Experimental papillary necrosis of the kidney. IV. Medullary plasma flow.
To test the thesis that vasoconstriction plays a significant role in the pathogenesis of papillary necrosis caused by bromoethylamine hydrobromide (BEA), medullary plasma flow was determined in rats treated with BEA. Medullary blood flow was normal (1/2) to 1 hour after BEA treatment, and was actually elevated 6 hours after BEA. There was no increase in plasma levels of prostaglandins A and E, which would have been expected if there had been medullary ischemia. Pretreatment with reserpine, which inhibited the development of papillary necrosis, had little effect on medullary plasma flow. These observations do not support the notion that vasoconstriction is the mechanism by which BEA causes papillary necrosis.
D000818:Animals; D001831:Body Temperature; D001965:Bromides; D003080:Cold Temperature; D003681:Dehydration; D003900:Desoxycorticosterone; D005021:Ethylamines; D005260:Female; D006801:Humans; D007511:Ischemia; D007668:Kidney / Q000098:blood supply*; D007679:Kidney Medulla / Q000098:blood supply* / Q000187:drug effects; D007681:Kidney Papillary Necrosis / Q000097:blood / Q000139:chemically induced / Q000209:etiology* / Q000378:metabolism / Q000652:urine; D011453:Prostaglandins / Q000032:analysis / Q000097:blood / Q000378:metabolism; D011863:Radioimmunoassay; D051381:Rats; D012039:Regional Blood Flow / Q000187:drug effects; D012110:Reserpine; D013217:Starvation; D013315:Stress, Psychological; D013997:Time Factors; D014682:Vena Cava, Inferior / Q000032:analysis; D014867:Water
D001965:Bromides; D005021:Ethylamines; D011453:Prostaglandins; D014867:Water; D003900:Desoxycorticosterone; D012110:Reserpine