(Circulation. 1999;100:107-112.)
© 1999 American Heart Association, Inc.
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Induction of Nitric Oxide Synthase and Dual Effects of Nitric Oxide and Cyclooxygenase Products in Regulation of Arterial Contraction in Human Septic Shock
Presented in abstract form at the British Pharmacological Society, Edinburgh, UK, September 2–4, 1997.
From Laboratoire de Pharmacologie et Physiologie Cellulaires, CNRS ERS 653, Faculté de Pharmacie, Illkirch, France (J.C.S., M.C.M., C.S., A.L.K., R.A.); Centre Hospitalier Universitaire de Hautpierre, Service de Réanimation Médicale, Strasbourg, France (P.O., F.S.); and Unité INSERM 338 de Biologie de la Communication Cellulaire, Centre de Neurochimie du CNRS, Strasbourg, France (S.C.).
Correspondence to Dr Ramaroson Andriantsitohaina, Laboratoire de Pharmacologie et Physiologie Cellulaires, CNRS ERS 653, Faculté de Pharmacie, 74, route du Rhin, F-67401 Illkirch, France. E-mail nain{at}pharma.u-strasbg.fr
Background—The role of endogenous nitric oxide (NO) and cyclooxygenase metabolites was investigated in contractile responses of small omental arteries from patients with hyperdynamic septic shock.
Methods and Results—Expression of inducible NO synthase (immunostaining) and a high but variable level of NO production (NO spin trapping) was detected in arteries from patients with septic shock. In these vessels, ex vivo contractile responses to the thromboxane A2 analogue U46619 and to low concentrations of norepinephrine (NE) (up to 10 µmol/L) were not significantly different from controls. However, higher concentrations of NE caused pronounced fading of contraction in septic but not in nonseptic arteries. Exposure to either the NO synthase inhibitor NG-nitro-L-arginine methyl ester or the cyclooxygenase inhibitor indomethacin had no effect in control vessels. However, both inhibitors increased the response to the contractile effects of the 2 agonists only in patients with septic shock. In contrast to NG-nitro-L-arginine methyl ester, which decreased the threshold concentration of the fading effect of NE, indomethacin abolished this effect in arteries from septic patients.
Conclusions—These results provide direct evidence for the induction of NO synthase in small arteries from patients with septic shock. They suggest that in these arteries, increased production of NO, in conjunction with vasodilatory cyclooxygenase metabolites, contributes to counteract hyperreactivity to agonists and decreases the cyclooxygenase product–mediated pronounced fading of contraction caused by a high concentration of NE.
Key Words: shock • nitric oxide synthase • prostaglandins • arteries • vasoconstriction
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