Experimental papillary necrosis of the kidney. IV. Medullary plasma flow

K. Solez, M. Miller, P. A. Quarles, P. M. Finer, R. H. Heptinstall

Research output: Contribution to journalArticle

Abstract

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 30 min to 1 hr after BEA treatment, and was actually elevated 6 hr 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.

Original languageEnglish (US)
Pages (from-to)521-528
Number of pages8
JournalAmerican Journal of Pathology
Volume76
Issue number3
StatePublished - Dec 1 1974

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Fingerprint Dive into the research topics of 'Experimental papillary necrosis of the kidney. IV. Medullary plasma flow'. Together they form a unique fingerprint.

  • Cite this

    Solez, K., Miller, M., Quarles, P. A., Finer, P. M., & Heptinstall, R. H. (1974). Experimental papillary necrosis of the kidney. IV. Medullary plasma flow. American Journal of Pathology, 76(3), 521-528.