Acetylcholine, decreased dramatically two weeks after isoflurane exposure. Donepezil, which is an antagonist of AChE, is a clinically approved medication used to treat Alzheimers disease patients. In the present study, we show that donepezil can prevent isoflurane-induced spatial memory impairment. This ZSTK474 finding suggests new possibilities for its clinical application to treat postoperative cognitive dysfunction. Lee found that animals that SB 203580 structure received donepezil had increased ChAT immunoreactivity in the cerebral cortex, which is similar to the present results. We demonstrated that intragastric donepezil administration for four weeks increased ChAT levels in the donepezil group and the donepezilisoflurane group. However, the MWM data indicate that donepezil does not make animals in the isofluranedonepezil and donepezil groups more clever than the control mice. The mechanism responsible for these effects is unknown. Kakinuma found that ChAT levels in the ventricular myocardium increased after donepezil treatment, which was accompanied by an increase in ChAT promoter activity. More studies should be performed to determine the detailed mechanism for these effects. Although Zivin found that AChE mRNA in the brain increased significantly after 28 days of donepezil treatment, we did not find any changes in AChE protein levels among the four groups. Alpha7-nAChRs are one of the major functional nAChR subtypes in the brain, and these receptors play an important role in learning and memory. Although Takadatakatori showed the upregulation of a7-nAChRs in primary culture rat cortical neurons after chronic donepezil treatment, we did not observe any significant changes in a7-nAChRs levels between groups. With the two-electrode voltage-clamp technique, Jackson demonstrated that isoflurane and halothane inhibited acetylcholine-evoked currents of a7-nicotinic acetylcholine receptors in Xenopus oocytes in a reversible and concentration-dependent manner. Studies are needed to examine a7-nAChRs after donepezil and volatile anesthetic exposure in vivo. Six-hour isoflurane exposure in 30 oxygen resulted in stable blood pressure and heart rate, normal oxygenation, adequate PCO2 and moderate acidosis. Similarly, Szczesny demonstrated that 0.8�C1.3 isoflurane exposure for 6.5 hours resulted in a stable mean blood pressure and heart rate in mice. With an oximeter probe, Ewald found that oxygen saturation remained at,97 at anesthesia levels of 0.9�C1.25 isoflurane. Because it is quite difficult to acquire a sufficient volume of arterial blood from mice without anesthesia for analysis, there is currently no record of normal blood gas values for mice. For this reason, many studies do not assess blood gases. Therefore, we do not know how to define and evaluate the effects of ac
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