Abstract
Purpose
T1he effect of halothane was compared on acetylcholine (ACh)-induced relaxation of the mesentenc artery and the aorta in rats
Methods
The responses of isolated rat aortic and mesentenc artenal nng segments precontracted with phenylephnne to ACh (10−8– 10−5M), in the presence of halothane 0–3%. were compared using isometric force tension recordings. Effects of NG -nitro-l-arginine (L-NOARG, 3 × 10−5), methylene blue (MB, 5 × 10−6 M), oxyhaemoglobin (OxyHB, 10−7 M), and vanous potassium channel inhibitors; tetraethylammonium (TEA, 10−5 M. 10−3 M), apamin (AP, 10−7 M), charybdotoxin (ChTx, 10−7M) and glibenclamide (GC, 10−5M) on ACh-induced relaxation in mesentenc artery were tested. Using radioimmunoassay, ACh (10−6M)-induced guanosine 3′:5′-cyclic monophosphate (cGMP) accumulation of mesentenc arterial rings pretreated with L-NAORG were also measured.
Results
L-NOARG partially inhibited ACh-induced relaxation in mesentenc arterial rings (P < 0.05. maximum relaxation reduced by approximately 50%), whereas it abolished them in aortic rings. The remaining relaxation resistant to L-NOARG in mesentenc artenal rings was insensitive to additional MB or OxyHB, and was not accompanied by increases in cGMP contents of rings. Halothane inhibited endothelium-dependent relaxation in aorta and mesentenc artenal rings. This inhibitory effect was larger in aorta. Halothane also inhibited NO independent EDHF-dependent relaxation in the mesentenc arterial rings.
Conclusion
Despite a similar inhibitory effect on the EDHF relaxing pathway, halothane has a larger effect on endothelium-dependent relaxation in the aorta (NO dependent mainly) than in the mesenteric rings (NO and EDHF dependent).
Résumé
Objectif
Comparer sur l’artère mésenténque et sur l’aorte du rat l’influence de l’halothane sur la vasodilatation induite par l’acétylcholine (ACh).
Méthodes
On a comparé les réactions d’anneaux arténels isolés de segments d’aorte et d’artère mésentérique préalablement contractés avec de la phényléphnne à l’ACh (10−8–10−5M), en présence d’halothane à 0 à 3% sur des enregistrements de la force de la tension isométrique. On a vérifié les effets de la NG-nitro-l-arginine (L-NOARG, 3 × 10−5 M), du bleu de méthylène (MB. 5 × 10−6 M), de l’oxyhémoglobine (OxyHB, 10−7 M) et de plusieurs inhibiteurs des canaux potassiques: le tétraéthylammonium (TEA, 10−5M, 10−3 M), l’apamine (AP, 10−7M), la charybdotoxine (ChTx, 10−7 M) et le glibenclamide (GC, 10−5M) sur la vasodilatation de l’artère mésentérique induite par l’ACh. Le radioxmmunodosage a servi en outre à mesurer l’accumulation de guanosine 3′:′5 — monophosphatase cyclique (cGMP) dans les anneaux arténels mésentériques prétraités à la L-NOARG.
Résultats
La L-NOARG n’abolissart que partiellement la vasodilatation des anneaux arténels mésentériques induite par l’ACh (P < 0,05. réduction de la dilatation maximale d’environ 50%) alors qu’elle abolissait celle des anneaux aortiques. La vasodilatation résiduelle L-NOARG-résistante des anneaux artériels mésentériques ne réagissait pas à l’ajout de MB ou d’OxyHB et ne s’accompagnait pas d’une augmentation du contenu en cGMP des anneaux. L’inhibition par l’halothane de la vasodilatation endothélium-dépendante des anneaux aortiques et artériels mésentériques était plus importante dans l’aorte. L’halothane inhibait aussi la vasodilatation NO-indépendante EDHP-dépendante des anneaux mésentériques.
Conclusion
Malgré des effets inhibiteurs similaires sur les voies de la vasodilation EDHF, l’halothane a un effet plus prononcé sur la vasodilatation endothélium-dépendante au niveau de l’aorte (principalement NO-dépendante) qu’au niveau des anneaux mésentériques (NO-et EDHF-dépendante).
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References
Palmer RMJ, Ferrige AG, Moncada S. Nitric oxide release accounts for biological activity of endotheliumderived relaxing factor. Nature 1987; 327: 524–6.
Palmer BMJ, Ashton DS, Moncada S. Vascular endothelial cells synthesize nitric oxide from L-arginine. Nature 1988; 333: 664–6.
