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Rump AF, Klaus W. Evidence for norepinephrine cardiotoxicity mediated by superoxide anion radicals in isolated rabbit hearts. Naunyn Schmiedebergs Arch Pharmacol. 1994;349(3):295-300doi: 10.1007/BF00169296.
Rump, A. F., & Klaus, W. (1994). Evidence for norepinephrine cardiotoxicity mediated by superoxide anion radicals in isolated rabbit hearts. Naunyn-Schmiedeberg's archives of pharmacology, 349(3), 295-300. https://doi.org/10.1007/BF00169296
Rump, A F, and Klaus, W. "Evidence for norepinephrine cardiotoxicity mediated by superoxide anion radicals in isolated rabbit hearts." Naunyn-Schmiedeberg's archives of pharmacology vol. 349,3 (1994): 295-300. doi: https://doi.org/10.1007/BF00169296
Rump AF, Klaus W. Evidence for norepinephrine cardiotoxicity mediated by superoxide anion radicals in isolated rabbit hearts. Naunyn Schmiedebergs Arch Pharmacol. 1994 Mar;349(3):295-300. doi: 10.1007/BF00169296. PMID: 7911559.
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Naunyn Schmiedebergs Arch Pharmacol. 1994 Mar;349(3):295-300. doi: 10.1007/BF00169296.

Evidence for norepinephrine cardiotoxicity mediated by superoxide anion radicals in isolated rabbit hearts.

Naunyn-Schmiedeberg's archives of pharmacology

A F Rump, W Klaus

Affiliations

  1. Institut für Pharmakologie, Universität Köln, Germany.

PMID: 7911559 DOI: 10.1007/BF00169296

Abstract

UNLABELLED: Catecholamines have been demonstrated to be cardiotoxic. Besides hemodynamic alterations, oxygen free radicals generated by the auto-oxidation of catecholamines might contribute to their deleterious effects. We examined the influence of exogenous norepinephrine (NE), after inhibiting functional alterations by alpha and beta-adrenoceptor blockade, on acute regional ischemia (MI).

METHOD: We used isolated electrically-driven rabbit hearts with depleted catecholamine stores (reserpine 7.0 mg/kg i.p. 16-24 h before preparation, Langendorff, constant pressure: 70 cm H2O, Tyrode solution, Ca2+ 1.8 mmol/l, 37 degrees C, 185-200 beats/min). Repetitive MI, separated by a reperfusion period of 50 min, was induced by coronary artery branch ligature and quantitated from epicardial NADH-fluorescence photography. Starting after a reperfusion period of 20 min, isolated hearts were treated with NE (10(-6) M), in the presence of propranolol (10(-6) M), phentolamine (10(-6) M) and vitamin C (3 x 10(-8) M) in the perfusion buffer to prevent the functional effects of NE. The influence of the free radical scavenger superoxide dismutase (SOD) (30 U/ml) or captopril (10(-6) M) on MI was also examined.

RESULTS: Left ventricular pressure or coronary flow were not significantly affected by either treatment (p > 0.05). Epicardial NADH-fluorescence area and intensity were, however, significantly enhanced by NE (+22%) (P < 0.05), although propranolol, phentolamine and vitamin C had no significant influence on MI (P > 0.05). SOD had no significant effect on MI in control hearts (P > 0.05) but completely prevented MI enlargement by NE (P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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