Hypoxic‐ischemic brain injury and narcotic drugs administration

Abstract

Following cerebral ischemia and hypoxia, disorders in brain metabolism, histological pathology, and neural function commonly could result in different nerve injuries, to some degree. Many researchers have revealed that some narcotic drugs hold a prominent efect of prevention and therapy on cerebral ischemic-hypoxic injury and ischemia-reperfusion injury. However, the underlying mechanism is largely unknown. In this paper, we summarized narcotic drugs' roles in antagonizing the neurotoxicity of excitatory amino acid, reducing excitatory injury and activating intracellular signaling cascade channel, adjusting the balance of Ca 2+ , increasing the expression of protective genes, reducing the generation of NO and free radical and anti-lipid peroxidation, and discussed and elucidated their relations.

Changes in postictal cerebral perfusion are related to the duration of electroconvulsive therapy‐induced seizures

“…Eight patients (33%) received midazolam 2–5 mg iv after ECT and before the ASL‐MRI acquisition because of severe postictal confusion. Studies on the influence of acute benzodiazepine administration have reported decreased CBF, cerebral metabolic rate, oxygen consumption, and intracranial pressure by enhancing the inhibitory effect of γ‐aminobutyric acid type A receptors 45,46 . The use of benzodiazepines may be associated with increased risk for ischemic stroke 47 .…”

“…Studies on the influence of acute benzodiazepine administration have reported decreased CBF, cerebral metabolic rate, oxygen consumption, and intracranial pressure by enhancing the inhibitory effect of γ-aminobutyric acid type A receptors. 45,46 The use of benzodiazepines may be associated with increased risk for ischemic stroke. 47 To verify whether our results were not driven by the administration of midazolam, we examined the groups of patients with or without postictal midazolam more closely and performed sensitivity analyses.…”