAONC>2.0.ZU;2-O
Abstract
The aim of this study was to investigate volatile anaesthetic action o n small splanchnic resistance arteries. Employing isometric tension re cording, we studied the effects of clinically relevant concentrations (0.25-1.25 minimum alveolar concentration (MAC)) of isoflurane, sevofl urane and enflurane on contractions induced by norepinephrine (NE) a s ympathetic neurotransmitter, in the rabbit small mesenteric artery. Rh ythmic oscillations were observed in contractile responses to NE. Both isoflurane (greater than or equal to 0.25 MAC, 0.5% (approximate to 0 .11 mM)) and sevoflurane (greater than or equal to 0.75 MAC, 2.8% (app roximate to 0.38 mM)) inhibited the NE (10 mu M)-induced contraction w ith concomitant inhibition of average amplitude of the oscillations. O nly enflurane (greater than or equal to 0.25 MAC, 0.7% (approximate to 0.20 mM)) generated vasoconstriction superimposed on the NE-induced c ontraction; however the vasoconstriction was transient and was followe d by vasorelaxation. Concurrently, enflurane (greater than or equal to 0.25 MAC) strongly inhibited the average amplitude of the oscillation s; higher concentrations (greater than or equal to 1.0 MAC) of enflura ne completely eliminated the oscillations. The frequency of the NE-ind uced oscillations was less affected by the anaesthetics. The observed vasodilator action of these anaesthetics in small resistance arteries may contribute to their hypotensive effects in vivo. The potent inhibi tion of the rhythmic oscillations also may play a role in volatile ana esthetic-induced alterations in cardiovascular homeostasis.