Endothelially-derived NO is an important modulator of sustained agonist-induced vasoconstriction. NO, as well as endothelially-derived cyclooxygenase products and EDHF, also contribute significantly to phenylephrine-induced oscillatory vasomotion.
Propofol is often used in patients with asthma, but it can induce bronchospasm. We report a patient with sick house syndrome (nonspecific complaints of mucosal irritation, headache, nausea, and chest symptoms) who suffered bronchospasm. This case suggests that propofol is not always a safe anesthetic for patients with asthma, especially drug-induced asthma.
Propofol and sevoflurane seem to have some different effects on endothelial function, which regulates the pacemaking of spontaneous contraction of lymphatic vessels.
Isolated spiral strips of rat thoracic aorta with endothelium were suspended for isometric tension recordings in a physiological salt solution. Endothelium-dependent vasorelaxation was elicited by carbachol 10(-6) and 10(-5) mol litre-1 during norepinephrine-induced contractions, and the effects of 1.5% and 3% halothane were evaluated with concomitant measurement of [Ca2+]i using fura-2-Ca2+ fluorescence. The effects of halothane on endothelium-dependent relaxation were compared with those of nitro G-L-arginine methyl ester 10(-4) mol litre-1 (L-NAME: an inhibitor of nitric oxide synthase). Carbachol reduced norepinephrine-induced contractions in a concentration-dependent manner, but augmented the norepinephrine-induced increase in [Ca2+]i in endothelium intact strips. In contrast, carbachol did not influence muscle tension or [Ca2+]i when the endothelium was completely denuded. Although 3% halothane and L-NAME 10(-4) mol litre-1 inhibited carbachol-induced vasorelaxation in a similar manner, halothane inhibited carbachol-induced increases in [Ca2+]i. These results indicate that halothane inhibited a carbachol-induced increase in [Ca2+]i in the endothelium, which subsequently attenuated the decrease in muscle tension.
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