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Progress in Medical World part 10

Renal Failure and Liver Dysfunction Hepatotoxic effects after inhalation anesthetic exposure thought to be caused by cytochrome P-450-mediated oxidative or reductive metabolism with the production of reactive metabolites. These metabolites may initiate an immune response that causes liver necrosis. Nephrotoxic effects associated with metabolism and the duration of the level of free Florida is very high in the blood. Toxic effects clinically relevant restricted to kidney and liver. Drugs that have been used in organ failure including halothane and gas klorofom currently has expired, trikloroetilen, and metoksifluran. Effects are severe, but rare, have been reported due to the use of enflurane and isofluran. Sevoflurane metabolism also have the potential to produce nephrotorik fluoride. Sevoflurane and expressed desfluran not cause liver dysfunction.
In addition to the effects of metabolites, inhalation anesthetic causing organ dysfunction due to decreased perfusion. Halothan significantly reduce portal venus and arterial blood flow to the liver in proportion to the degree of anesthesia. Reduction in blood flow in heart arteries causing reduction of oxygen delivery that causes the organ injured. This mechanism is particularly important for patients who develop chronic liver disease and portal hypertension.  

Marginal hepatocellular function can be adjusted with a total reduction of blood flow in heart arteries and acute liver failure that begins at the postoperative period. However, a decrease in blood flow in heart arteries that total may be due to the use of anesthesia given in a way not inhaled, manipulation operation, or use of vasopressor. Likewise, postoperative renal dysfunction may be the result of hemodynamic effects of inhalation anesthesia or blood flow in the renal and secretion of antidiuretic hormone.

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