Hypotension during septic shock does not correlate with exhaled nitric oxide in anesthetized rat.
Sepsis is characterized by hypotension, acidosis, and increased nitric oxide (NO) production. The role of NO in the development of sepsis-related hypotension is still unclear. The relationship among exhaled nitric oxide (ENO), arterial blood pressure (BP), and pH after administration of lipopolysaccharide (LPS) and tumor necrosis factor alpha (TNFalpha) was investigated in anesthetized rats. Forty-three adult male Sprague-Dawley rats were randomized into five groups: group 1 (C, n = 8) received normal saline; group 2 (LPS-I, n = 8) received Escherichia coli (LPS) 10 mg/kg intravenously (i.v.); group 3 (LPS-h, n = 10) received 100 mg/kg LPS i.v.; group 4 (n = 9) was treated with 100 mg/kg i.v. aminoguanidine (AG) 1 h after receiving 100 mg/kg i.v. LPS; group 5 (TNFalpha, n = 8) received 1 microg recombinant rat TNFalpha i.v.. ENO, BP, and pH were measured every 30 min for 4 h whereas arterial blood gases and pH were measured every hour. LPS administration induced a dose-related increase in ENO and a dose-related decrease in BP and pH. AG blocked the increase in ENO after LPS but had minimal effect on BP and pH. TNFalpha administration increased ENO without changing BP and pH. In LPS-treated rats, no significant correlation was found between ENO and BP (r2 = 0.13, P= ns). However, there was a significant correlation between pH and BP (r2 = 0.7, P < 0.01). Our results suggest that, in this animal model, ENO may not be a key mediator in the development of systemic hypotension during sepsis, while acidosis may significantly contribute to it.