NG-monomethyl-l-arginine (NMA) restores arterial blood pressure but reduces cardiac output in a canine model of endotoxic shock.

Abstract

Previous studies have suggested that NMA or similar inhibitors of nitric oxide synthesis from L-arginine reverses or prevents the hypotension associated with endotoxin administration. We wanted to determine if vascular and cardiac responses to NMA support the idea that inhibitors of nitric oxide synthesis might be useful in the treatment of septic shock. Pentobarbital-anesthetized beagle dogs were administered endotoxin for 2 hours at a dose of 250 ng/kg/min. This resulted in reductions in systemic vascular resistance (34% decrease) and mean arterial pressure (25% decrease). Administration of NMA (30 mg/kg, IV) caused large and sustained increases in mean arterial pressure and systemic vascular resistance, and a large decrease in cardiac output and femoral arterial blood flow. Although NMA restored arterial pressure, the large and sustained fall in cardiac output suggests that the cardiovascular action of NMA is detrimental to dogs treated with endotoxin.

• Authors: R E Klabunde, R C Ritger
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 178 Issue 3 Pg. 1135-40 (Aug 15 1991) ISSN: 0006-291X [Print] United States
• PMID: 1872835 (Publication Type: Journal Article)

Chemical References

• Endotoxins
• omega-N-Methylarginine
• Arginine

Topics

• Animals
• Arginine (analogs & derivatives, pharmacology)
• Blood Pressure (drug effects)
• Cardiac Output (drug effects)
• Dogs
• Endotoxins
• Femoral Artery (physiopathology)
• Hemodynamics (drug effects)
• Male
• Regional Blood Flow (drug effects)
• Shock, Septic (physiopathology)
• Vascular Resistance (drug effects)
• omega-N-Methylarginine