nitroarginine and Shock

This work was done on rat tourniquet shock (ToS) model. It was found that reactivity of isolated perfused aortic ring to noradrenaline decreased, while cGMP content of the aortic tissue increased. These changes could be potentiated by perfusion with L-arginine (NO-precursor). On the other side, when the aortic ring was perfused with L-NNA (NO-synthesis inhibitor) or methylene blue (soluble cGMPase inhibitor), the changes could be attenuated. The effect of these drugs are independent of the presence of vascular endothelium. The results suggest that non-endothelium-derived NO-like relaxing factor may be one of the factors causing low vascular reactivity of the ToS animals.

Topics: Animals; Cyclic GMP; Guanylate Cyclase; Male; Methylene Blue; Nitric Oxide; Nitric Oxide Synthase; Nitroarginine; Rats; Rats, Wistar; Shock; Tourniquets; Vasoconstriction

When NG-nitro-L-arginine, a nitric oxide synthase inhibitor, administration was started 5 min prior to shock induction in anesthetized dogs, a partial restoration was observed in endotoxin-induced shock and a complete recovery in platelet activating factor (PAF)-induced shock. When NG-nitro-L-arginine infusion was started 5 min after shock induction, no significant recovery was observed in endotoxin-induced shock and a complete recovery in PAF-induced shock. These data indicate that enhanced production of nitric oxide by vascular endothelial cells may contribute to endotoxin- or PAF-induced shock and also that some mediators including inducible nitric oxide synthase and/or cellular damage might be involved in endotoxin-induced shock.

Topics: Amino Acid Oxidoreductases; Analysis of Variance; Animals; Arginine; Dogs; Endothelium, Vascular; Endotoxins; Female; Male; Nitric Oxide; Nitric Oxide Synthase; Nitroarginine; Platelet Activating Factor; Shock; Shock, Septic

On tourniquet shock (ToS) rat model, it was found that the reactivity of isolated perfused aortic ring to noradrenaline was decreased, while the cGMP content of the aortic tissue was increased. These ToS-induced changes could be potentiated or attenuated respectively by perfusion with NO-precursor, L-arginine, or NO-synthesis inhibitor L-NNA independent of the presence of vascular endothelium. Guanylate cyclase inhibitor, methylene blue, could also attenuate the aortic reactivity. All these results suggest that the aortic musculature can produce a NO-LRF factor capable of lowering the vascular reactivity of the ToS animals. That L-arginine can ameliorate while L-NNA can exacerbate ToS, suggest that NO-LRF do play an adaptive role in the protective mechanism of the organism during ToS.

Topics: Animals; Aorta; Arginine; Blood Pressure; Cyclic GMP; In Vitro Techniques; Male; Nitric Oxide; Nitroarginine; Rats; Rats, Wistar; Shock; Tourniquets; Vasodilator Agents