• X Wu, S Zhang, and G Shan.
• Department of Anesthesiology, First Hospital, Beijing Medical University, No. 8 Xishiku Street, 100034, Beijing, China.
• J Anesth. 1997 Jun 1;11(2):130-5.

AbstractTo verify the effect of nitric oxide pathway modification during sepsis, experiments were conducted in four groups of anesthetized dogs which received lipopolysaccharide (LPS) intravenously (group 1), 300 mg·kg(-1) ofL-arginine plus LPS (group 2), 20 mg·kg(-1) ofN-nitro-L-arginine plus LPS (L-NNA, group 3), and normal saline as the control group. Hemodynamic and oxygenation data as well as extravascular lung water (EVLW) were measured or calculated. The results showed thatL-arginine increases cardiac output index (CI) and decreased the peripheral vascular resistance index (PVRI) without a significant influence on oxygen extraction ratio (O2ER), oxygen delivery (DO2), or oxygen consumption (VO2). All of the untoward hemodynamic effects of LPS were exacerbated by the addition ofL-NNA. Therefore, as DO2 was significantlys decreased byL-NNA, and although O2ER was increased (insufficiently), VO2 was still decreased significantly. EVLW was markedly increased byL-NNA. These results support the hypothesis that inhibition of nitric oxide synthesis may exacerbate hemodynamic and oxygenation consequences in septic shock.

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