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Biomedical subjects

M A Dillingham

Publications and source records attributed to M A Dillingham.

22 records · Page 2Linked to original sources
PubMed1983

The renal concentrating defect after gentamicin administration in the rat.

The present studies were carried out to delineate the mechanism of the polyuric state and renal concentration defect seen after gentamicin. Gentamicin was given at a dosage of 100 mg/kg/day subcutaneously for either 4 or 5 days to Sprague-Dawley rats and resulted in a reversible, polyuric form of acute renal failure. This nonoliguric acute renal failure was accompanied by significant polydipsia and a renal concentrating defect 11 days after gentamicin. To assess the role of polydipsia in the polyuria and renal concentrating abnormality, water intake was restricted in gentamicin-treated animals to match intake of control animals. Elimination of the polydipsia failed to eliminate the polyuria and to improve the renal concentrating abnormality. Postdehydration plasma vasopressin levels were higher in gentamicin-treated than control animals, suggesting that the renal concentrating defect was nephrogenic in origin. Daily urinary prostaglandin E2 excretion was comparable in gentamicin-treated and control animals. However, indomethacin failed to improve urinary concentrating ability, suggesting that the renal concentrating defect was prostaglandin E2 independent. Finally, depressed postdehydration inner medullary tonicity was found in gentamicin-treated animals In summary, gentamicin administration in the rat was associated with a reversible polyuric form of acute renal failure and a renal concentrating defect. This concentration defect was nephrogenic in origin, independent of polydipsia and prostaglandin E2, and was associated with a decrease in inner medullary tonicity.

Acute Kidney Injury↗
PubMed1982

Role of renal nerves, angiotensin II, and prostaglandins in the antinatriuretic response to acute hypercapnic acidosis in the dog.

Although clinical studies suggest that chronic hypercapnic acidosis may be associated with renal sodium retention, little information is available on the effect of acute hypercapnic acidosis on renal sodium excretion. We, therefore, increased PCO2 from 23 to 74 mm Hg in anesthetized dogs and observed a marked antinatriuresis as absolute sodium excretion (235 to 60 muEq/min, P less than 0.001) and fractional excretion of sodium (4.0 to 1.2 %, P less than 0.02) decreased significantly. This decrease in sodium excretion occurred independent of consistent changes in renal perfusion pressure, PO2, glomerular filtration rate, renal blood flow, extraction of P-aminohippuric acid, and filtration fraction. The antinatriuretic response to acute hypercapnic acidosis could be attenuated significantly by surgical renal denervation, intrarenal phenoxybenzamine, and by intrarenal infusion of 1-sarcosine,8-glycine angiotensin II. Administration of 10 mg/kg indomethacin enhanced the antinatriuretic response to hypercapnic acidosis in denervated kidneys. These results suggest that renal alpha-adrenergic nerves and the renal angiotensin system result in an antinatriuretic effect during acute hypercapnic acidosis. Renal prostaglandins or related substances may serve to attenuate this antinatriuretic response.

Acidosis↗
PubMed1980

Normalization of triglycerides in type IV hyperlipoproteinemia fails to correct low levels of high-density-lipoprotein cholesterol.

High-density-lipoprotein (HDL) cholesterol protects against coronary heart disease, and ways to raise low HDL values are being sought. Cross-sectional population surveys have shown that HDL cholesterol is inversely related to plasma triglycerides, yet to our knowledge no longitudinal studies have shown that a decrease in elevated triglycerides will raise depressed HDL levels. We therefore used dietary therapy to lower the triglyceride levels of 29 men with Type IV hyperlipoproteinemia and evaluated the effects on HDL-cholesterol levels. Despite a reduction in triglyceride levels from 697 +/- 90 to 333 +/- 37 mg per deciliter (P < 0.01), initially low HDL-cholesterol values did not change (29 +/- 1 to 30 +/- 1 mg per deciliter). Even in a subgroup of 12 men whose triglyceride levels fell to normal (from 670 +/- 99 to 170 +/- 7, P < 0.01) and whose weight and triglycerides remained stable for two years, HDL cholesterol remained unchanged (29 +/- 1 vs. 32 +/- 1). The persistently low HDL-cholesterol level in the presence of normalization of triglycerides suggests that depressed HDL cholesterol may be an independent metabolic abnormality in Type IV hyperlipoproteinemia.

Adult↗