Anesthesiology
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Review Case Reports
Case scenario: perianesthetic management of laryngospasm in children.
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Propofol exposure to neurons during synaptogenesis results in apoptosis, leading to cognitive dysfunction in adulthood. Previous work from our laboratory showed that isoflurane neurotoxicity occurs through p75 neurotrophin receptor (p75(NTR)) and subsequent cytoskeleton depolymerization. Given that isoflurane and propofol both suppress neuronal activity, we hypothesized that propofol also induces apoptosis in developing neurons through p75(NTR). ⋯ These results demonstrate that propofol induces apoptosis in developing neurons in vivo and in vitro and implicate a role for p75(NTR) and the downstream effector RhoA kinase.
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Subarachnoid hemorrhage (SAH) in pregnancy occurs because of a variety of etiologies, which range from ruptured aneurysms to benign venous bleeding. The more malignant etiologies represent an important cause of maternal morbidity and mortality. We sought to investigate the epidemiology and mechanisms of pregnancy-related SAH. ⋯ SAH during pregnancy results from a range of etiologies, and is less likely to be because of a cerebral aneurysm than SAH occurring in the nonpregnant patient. Peripartum SAH frequently occurs in the setting of hypertensive disorders.
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Exposure of rhesus macaque fetuses for 24 h or neonates for 9 h to ketamine anesthesia causes neuroapoptosis in the developing brain. The current study clarifies the minimum exposure required for and the extent and spatial distribution of ketamine-induced neuroapoptosis in rhesus fetuses and neonates. ⋯ The developing rhesus macaque brain is sensitive to the apoptogenic action of ketamine at both a fetal and neonatal age, and exposure duration of 5 h is sufficient to induce a significant neuroapoptosis response at either age. The pattern of neurodegeneration induced by ketamine in fetuses was different from that in neonates, and loss of neurons attributable to ketamine exposure was 2.2 times greater in the fetal than neonatal brains.