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The Science Journal of the Lander College of Arts and Sciences

Abstract

Recent studies suggest that general anesthetic (GA) agents administered to developing rats, through its mechanism as an NMDA antagonist or a GABAa mimetic, may damage developing neural cells by inducing a higher rate of programmed cell death (apoptosis). Similar heightened degeneration was also apparent in higher primates such as the monkey. This warrants strong concern, as every year thousands of pregnant women and children below 1 year of age undergo a surgical procedure in which GAs are used. A spike in neuroapoptosis may lead to long term cognitive deficiencies lingering into adulthood. Are humans vulnerable to these affects? Different pathways are under investigation as to the cause of the damage in animals, but humans have different metabolic pathways than even higher primates, and the basic mechanism by which GAs take affect is not well understood. Scientists continue to unravel the underlying mechanism, seeking to stop the apoptotic cascade, all the while maintaining the benefits of the sedative effect. Promising new hope comes.

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