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Heme nitric oxide synthesis effects

TABLE II Effects of Endogenous Nitric Oxide Synthesis on Total Cytochrome M50 Heme and Total Microsomal Heme in Microsomes from Freshly Isolated and Cultured Hepatocytes of Corynebacterium parvum-Treated Rats ... [Pg.281]

The mechanism of the acute kidney injury is thought to be multifactorial and similar to other cases of myoglobinuric renal failure [118, 121-126]. These factors include obstruction of tubules, toxic effects of the pigment or iron on renal tubular cells and altered hemodynamics in association with inhibition of the vasodilator nitric oxide by myoglobin. Experimental animals exposed to heme pigment have increases in the renal synthesis of both heme oxidase and ferritin [125]. This allows for more rapid heme degradation and greater sequestration of potentially toxic iron by the tubular cells [125]. Whether narcotics or the hypotensive, hypoxic environment associated with rhabdomyolysis interfere with these protective effects of the kidney is unknown. [Pg.604]


See other pages where Heme nitric oxide synthesis effects is mentioned: [Pg.924]    [Pg.363]    [Pg.729]    [Pg.146]    [Pg.190]    [Pg.730]    [Pg.121]    [Pg.249]    [Pg.503]   
See also in sourсe #XX -- [ Pg.279 , Pg.280 , Pg.281 ]




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