PubMed · 16335515
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Nischol K Raval, Chittanranjan Andrade. Unmodified ECT vs modified ECT.. https://pubmed.ncbi.nlm.nih.gov/16335515/
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A great variety of mishaps can occur during or following the administration of anesthesia and operative or investigational procedures that do not necessarily convey an error of judgment or negligence on the part of the surgeon or the anesthetist. However, all deaths occurring during the course of anesthesia and surgery or within a reasonable period thereafter (commonly referred to as peri-operative period) have to be reported to the police as these deaths cannot be regarded as natural. Despite the death occurring due to some preexisting disease or some co-existent condition, there may be a tendency on the part of the relatives of the deceased to impute negligence on the part of the anesthetist and/or the surgeon merely because of the fact that the death was closely associated with the anesthesia and surgical intervention. As such, any death suspected to be caused, or contributed to, by any of these procedures needs to be adequately investigated both from the point of view of the relatives of the deceased as well as instituting future safety measures. This paper examines the medical, ethical and legal aspects of such deaths with reference to the allegations of medical negligence in these cases.
In contrast with most inhalational anesthetics, the anesthetic gases xenon (Xe) and nitrous oxide (N(2)O) act by blocking the N-methyl-d-aspartate (NMDA) receptor. Using x-ray crystallography, we examined the binding characteristics of these two gases on two soluble proteins as structural models: urate oxidase, which is a prototype of a variety of intracellular globular proteins, and annexin V, which has structural and functional characteristics that allow it to be considered as a prototype for the NMDA receptor. The structure of these proteins complexed with Xe and N(2)O were determined. One N(2)O molecule or one Xe atom binds to the same main site in both proteins. A second subsite is observed for N(2)O in each case. The gas-binding sites are always hydrophobic flexible cavities buried within the monomer. Comparison of the effects of Xe and N(2)O on urate oxidase and annexin V reveals an interesting relationship with the in vivo pharmacological effects of these gases, the ratio of the gas-binding sites' volume expansion and the ratio of the narcotic potency being similar. Given these data, we propose that alterations of cytosolic globular protein functions by general anesthetics would be responsible for the early stages of anesthesia such as amnesia and hypnosis and that additional alterations of ion-channel membrane receptor functions are required for deeper effects that progress to "surgical" anesthesia.
Heme oxygenase (HO), the rate limiting enzyme in the breakdown of heme into carbon monoxide (CO), iron and bilirubin, has recently received overwhelming research attention. To date three mammalian HO isozymes have been identified, and the only inducible form is HO-1 while HO-2 and HO-3 are constitutively expressed. Advances in unveiling signal transduction network indicate that a battery of redox-sensitive transcription factors, such as activator protein-1 (AP-1), nuclear factor-kappa B (NF-kappaB) and nuclear factor E2-related factor-2 (Nrf2), and their upstream kinases including mitogen-activated protein kinases play an important regulatory role in HO-1 gene induction. The products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin have been shown to exert protective effects in several organs against oxidative and other noxious stimuli. In this context, it is interesting to note that induction of HO-1 expression contributes to protection against liver damage induced by several chemical compounds such as acetaminophen, carbon tetrachloride and heavy metals, suggesting HO-1 induction as an important cellular endeavor for hepatoprotection. The focus of this review is on the significance of targeted induction of HO-1 as a potential therapeutic strategy to protect against chemically-induced liver injury as well as hepatocarcinogenesis.