Open AccessHalothane and Isoflurane Inhibit Endothelium-Dependent Relaxation Elicited by Acetylcholine
Author(s) -
Hiroshi Toda,
Kumi Nakamura,
Yoshio Hatano,
Makoto Nishiwada,
Masahiro Kakuyama,
Kenjiro Mori
Publication year - 1992
Publication title -
anesthesia and analgesia/anesthesia and analgesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.404
H-Index - 201
eISSN - 1526-7598
pISSN - 0003-2999
DOI - 10.1213/00000539-199208000-00008
Subject(s) - halothane , isoflurane , acetylcholine , medicine , phenylephrine , guanosine , anesthesia , endothelium , endocrinology , sodium nitroprusside , vasodilation , endothelium derived relaxing factor , pharmacology , nitric oxide , chemistry , biochemistry , blood pressure
The purpose of this study was to determine whether volatile anesthetics modify the release of endothelium-derived relaxing factor. We examined the effects of halothane and isoflurane on endothelium-dependent relaxation and 3',5'-cyclic guanosine monophosphate formation elicited by acetylcholine and ionophore A23187 in isolated rat aorta. Halothane and isoflurane (1%-2%) significantly attenuated acetylcholine-induced relaxation of the phenylephrine-contracted aorta but had no significant effect on relaxation induced by A23187, nitroprusside, and nitroglycerin. Basal and A23187 (10(-7) M)-stimulated levels of 3',5'-cyclic guanosine monophosphate were slightly lowered by halothane and isoflurane (2%). In contrast, the increase of 3',5'-cyclic guanosine monophosphate elicited by acetylcholine (10(-5) M) was significantly attenuated by halothane (2%) and abolished by isoflurane (2%). These findings indicate that halothane and isoflurane strongly inhibit the release of endothelium-derived relaxing factor elicited by acetylcholine.