الفهرس 
Thiopentone sodiumOnly 14 pages are availabe for public view
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Abstract
Barbiturates are known to suppress contraction of isolated smooth muscle of various origins. However, it has been shown that some of them, thiamylal and thiopental, can also induce vasoconstriction in isolated arteries depending on the experimental conditions. Although vasodilatation by barbiturates has been explained by inhibition of voltage-operated ca2’ channels and suppression of the contractility of muscle proteins, mechanism(s) of contraction by barbiturates is little known. There are several evidences suggesting that ca2’ plays an important role in barbiturae-induced contraction. It has been demonstrated in rat aorta, using a ca2’ indicator dye, that the contraction induced by thiopental and thiamylai under basal tension was associated with increased free cytosolic ca2’ concentration while they did not specify the source of ca2’. Moreover, by recording the tension in various extraceluular conditions, it has been suggested that thiamylal-induced contraction was mainly due to influx of ca2’ from the extacellular fluid via pathways other than the voltage operated ca2’ channels. However, the mechanism of ca2’ mobilization by thiopental has not been explored. Anesthetic induction and maintenance with propofol is often accompanied by hypotension, which has been ascribed to a decrease in either systemic vascular resistance or cardiac output or both. However, in the presence of ca2’ antagonists, propofol produced constriction in bovine coronary artery rings denuded of endothelium. Experiments with isolated arteries may clarify if agents have direct vascular effects, as the influences of the nervous system and humoral factors are eliminated. Moreover, such experiments may demonstrate different responses of arteries from different sites. Halogenated volatile anesthetics, halothane and isoflurane modify vascular contractility through acting on various mechanisms of contraction. While they are thought to inhibit vascular contraction, they can also contract vessels depending on the type of vessels and on experimental conditions. In canine and rat mesenteric arteries, halothane caused a transient contraction, which has been clearly explained by anesthetic-induced ca2’ release from the sarcoplasmic reticulum. In contrast, halothane .and isoflurane induced a slowly developing sustained contraction in rat and rabbit aortae which has been treated with verapamil and precontracted with phenylephrine. Also, it has been clearly demonstrated that anesthetic-induced contraction in rat aorta was mediated by raised free intracellular ca2’ concentration, but the source of this mobilized ca2’ has not been examined in details. This study aimed to examine the contractile effect of thiopental, propofol, halothane and isoflurane and to elucidate the underlying mechanism(s) by conducting tension experiments, 45ca2+ flux measurements and fura 2 experiments. Endothelium denuded and intact rat aortic thoracic rings were used. We measured thiopental-induced contraction in denuded rings under basal tension, in verapamil treated rings subrnaximally contracted with phenylephrine, in ca2’-free solution, after ryanodine, before and after caffeine and after thapsigargin treatment. 45~aZin’f lux and 45~a2’ efflux experiments were performed to elucidate the role of ca2’ influx or ca2’ release respectively in the mechanism of contraction. For propofol (as well as intralipid), we examined its contractile effect in both endothelium intact and denuded rings. For halothane and isoflurane we measured their contractile effect in denuded rat aortic rings under basal tension, in verapamil treated rings submaximally contracted with phenylephrine, in ca2’-free solution, after ryanodine and after SK&F96365. 45~a2’influx experiment with and without SK&F96365 was performed. Simultaneous tension recordings and ca2’ monitoring before and after ryanodine was done using a flurescent dye for 4% halothane and 2.3% isoflurane. Our results showed that thiopental induced a dose-dependent contraction under basal tension. This contraction was enhanced after verapamil treated and phenylephrine precontracted rings. In ca2’-free solution, thiopental-induced contraction was inhibited at higher concentrations and abolished at lower concentrations. Ryanodine or caffeine pretreatment significantly reduced thiopental-induced contraction whereas thiopental pretreatment completely abolished caffeine-induced contraction. Thapsigargin pretreatment completely abolished thiopental -induced contraction. ca2’ influx experiment showed that thiopental could not induce any ca2’ influx. ca2’ efflux experiment confirmed the induced-release of ca2’ by thiopental.