[en] In acute experiments on nembutal-urethan-anaesthetized rats, a slow infusion of subseptic dose of lipopolysaccharide (LPS) Escherichia coli (1 mg/ml) via the right jugular vein immediately led to bradycardia and extrasystoles. Preliminary administration of 20 mg/kg N(G)-nitro-L-arginine methyl ester (L-NAME) or 30 mg/kg aminoguanidine hydrochloride prevented the LPS-induced extrasystoles but did not affect the pattern of bradycardia. We conclude that nitric oxide (NO)-ergic mechanisms are involved in provoking electrical instability of the heart in conditions of endotoxemia.
Baykal, A., Kavuklu, B., Iskit, A.B., Guc, M.O., Hascelik, G., Sayek, I., Experimental study of the effect of nitric oxide inhibition on mesenteric blood flow and interleukin-10 levels with a lipopolysaccharide challenge (2000) World J. Surg., 24, pp. 1116-1120
Chen, C.C., Lin, Y.C., Chen, S.A., Luk, H.N., Ding, P.Y., Chang, M.S., Chiang, C.E., Shortening of cardiac action potentials in endotoxic shock in guinea pigs is caused by an increase in nitric oxide activity and activation of the adenosine triphosphate-sensitive potassium channel (2000) Crit. Care Med., 6, pp. 1713-1720
Comstock, K.L., Krown, K.A., Page, M.T., Martin, D., Ho, P., Pedraza, M., Castro, E.N., Sabbadini, R.A., LPS-induced TNF-alpha release from and apoptosis in rat cardiomyocytes: Obligatory role for CD14 in mediating the LPS response (1998) J. Mol. Cell. Cardiol., 30, pp. 2761-2775
Curtis, M.J., Pabla, R., Nitric oxide supplementation or synthesis block - Which is the better approach to treatment of heart disease? (1997) Trends Pharmacol. Sci., 18, pp. 239-244
Decking, U.K.M., Flesche, C.W., Gödecke, A., Schrader, J., Endotoxin-induced contractile dysfunction in guinea pig hearts is not mediated by nitric oxide (1995) Am. J. Physiol., 268, pp. H2460-H2465
Deitch, E.A., Bacterial translocation of the gut flora (1990) J. Trauma, 30, pp. S184-S189
Hales, J.R.S., Hubbard, R.W., Gaffin, S.L., Limitation of heat tolerance (1996) Handbook of Physiology, pp. 285-355. , M.J. Fregly, & C.M. Blatteis. New York: Oxford Univ. Press
Koulchitsky, S.V., Does selective destruction of the vagal afferent inflow facilitate or reduce the development of fever? (2000) J. Therm. Biol., 25, pp. 39-43
Koulchitsky, S.V., Kulchitsky, V.A., Central and peripheral mechanisms of nociceptive reflexes in conditions of acute phase reaction (2001) Proc. Natl. Sci. Counc., Repub. China, Part B, 25, pp. 197-213
Koulchitsky, S.V., Levkovets, V.S., Tchitchkan, D.N., Soltanov, V.V., Kulchitsky, V.A., Role of the solitary tract nucleus and caudal ventrolateral medulla in temperature responses in endotoxemic rats (1999) Life Sci., 64, pp. 37-43
McDonough, K.H., Smith, T., Patel, K., Quinn, M., Myocardial dysfunction in the septic rat heart: Role of nitric oxide (1998) Shock, 10, pp. 371-376
Shan, Q., Bourreau, J., Cardiac and vascular effects of nitric oxide synthase inhibition in lipopolysaccharide-treated rats (2000) Eur. J. Pharmacol., 406, pp. 257-264
Suffredini, A.F., From, R.E., Parker, M.M., Brenner, M., Kovacs, J.A., Wesley, R.A., Parrillo, J.E., The cardiovascular response of normal humans to the administration of endotoxin (1989) N. Engl. J. Med., 321, pp. 280-287
Swank, G.M., Deitch, E.A., Role of the gut in multiple failure: Bacterial translocation and permeability changes (1996) World J. Surg., 20, pp. 411-417
Ullrich, R., Scherrer-Crosbie, M., Bloch, K.D., Ichinose, F., Nakajima, H., Picard, M.H., Zapol, W.M., Quezado, Z.M., Congenital deficiency of nitric oxide synthase 2 protects against endotoxin-induced myocardial dysfunction in mice (2000) Circulation, 102, pp. 1440-1446
Wolff, D.J., Lubeskie, A., Aminoguanidine is an isoform-selective, mechanism-based inactivator of nitric oxide synthase (1995) Arch. Biochem. Biophys., 316, pp. 290-301
Xia, Y., Krukoff, T.L., Cardiovascular responses to subseptic doses of endotoxin contribute to differential neuronal activation in rat brain (2001) Brain Res. Mol. Brain Res., 89, pp. 71-85