Volatile anaesthetics restore bradykinin and serotonin-induced coronary vasodilation after blocking nitric oxide synthase: lack of anaesthetic effects on K_<ATP> channels and prostaglandin pathways
著者
藤田, 智
(Fujita, Satoshi)
Stowe, DF
Heisner, JS
Chung, WW
上位タイトル
European Journal of Anaesthesiology
Vol.18,
No.4
(2001.
)
,p.219-
230
Background and objective: Volatile anaesthetic effects on altering tone after blocking nitric oxide synthase, cyclo-oxygenase-prostaglandin synthase and K_<ATP> channel pathways are controversial. We examined in isolated guinea pig hearts whether anaesthetics alter bradykinin and 5-hydroxytryptamine-induced effects on coronary flow and percentage oxygen extraction after blocking these pathways. Methods: Before and during exposure to sevo-flurane, halothane or isoflurane, hearts were infused with 10^<−13>–10^<−8> M bradykinin, or 10^<−8>–10^<−6> M 5-hydroxytryptamine (serotonin), with either L-NAME, indomethacin, or glibenclamide. Bradykinin or 5-hydroxytryptamine alone increased flow and decreased percentage oxygen extraction in a concentration-dependent manner; these effects were largely blocked by L-NAME (nitro-L-arginine methylester), which also decreased basal flow and increased basal percentage oxygen extraction. Results: The anaesthetics restored bradykinin and 5-hydroxytryptamine-induced increases in flow or decreases in percentage oxygen extraction after inhibition by L-NAME. Indomethacin or glibenclamide alone had little effect on basal flow and percentage oxygen extraction. The anaesthetics restored bradykinin and 5-hydroxytryptamine-induced increases in flow or decreases in percentage oxygen extraction after inhibition by L-NAME. Indomethacin or glibenclamide alone had little effect on basal flow and percentage oxygen extraction. Drug-induced increases in flow and decreases in percentage oxygen extraction in the absence or presence of glibenclamide or indomethacin were not altered at either of the two concentrations of anaesthetics. Conclusions: Endothelium-dependent vasodilatation is not affected by blocking prostaglandin release or K_<ATP> channels in the intact heart even in the presence of an anaesthetic. However, the diminished responses to vasodilators after nitric oxide synthase inhibition is largely restored or enhanced by anaesthetics.
