Influence of L-arginine in the pulmonary vasculature during ovine sepsis

Research output: Contribution to journalArticle

Abstract

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 languageEnglish (US)
JournalCritical Care Medicine
Volume26
Issue number1 SUPPL.
StatePublished - 1998

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Arginine
Sheep
Sepsis
Norepinephrine
Nitric Oxide
Lung
Blood Vessels
Arterial Pressure
Pulmonary Veins
Baths
Pulmonary Hypertension
Pulmonary Artery
Veins
Analysis of Variance
Stem Cells
arginine methyl ester

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

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Influence of L-arginine in the pulmonary vasculature during ovine sepsis. / Fischer, Stefanie.

In: Critical Care Medicine, Vol. 26, No. 1 SUPPL., 1998.

Research output: Contribution to journalArticle

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abstract = "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.",
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