PROTECTIVE EFFECTS OF NO-SYNTHASE INHIBIT OR DURING HEAT-SHOCK

Acute hypotension related to the excessive production of a potent endo genous vasodilator nitric oxide (NO) is a most important link of heat shock pathogenesis, It was shown that inhibition of inducible NO-synth ase by N-W-nitro-L-arginine (L-NNA) at 10 mg/kg reduces the mortality of animals due to heat shock, prevents the fail of arterial blood pres sure and abnormal inhibition of constriction and stimulation of dilati on reactions related to NO hyperproduction. A total blockade of NO syn thesis by L-NNA at 300 mg/kg did not exert a protective effect from he at shock. The data obtained suggest the importance of inducible NO-syn thase in heat shock pathogenesis and show promise for the application of selective inhibition of inducible NO-synthase at pathological state s related to NO hyperproduction.