@article {Stern65, author = {Paula H. Stern and Theodore M. Brody}, title = {CATECHOLAMINE EXCRETION FOLLOWING CARBON TETRACHLORIDE ADMINISTRATION}, volume = {141}, number = {1}, pages = {65--73}, year = {1963}, publisher = {American Society for Pharmacology and Experimental Therapeutics}, abstract = {Oral administration of 2.5 ml/kg CCl4 in peanut oil to rats produced elevated free epinephrine and norepinephrine levels in plasma and urine. The elevated urinary free catecholamine levels were probably the result of increased secretion, rather than decreased metabolism or tissue depletion. There was less excretion of catecholamines after CCl4 during the summer months. Cord section, trimethidinium, guanethidine and β-TM-10 reduced the elevated norepinephrine excretion of CCl4-treated animals; the elevated epinephrine excretion was prevented by cord section, adrenalectomy and trimethidinium. Thyroxin, which exacerbated the CCl4 toxicity and mitochondrial damage, markedly potentiated epinephrine excretion following CCl4. The finding of elevated urinary catecholamine levels following CCl4 administration and the further demonstration that this elevation was the result of increased secretion is evidence that CCl4 does stimulate the sympathetic nervous system. That agents which prevent the CCl4-induced increase in catecholamine excretion have been shown to prevent the CCl4-induced hepatic necrosis, lipid accumulation and mitochondrial enzyme changes lends strong support to the hypothesis that hepatic damage is at least in part a consequence of stimulation of the sympathetic nervous system.}, issn = {0022-3565}, URL = {https://jpet.aspetjournals.org/content/141/1/65}, eprint = {https://jpet.aspetjournals.org/content/141/1/65.full.pdf}, journal = {Journal of Pharmacology and Experimental Therapeutics} }