The physiologic changes associated with se ptic shock result from a so phisticatedrninterplay of a number of mediators. The initiating factor in the complex cascade ofrninflammatory events leading to clinical sepsis in most cases is the release of endotoxin; arnlipopolysaccharide component of the cell wall of Gram-negative bacteria. Once released,rnendotoxin triggers the cascade of inflammatory mediators ipcreasing capillary permeabilityrnand vasodilation, with resultant disturbances of microcirculation in many organs.rnEvidences have been presented supporting the view that sepsis-induced disturbancesrnin vascular smooth muscle contractility are mediated mainly by nitric oxide. Endotoxin andrnsome other cytokines stimulate nitric oxide production by the activation of an induciblernnitric oxide ;ynthase, transforms an amino acid L-arginine into nitric oxide and L-citrullinernin endothelial cells, macrophages and other cells. This induction of nitric oxide sy nthasernwith the consequent excessive production of nitric oxide, is thus proposed to be involvedrnin pathologic vasodilation and tissue damage seen in septic shock.rnIn the present study, intravenous administration of endotoxin (LPS, E.coli extract,rn70 jJg/ICg) in six unanesthetized ewes resu teCrillaaecrease illMA-P by 38%; and SYR-byrn37.5% compared to the control baseline values. Injection of 50 mg/kg carboxy-PTIO, as anrnantidote, after an hour of LPS dose, reestablished the baseline values .rnThe pulmonary atterial pressure was increased by 55.56%; rectal temperature, healtrnrate and respiratOIY rate increased linearly; and the cardiac index and the central venousrnI pressure increased after initial fall due to endotoxin. Carboxy-PTIO showed to have nornsignificant effect on these parameters. The renal blood flow decreased significantly (p