Introdnction: In sepsis, nitric oxide (NO) acts a a mediator for the depression of vascular contractility of systemic vessels. Contractility is unproved by NO synuuse inhibitors like L-nitro-arginine methyl ester (L-NAME). We investigated the effect of sepsis, the NO precursor L-arginine, and L-NAME on pulmonary vessel contractility. Methods: Third order pulmonary arteries and veins were collected from chronically instrumented healthy (n=6), septic (24h infusion of 6-104 colony-forming units/kg/h Ps. aeruginosa, n=6) and septic, L-arginine supplemented (100 mg/Vg/h started Ih before bacterial infusion, n=6) sheep and sustained in Krcbs-bicarbonale baths. Contraction with 10-5 M norepinephrine (NE) was measured without and after 30 mm incubation with 10-4 M L-NAME. Statistical analysis by t-lest and ANOVA. Results: Pulmonary arterial pressure (PAP) and cardiac index rose from baseline values by 43±12% and 7±5% (septic) and 25±7%‡ and 34±9%‡ (sepsis-t-L-arg.); ‡ p<0.05 vs. sepsis group. Data in the graphs are presented as means ±SEM. Numbers in graph are ratio of NE+L-NAME contraction divided by NE contraction. * p<0.05 vi. NE contraction, † p<0.05 vs. ratio of healthy animals. (Figure Presented) Discnuion: The enhancement of vascular contractions with L-NAME may be responsible for the pulmonary hypertension seen with NO synuse inhibitors. This enhancement was more pronounced in veins. The lesser increase in PAP in L-arginine treated septic animals suggests die clinical use of L-arginine but is not explained by changes in vessel contractility.
|Original language||English (US)|
|Journal||Critical care medicine|
|Issue number||1 SUPPL.|
|State||Published - Dec 1 1998|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine