Carbon disulfide exposure attenuates adrenergic inotropic response in rats.
Catecholamine-induced myocardial necrosis is enhanced in carbon disulfide exposed rats. We investigated whether the reported morphological findings after carbon disulfide exposure are accompanied by functional disturbances of the adrenergic inotropic response as well as by biochemical alterations. The cardiac effects of epinephrine and norepinephrine were studied in urethane-anesthetized rats which had been subacutely exposed to carbon disulfide. Compared with not exposed control animals left ventricular inotropic response was diminished and the transient T-wave elevation of the ECG due to ischemic episodes was enhanced in carbon disulfide-exposed rats. Activity of LDH-isozymes in the myocardium was shifted toward LDH-M. Our results support the hypothesis that carbon disulfide causes disturbances of energy supply in the heart.
Institute of Industrial Toxicology, Martin-Luther-University, Halle, Saale BRD.
M
M
Klapperstück
S
S
Müller
P
P
Hoffmann
D000818:Animals; D002246:Carbon Disulfide / Q000633:toxicity*; D004837:Epinephrine / Q000494:pharmacology*; D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase / Q000032:analysis; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000201:enzymology; D009638:Norepinephrine / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D013268:Stimulation, Chemical; D016277:Ventricular Function, Left / Q000187:drug effects
D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase; D002246:Carbon Disulfide; D009638:Norepinephrine; D004837:Epinephrine