Minocycline (25 to 100 ,ug/g) dose dependently increased serum glutamic oxalacetic transaminase, urea, and bilirubin levels, and the hepatic triglyceride content in mice. In animals pretreated with phenobarbital to enhance minocycline metabolism, the effects on liver triglycerides were attenuated, while the changes in serum glutamic oxalacetic transaminase, urea, and bilirubin were enhanced. It is concluded that part of the toxic effects of minocycline may be produced by a metabolite of minocycline.

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The influence of 17 recently developed trypanocidal amidino compounds on blood pressure, heart rate, and carotid blood flow has been investigated in rats. Their cardiovascular effects were compared with those produced by pentamidine (Lomidine@) and diminazen (Berenil@). All compounds lowered the arterial blood pressure, especially the diastolic pressure, and almost all agents caused a reflex tachycardia and some reduction of the carotid blood flow. The hypotensive potency of the compounds can be reduced by alterations of the chain length between the cation moieties.