Their EC 50 values are mostly of the order of 1 mM, and experiments have shown that they bind to proteins as diverse as myoglobin ( Schoenborn et al., 1965), adenylate kinase ( Sachsenheimer et al., 1977), cholesterol oxidase ( Bertaccini et al., 1998) or even albumin ( Bhattacharya et al., 2000). This method, however, yielded few useful results for gaseous GAs, because they associate with many proteins non-specifically (they bind to more than one sites). ![]() In pharmacology, specific binding is very often used to locate the site of action of a drug. Lastly, I provide a ‘road map’ of GA research, to define what is needed to complete our understanding of these drugs, and suggest physical and chemical methods that could potentially revolutionize GA research at the molecular level. I shall also delineate our ignorance to show how far we are from a proper understanding of these mechanisms. ![]() A recent review has discussed the nervous system pathways involved in greater detail ( Franks, 2008), so the main emphasis here is on recent progress towards elucidating the molecular mechanisms of general anaesthesia. I shall first provide a brief review of previous results, concentrating on those which have an impact on future directions. In this review, I focus mainly on their action as agents to cause loss of consciousness. Without them, modern medicine, especially surgery, would not have been possible.Īlthough the primary event of GAs is loss of consciousness, they have additional actions which include analgesia, amnesia and muscle relaxation. GAs comprise one of the most important drug groups in clinical use. Towards the middle of the 20th century, the haloalkane gaseous GAs were synthesized, and they have remained the family of GA drugs most widely used. Over time, more chemicals were found to have general anaesthetic action. ![]() The first such drugs were chloroform and ether. General anaesthetics (GAs) have been in use since the mid-19th century.
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