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The ability to pharmacologically render patients insensible to noxious stimulation using general anesthetics and sedatives represents one of the greatest discoveries in medicine. Advanced physiological monitoring and meticulous administration of modern anesthetic drugs have facilitated surgical interventions to mitigate life-threatening conditions in very young children. Moreover, sedation during mechanical ventilation and for painful procedures in intensive care units has shielded neonates from the deleterious effects of pain and suffering. Accordingly, every year, anesthetics and sedatives are used in millions of young children worldwide to ablate the stress response to noxious stimulation and to mitigate potential, stress-related morbidity during painful procedures and imaging studies.
However, recent findings in laboratory animals have demonstrated structural alterations, such as a widespread increase in apoptotic brain cell death, an inborn cell suicide program, immediately following exposure to all currently and commonly used sedatives and anesthetics. Moreover, several preclinical studies have also observed alterations in synaptic formation and subsequent impairment in neurocognitive function. These findings in newborn animals have led to significant concerns among pediatric anesthesiologists and parents.
Given the potentially serious consequences of long-term neurological sequelae following uneventful pediatric surgery with anesthesia, our research aims to clarify the underlying mechanisms and to delineate the selectivity of anesthesia-induced neuroapoptosis, which will be critical for assessing human relevance of this phenomenon, and if necessary, for developing mitigating strategies.
Along those lines, our laboratory has demonstrated similar neuronal apoptosis following prolonged exposure to equipotent doses of the three most commonly used anesthetics: Desflurane, Isoflurane and Sevoflurane. Furthermore, we were able to demonstrate that anesthetics selectively affect immature neurons, explaining the shift in brain regional vulnerability, changing with age. We characterized the age of susceptible neurons to be around two weeks of age. Given the phenomenon’s potential dramatic clinical impact, we will continue our research efforts to improve the understanding of the underlying mechanism, to delineate human applicability, and to determine alternative anesthetic techniques. Our translational efforts are geared toward examining the effects of surgery with anesthesia early in life on subsequent brain structure and function using noninvasive imaging technology and validated individualized testing.
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