The effect of nitric oxide synthase inhibition on hypertonic saline treatment of controlled hemorrhagic shock.

The effect of the nitric oxide (NO) donor, L-arginine, and the NO synthase inhibitor, L-NAME on hypertonic saline (HTS) infusion in controlled hemorrhagic shock was studied in anesthetized rats. Hemorrhagic shock was induced by arterial bleeding of 35% of the total blood volume in 90 min. After 110 min, the animals were divided into two groups: in Group A, 5 mL/kg NaCl 7.5% (HTS) was infused. In Group B HTS was not infused. After 135 min the animals in both groups were divided into 4 subgroups: Group 1 (n = 8) was untreated, Group 2 (n = 8) was treated after 135 min with 100 mg/kg L-arginine, in Group 3 (n = 8) 100 mg D-arginine was infused, and in Group 4 (n = 8) 50 mg/kg L-NAME was infused. Arterial bleeding in Group A1 resulted in a fall in mean arterial pressure (MAP) to 43.5 +/- 5 mmHg (p < .001)) in 90 min. A similar fall in MAP was observed in all groups. HTS infusion in Group A1 was followed by an increase in MAP to 82.3 +/- 6 (p < .01)) after 125 min followed by a gradual decrease to 61.5 +/- 8 mmHg (p < .01)) after 4 h. Infusion of L-NAME in Group A4 resulted in an increase in MAP to 87.4 +/- 5 mmHg (p < .01)) that then rapidly dropped to 61.7 +/- 11 (p < .01)) after 4 h. Infusion of L-NAME in Group B4 resulted in an increase in MAP to 96.7 +/- 9 mmHg (p < .001)) which was maintained after 4 h at 92.2 mmHg, and was significantly higher than MAP in Group A4 (p < .01). We concluded that HTS infusion leads to a significant increase in MAP in controlled hemorrhagic shock. NO synthase inhibition by L-NAME in hemorrhagic shock leads to a protracted, significant increase in MAP. Infusion of HTS prevented the significant and sustained rise in MAP induced by L-NAME.