Such_Saturation
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Clinical concentrations of chemically diverse general anesthetics minimally affect lipid bilayer properties
In the study, published March 6 in the Proceedings of the National Academy of Sciences, researchers demonstrated that general anesthetics at clinically relevant concentrations do not affect the properties of the part of cellular membranes composed of fat, called the lipid bilayer, contrary to previous ideas. Their discovery strongly supports a modern hypothesis that anesthesia interacts directly with membrane proteins – rather than indirectly through the membrane itself – to inhibit the electrical communications between neurons, triggering unconsciousness.
"We have debunked a century-old hypothesis and finally have proof that these anesthetics must have a direct effect on integral membrane proteins – and not an indirect effect on proteins through the lipid bilayer – to put patients in a coma-like state, allowing them to undergo painful procedures with no memory or pain," said co-senior author Dr. Hugh Hemmings, chair of the Department of Anesthesiology at Weill Cornell Medicine.
Since the first successful use of ether to induce unconsciousness for surgery in 1846, scientists have simultaneously hailed general anesthesia as one of the most important advances in medicine while also striving to understand how it exerts its desired clinical effects. Two 19th-century pharmacologists hypothesized that anesthetic potency correlates with drug solubility in fats; experiments in which they dissolved anesthetic agents into olive oil confirmed their suspicions. Their findings produced the prevailing scientific explanation for anesthesia that held sway for a century: General anesthetics work by altering lipid bilayer properties and disrupting neuronal function, leading to unconsciousness. By the 1970s, some investigators began challenging that dogma, suggesting that proteins are in fact anesthetics' targets, and a vigorous controversy ensued.
In the study, published March 6 in the Proceedings of the National Academy of Sciences, researchers demonstrated that general anesthetics at clinically relevant concentrations do not affect the properties of the part of cellular membranes composed of fat, called the lipid bilayer, contrary to previous ideas. Their discovery strongly supports a modern hypothesis that anesthesia interacts directly with membrane proteins – rather than indirectly through the membrane itself – to inhibit the electrical communications between neurons, triggering unconsciousness.
"We have debunked a century-old hypothesis and finally have proof that these anesthetics must have a direct effect on integral membrane proteins – and not an indirect effect on proteins through the lipid bilayer – to put patients in a coma-like state, allowing them to undergo painful procedures with no memory or pain," said co-senior author Dr. Hugh Hemmings, chair of the Department of Anesthesiology at Weill Cornell Medicine.
Since the first successful use of ether to induce unconsciousness for surgery in 1846, scientists have simultaneously hailed general anesthesia as one of the most important advances in medicine while also striving to understand how it exerts its desired clinical effects. Two 19th-century pharmacologists hypothesized that anesthetic potency correlates with drug solubility in fats; experiments in which they dissolved anesthetic agents into olive oil confirmed their suspicions. Their findings produced the prevailing scientific explanation for anesthesia that held sway for a century: General anesthetics work by altering lipid bilayer properties and disrupting neuronal function, leading to unconsciousness. By the 1970s, some investigators began challenging that dogma, suggesting that proteins are in fact anesthetics' targets, and a vigorous controversy ensued.