[The protective effect of a NO-synthase inhibitor in heat shock].
Acute hypotension related to the excessive production of a potent endogenous vasodilator nitric oxide (NO) is a most important link of heat shock pathogenesis. It was shown that inhibition of inducible NO-synthase by N(W)-nitro-L-arginine (L-NNA) at 10 mg/kg reduces the mortality of animals due to heat shock, prevents the fall of arterial blood pressure and abnormal inhibition of constriction and stimulation of dilation reactions related to NO hyperproduction. A total blockade of NO synthesis by L-NNA at 300 mg/kg did not exert a protective effect from heat shock. The data obtained suggest the importance of inducible NO-synthase in heat shock pathogenesis and show promise for the application of selective inhibition of inducible NO-synthase at pathological states related to NO hyperproduction.
Manukhina
E B
EB
Pokidyshev
D A
DA
Golubeva
L Iu
LIu
Zenina
T A
TA
Malyshev
I Iu
IIu
D000208:Acute Disease; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004353:Drug Evaluation, Preclinical; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D018882:Heat Stress Disorders / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D007022:Hypotension / Q000150:complications / Q000503:physiopathology / Q000517:prevention & control; D008297:Male; D009569:Nitric Oxide / Q000037:antagonists & inhibitors; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D019335:Nitroarginine / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D012769:Shock / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control
D004791:Enzyme Inhibitors; D019335:Nitroarginine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase