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Ropivacaine cardiac toxicity of -aminobutyric acid A receptor mechanism
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Ropivacaine cardiac toxicity of -aminobutyric acid A receptor mechanism
Of: Zhuyao Min, Yuan Zu Yi, Wu Hui, Wang Ning, King Guixia
[Abstract] Objective To investigate the cardiac toxicity of ropivacaine on the -aminobutyric acid A receptor mechanism. Methods New Zealand white rabbits by intracerebroventricular injection of -aminobutyric acid A receptor agonist muscimol and -aminobutyric acid A receptor blocker picrotoxin, intravenous infusion of ropivacaine induced cardiotoxicity occurs in plasma concentrations of ropivacaine. Results intracerebroventricular injection of muscimol can significantly prolong the cardiac toxicity of ropivacaine time of occurrence to improve the cardiac toxicity of ropivacaine occurred ropivacaine plasma concentration; intracerebroventricular injection of picrotoxin can significantly reduce the cardiac toxicity of ropivacaine time of occurrence, lower cardiac toxicity of ropivacaine occurred in plasma ropivacaine tetracaine concentration. Conclusion Ropivacaine cardiac toxicity of ropivacaine mechanisms in addition to direct toxicity of the heart, the part of the central nervous system by -aminobutyric acid A receptor mediated.
[Keywords:] ropivacaine; cardiac toxicity; -aminobutyric acid A receptor
ABSTRACT: ObjectiveTo investigate the mechanism of ropivacaine in GABAA receptor-mediated cardiotoxicity.MethodsBy intravenous injection of ropivacaine into New Zealand white rabbits, we examined the plasma concentration of the drug when cardiotoxicity occurred after intracerebroventricular pretreatment with muscimol (a drug that enhances GABAA activity) and picrotoxin (a drug that decreases GABAA activity). ResultsIntracerebroventricular infusion of muscimol could significantly prolong the time of ropivacaine-induced cardiotoxicity and significantly increase the plasma concentration of ropivacaine. In contrast, intracerebroventricular infusion of picrotoxin significantly shortened the time of ropivaca
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