title: Effects of nitric oxide on blood flow distribution and O2 extraction capabilities during endotoxic shock.
abstract: The effects of the nitric oxide (NO) synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) and the NO donor 3-morpholinosydnonimine (SIN-1) were tested in 18 endotoxic dogs. L-NMMA infusion (10 mg . kg-1 . h-1) increased arterial and pulmonary artery pressures and systemic and pulmonary vascular resistances but decreased cardiac index, left ventricular stroke work index, and blood flow to the hepatic, portal, mesenteric, and renal beds. SIN-1 infusion (2 microg . kg-1 . min-1) increased cardiac index; left ventricular stroke work index; and hepatic, portal, and mesenteric blood flow. It did not significantly influence arterial and pulmonary artery pressures but decreased renal blood flow. The critical O2 delivery was similar in the L-NMMA group and in the control group (13.3 +/- 1.6 vs. 12.8 +/- 3.3 ml . kg-1 . min-1) but lower in the SIN-1 group (9.1 +/- 1.8 ml . kg-1 . min-1, both P < 0.05). The critical O2 extraction ratio was also higher in the SIN-1 group than in the other groups (58.7 +/- 10.6 vs. 42.2 +/- 7.6% in controls, P < 0.05; 43.0 +/- 15.5% in L-NMMA group, P = not significant). We conclude that NO is not implicated in the alterations in O2 extraction capabilities observed early after endotoxin administration.
authors.affiliation: Department of Intensive Care, Erasme University Hospital, Free University of Brussels, B-1070 Brussels, Belgium.
authors.forename: H
authors.initials: H
authors.lastname: Zhang
authors.forename: P
authors.initials: P
authors.lastname: Rogiers
authors.forename: N
authors.initials: N
authors.lastname: Smail
authors.forename: A
authors.initials: A
authors.lastname: Cabral
authors.forename: J C
authors.initials: JC
authors.lastname: Preiser
authors.forename: M O
authors.initials: MO
authors.lastname: Peny
authors.forename: J L
authors.initials: JL
authors.lastname: Vincent
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D002305:Cardiac Tamponade / Q000378:metabolism / Q000503:physiopathology; D004285:Dogs; D004731:Endotoxins / Q000633:toxicity; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008981:Molsidomine / Q000031:analogs & derivatives / Q000494:pharmacology; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D010101:Oxygen Consumption / Q000187:drug effects / Q000502:physiology*; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012772:Shock, Septic / Q000378:metabolism / Q000503:physiopathology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D004731:Endotoxins; D004791:Enzyme Inhibitors; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; C002385:linsidomine; C044101:endotoxin, Escherichia coli; D008981:Molsidomine; D019001:Nitric Oxide Synthase; D000254:Sodium-Potassium-Exchanging ATPase