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R H Heptinstall

Publications and source records attributed to R H Heptinstall.

At least 55 records · Page 3Linked to original sources
PubMed1974

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.

Animals↗
PubMed1972

Experimental papillary necrosis of the kidney. 3. Effects of reserpine and other pharmacologic agents on the lesion.

Reserpine is able to exert a pronounced inhibitory effect on the development of papillary necrosis following the administration of bromoethylamine hydrobromide to the rat. This inhibitory effect has been observed using light microscopy, histochemistry, indigo carmine excretion and urine output. These observations suggest that vasoconstriction may play a significant role in the pathogenesis of papillary necrosis, but the evidence for this is incomplete.

Adenosine Triphosphatases↗
PubMed1972

Experimental papillary necrosis of the kidney. I. Morphologic and functional data.

Papillary necrosis was produced in rats by a single intravenous injection of bromoethylamine hydrobromide (BEA). The earliest changes as seen by light microscopy were necroses of the limbs of Henle and eosinophilic droplets in collecting ducts. Complete necrosis of the papilla took place between 4 and 7 days and the dead papilla was usually sequestered completely by 21 days. Cortical changes occurred secondary to papillary necrosis. Tubular atrophy and loss was greatest in the deeper parts of the central cortex, the more superficial nephrons frequently being spared. The perihilar cortex was the least involved. This distribution was considered to be related to the respective lengths of the limbs of Henle, nephrons with limbs extending into the papilla being those undergoing change. Increased urine output occurred during the first day and continued thereafter. There was a profound defect in concentrating ability.

Animals↗
PubMed1969

Renal biopsy.

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Biopsy↗