A method for assessing the gas exchange through the middle ear (ME) mucosa using nitrous oxide is introduced. Increases in the ME pressure was determined by a tympanogram or a micropressure sensor inserted into the mastoid cavity during ear surgery under general anesthesia using 67% nitrous oxide, 33% oxygen, and sevoflurane on 30 normal ears, 12 ears with otitis media with effusion (OME), and 3 postoperative ears with chronic adhesive otitis media or cholesteatoma. All the 30 normal ears except one showed varying pressure increase, and an inverse correlation was observed between pressure increase and area of mastoid on radiographs. Pressure increase was observed in 6 (50%) ears with OME, and this finding correlated well with the presence or absence of air space in the ME on computed tomography images examined preoperatively, on ears which had ear surgery, the presence or absence of pressure increase correlated with the degree of previous surgical intervention on the mastoid. The rationale and possibility of clinical application of this method is discussed.

Our finding that the inhibitory effects of isoflurane and sevoflurane on Ang II-induced vasoconstriction are enhanced in SHR may, at least in part, account for the anesthesia-induced systemic hypotension frequently seen in hypertensive patients.

The current study indicates that Ca2+ and cPKC-alpha are involved in angiotensin II-induced vascular contraction. Sevoflurane dose-dependently inhibited the angiotensin II-stimulated, cPKC-mediated but not Ca2+-elicited contraction of rat aortic smooth muscle.

The present study was designed to examine the role of basally released nitric oxide in relaxations to an ATP-sensitive K+ channel opener. Whether relaxations to levcromakalim are modulated by endothelial removal or the inhibitors of vasodilator effects of endothelium-derived nitric oxide, were investigated in the rat aorta. During contractions to phenylephrine (3 x 10(-7) to 10(-6) M), levcromakalim (10(-8) to 10(-5) M) or a nitric oxide donor, 1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-1-triazene (NOC-7, 10(-9) to 10(-5) M), was added in a cumulative fashion. Relaxations to levcromakalim (10(-8) to 10(-5) M) were significantly reduced by the endothelium-removal. In aortas with endothelium, relaxations in response to levcromakalim were decreased by selective inhibitors of nitric oxide synthase (N(G)-nitro-L-arginine methyl ester, 10(-4) M) and soluble guanylate cyclase (1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one; ODQ, 10(-5) M) and a scavenger of nitric oxide (carboxy-PTIO, 10(-3) M). Relaxations to levcromakalim in aortas treated with these inhibitors are comparable to those seen in aortas without endothelium. KCl (30 mM) and an ATP-sensitive K+ channel inhibitor, glibenclamide (10(-5) M), abolished relaxations to levcromakalim in aortas with or without endothelium, whereas glibenclamide did not alter relaxations to NOC-7 (10(-9) to 10(-5) M) in aortas without endothelium. These results suggest that in rat aortas, inhibition of vasodilator effects of basally released nitric oxide can reduce relaxations via ATP-sensitive K+ channels, although these channels do not mediate relaxations to exogenously applied nitric oxide.

The effects of sevoflurane and isoflurane on the development of nitroglycerin (TNG) tolerance were investigated in isolated rat aorta. TNG tolerance was induced by incubation of the vascular tissue in the bathing media containing TNG (10-5 M) for 30 min. Sevoflurane, but not isoflurane, enhances TNG tolerance, possibly by additive generation of oxygen-derived free radicals.