Muldoon SM, Hart JL, Bowen KA, Freas W. Attenuation of endothelium-mediated vasodilation by halothane. Anesthesiology 1988; 68: 31–7.
Uggeri MJ, Proctor GJ, Johns RA. Halothane, enflurane and isoflurane attenuate both receptor- and non receptor-mediated EDRF production in rat thoracic aorta. Anesthesiology 1992; 76: 1012–7.
Stone DJ, Johns RA. Endothelium-dependent effects of halothane, enflurane, and isoflurane on isolated rat aortic vascular rings. Anesthesiology 1989; 71: 126–32.
Nakamura K, Terasako K, Toda H, et al. Mechanisms of inhibition of endothelium-dependent relaxation by halothane, isoflurane, and sevoflurane. Can J Anaesth 1994; 41: 340–6.
Toda H, Nakamura K, Hatano Y, Nishiwada M, Kakuyama M, Mori K. Halothane and isoflurane inhibit endothelium-dependent relaxation elicited by acetylcholine. Anesth Analg 1992; 75: 198–203.
Hart JL, Jing M, Bina S, Freas W, Van Dyke RA, Muldoon SM. Effects of halothane on EDRF/cGMP-mediated vascular smooth muscle relaxations. Anesthesiology 1993; 79: 323–31.
Toda N, Fujita T. Responsiveness of isolated cerebral and peripheral arteries to serotonin, norepinephrine, and transmural electrical stimulation. Circ Res 1973; 33: 98–104.
Su JY, Chang YI, Tang LJ. Mechanisms of action of enflurane on vascular smooth muscle. Anesthesiology 1994; 81: 700–9.
Garland CJ, McPherson GA. Evidence that nitric oxide does not mediate the hyperpolarization and relaxation to acetylcholine in the rat small mesenteric artery. Br J Pharmacol 1992; 105: 429–35.
Feletou M, Vanhoutte PM. Endothelium-dependent hyperpolarization of canine coronary smooth muscle. Br J Pharmacol 1988; 93: 515–24.
Brayden JE. Membrane hyperpolarization is a mechanism of endothelium-dependent cerebral vasodilation. Am J Physiol 1990; 259: H668–73.
Chen G, Suzuki H. Some electrical properties of the endothelium-dependent hyperpolarization recorded from rat arterial smooth muscle cells. J Physiol (Lond) 1989; 410: 91–106.
Tayler SG, Weston AH. Endothelium-derived hyperpolarizing factor; a new endogenous inhibitor from the vascular endothelium. Trends Pharmacol Sci 1988; 9: 272–4.
Garland CJ, Plane F, Kemp BK, Cocks TM. Endotheliumdependent hyperpolarization: a role in the control of vascular tone. Trends Pharmacol Sci 1995; 16: 23–30.
Standen NB, Quayle JM, Davies NW, Brayden JE, Huang Y, Nelson TM. Hyperpolarizing vasodilators activate ATP-sensitive K+ channels in arterial smooth muscle. Science 1989; 245: 177–80.
Bolton TB, Lang RJ, Takewaki T. Mechanisms of action of noradrenaline and carbachol on smooth muscle of guinea-pig anterior mesenteric artery. J Physiol (Lond) 1984; 351: 549–72.
Chen G, Cheung DW. Modulation of endotheliumdependent hyperpolarization and relaxation to acetylcholine in rat mesenteric artery by cytochrome P450 enzyme activity. Circ Res 1996; 79: 827–33.
Kajioka S, Nakashima M, Kitamura K, Kuriyama H. Mechanisms of vasodilation induced by potassiumchannel activators. Clin Sci 1991; 81: 129–39.
Johns RA. Endothelium, anesthetics, and vascular control. Anesthesiology 1993; 79: 1381–91.
Akata T, Nakashima M, Kodama K, Boyle WA III, Takahashi S. Effects of volatile anesthetics on acetylcholine-induced relaxation in the rabbit mesenteric resistance artery. Anesthesiology 1995; 82: 188–204.
Lischke V, Busse R, Hecker M. Inhalation anesthetics inhibit the release of endothelium-derived hyperpolarizing factor in the rabbit carotid artery. Anesthesiology 1995; 83: 574–82.
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Iranami, H., Hatano, Y., Tsukiyama, Y. et al. Halothane inhibition of acetylcholine-induced relaxation in rat mesenteric artery and aorta. Can J Anesth 44, 1196–1203 (1997). https://doi.org/10.1007/BF03013345
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DOI: https://doi.org/10.1007/BF03013345