The effects of l-epinephrine, l-norepinephrine, phenylephrine, methoxamine, metaraminol and mephentermine on renal hemodynamics were studied in six groups of dogs. Although comparable rises in blood pressure were obtained, there were marked differences in the effects on renal hemodynamics. While infusion of mephentermine led to only slight reductions in glomerular filtration rate and renal blood flow, and only a slight increase in renal vascular resistance, methoxamine produced a marked fall in flow and a marked increase in resistance. The other agents tested had effects which were intermediate between these two. The effects of these same drugs on renal hemodynamics were also compared in dogs made hypotensive by bleeding. While blood pressure increased significantly in all groups, glomerular filtration rate and renal blood flow increased significantly only during infusion of mephentermine, metaraminol and phenylephrine. Since assays relative to the inherent vasodilator properties of these agents revealed epinephrine to be the only agent with marked activity, it seems unlikely that the observed effects were due to this factor. It is concluded that the observed changes were due to a greater reactivity of renal vascular vasoconstrictor adrenergic receptors with certain sympathicomimetic drugs than those of the vasculature in general.
Myopathy was induced in dogs with large doses of anti-inflammatory steroids (cortisol, prednisolone, methylprednisolone, dexamethasone and triamcinolone). Weight loss and muscle atrophy occurred in all groups except the control group but was most pronounced in the triamcinolone\x=req-\ treated dogs. There was a marked difference between the treated groups in decrease of muscle size (occurring the least with cortisol) and also in fiber thickness of muscle tissue (changing the least methylprednisolone and diminishing the most triamcinolone).The diagnosis of steroid myopathy could be made by clinical observation, electromyography and biopsy. The only specific histological change detectable was the diminished size of muscle fiber. Further investigation is necessary to understand the pathogenesis and to explain the peculiar localization of the myopathy.
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