[Effects of anesthetic agents on arterial reactivity]

To review the effects of halogenated and intravenous anaesthetics on arterial vasoreactivity.

Articles were obtained from a MEDLINE review (search terms: 'vascular smooth muscle, endothelium' used separately or associated with following anaesthetic agents: 'halothane, isoflurane, enflurane, desflurane, sevoflurane, thiopentone, propofol, ketamine, etomidate'. Other sources included review articles and textbooks.

All experimental studies published since 1975 were analysed and pertinent data extracted.

Within the vascular wall, arterial vasoreactivity involves the endothelium and the vascular smooth muscle. In vivo, arterial vasoreactivity is regulated by neuronal, hormonal, and metabolic factors. In vitro, the direct action of anaesthetic agents on the vessel can be studied in the absence of such factors. In vitro studies with arterial rings have shown that inhalational anaesthetics directly decrease endothelium-independent contraction induced by various pharmacological agents. This direct effect of anaesthetics results from a decrease in intracellular calcium, mainly caused by an inhibition of transsarcoplasmic calcium influx. Volatile anaesthetics decrease endothelium-dependent vasorelaxation at a site(s) within the nitric oxide (NO) signalling pathway, located downstream from the NO-related receptors and upstream from guanylyl cyclase. They may also decrease endothelium-independent vasorelaxation by inhibiting NO activation of guanylate cyclase. Intravenous anaesthetics, such as propofol, barbiturates, ketamine and etomidate also decrease vasoconstriction by various degrees. Propofol is the most potent inhibitor of vasoconstriction and thiopental the least one. All these IV anaesthetics have been shown to inhibit in some circumstances both endothelium-dependent and -independent vasorelaxation. Further studies are required to enable a better understanding of the mechanism and the site of action of these vascular effects of anaesthetics. For example, the investigation of the effects of anaesthetic agents on vascular reactivity in diseases associated with endothelial dysfunction may indirectly provide insight into the role of endothelium.