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Biomedical subjects

R D Lindeman

Publications and source records attributed to R D Lindeman.

At least 55 records · Page 3Linked to original sources
PubMed1981

Differences in blood glutathione levels of tumor-implanted or zinc-deficient rats.

Previously we found that blood glutathione (GSH) levels were decreased in rats that were both zinc-deficient and tumor-bearing. In this study the separate effects of zinc deficiency and tumor were investigated. Young, male rats were pair-fed either a complete, control diet or a zinc-deficient diet, and some of each group were implanted intramuscularly (i.m.) with Walker 256/Ml carcinosarcoma. Then half of the tumor-implanted, zinc-deficient rats were repleted with zinc. All rats were killed 7 days after tumor implantation. Zinc deficiency was validated by poor growth, low food efficiency and decreased concentrations of zinc in liver, kidney and plasma. Relative to controls rats, the blood GSH level increased 21% as a result of tumor alone (P less than 0.005) and decreased 19% with zinc-deficiency alone (P less than 0.025). In rats that were both tumor-bearing and zinc-deficient, the GSH level was 16% higher than the controls (P less than 0.005). Zinc repletion of the tumor-bearing rats restored GSH levels to control values. These results indicate that the marked and opposite changes in blood GSH levels as a result of tumor implantation or of zinc deficiency occur by different mechanisms.

Animals↗
PubMed1981

Effects of diet on exaggerated natriuresis in hypertension.

The effects of high and low salt diet on exaggerated natriuresis after volume expansion were examined in two groups of hypertensive patients, 6 with labile and 6 with fixed uncomplicated essential hypertension. Fixed hypertensives eliminated the administered salt-load faster than the labile hypertensives, and diet had no effect on the exaggerated natriuresis of both groups. No association was observed between plasma renin activity and natriuresis in both groups of patients. We conclude that, 1) diet did not affect the saline-induced natriuresis in hypertensive patients, 2) there was no apparent association between plasma renin activity and exaggerated natriuresis in hypertension, 3) other factors such as the capacitance system and vasopressin may play an important role in volume expansion natriuresis, especially in fixed hypertensives.

Blood Pressure↗
PubMed1978

Urinary zinc excretion following infusions of zinc sulfate, cysteine, histidine, or glycine.

Zinc sulfate (40 mg elemental zinc) or one of three amino acids (5 or 10 g cysteine, 10 g histidine, or 10 g glycine) was infused into anesthetized dogs over a 60-min period. Plasma concentrations and urine excretions of zinc and five other cations, and glomerular filtration rates were determined before, during, and after these infusions. Infusions of zinc sufficient to produce a 20-fold increase in total plasma zinc concentrations had little effect on urinary zinc excretions (threefold increase) or plasma ultrafilterable zinc concentrations. Ten grams of cysteine urinary zinc excretions more than 100-fold, 5 g of cysteine increased zinc excretions more than 30-fold, 10 g of histidine increased zinc excretions sixfold, and 10 g of glycine had no effect. Cysteine infusions appeared to produce a net tubular secretion of zinc. Only histidine appeared to increase serum ultrafilterable zinc concentrations significantly. It would appear that plasma and urine concentrations of certain amino acids, specifically cysteine and histidine, along with polypeptides and other metabolites containing these amino acids, may be major determinants of urinary zinc excretion.

Animals↗
PubMed1978

Effects of acute and chronic splenectomy on experimental acute renal tubular lesions.

The first half of this study describes the effects of acute splenectomy on epinephrine-induced ATL in the dog. Renal morphology and hematocrit were compared in 12 dogs without splenectomy (group I), six dogs with antecedent splenectomy (group II), and seven dogs with antecedent splenectomy after splenic contraction was induced by topical application of epinephrine (group III). Splenectomy was performed in groups II and III 20 to 30 min prior to epinephrine infusion; all three groups received equal infusions (4 microgram/kg/min) for 6 hr before the kidneys were harvested. ATL and renal congestion were consistently severe in group I but infrequent and less severe in groups II and III. The second half of this study describes the apparent protective effect of chronic (2-week) splenectomy on epinephrine-induced ATL. Renal morphology and hematocrits were compared in 13 intact dogs (group IV) and 10 dogs splenectomized 2 weeks before the epinephrine infusion (group V). The severity of the ATL and the degree of renal congestion were significantly less in the chronically splenectomized dogs. This chronic protection afforded by acute and chronic splenectomy observed after epinephrine infusion remains unclear.

Animals↗
PubMed1977

Hereditary (familial) renal disease: clinical and genetic studies.

Four or more generations of three Oklahoma-Kansas families in which multiple members have been found to have glomerulonephritis or interstitial nephritis have been studied. Twenty-five of 146 members in kindred A, 16 of 50 members in kindred B, and 33 of 156 members in kindred C were identified as probably to definitely afflicted. Renal tissue from members of the first two families showed an acute or chronic glomerulonephritis. Renal failure often appeared by the third decade. The lesions were less frequent but more rapidly lethal in the male members. Renal tissue from members of the third kindred showed an interstitial nephritis. This appeared later in life and followed a more chronic course. Hearing loss was common in both groups. The hereditary studies are consistent with the hypothesis that the disease is transmitted by an autosomal dominant gene with imcomplete penetrance (not all members carrying the gene develop renal disease) and variable expressivity. Male-to-male transmission was present in all three families but less frequently than would be predicted, suggesting a reduced clinical expression of the disease in males who receive the mutant gene from their father.

Adult↗
PubMed1977

Zinc metabolism in renal disease and renal control of zinc excretion.

Serum zinc concentrations are decreased in patients with a variety of clinical disorders including cirrhosis, nephrotic syndrome and renal insufficiency. Urinary zinc excretions are increased in the first two disease states. Symptoms of acute zinc deficiency (anorexia, dysfunction of smell and taste, and mental and cerebellar disturbances) and chronic zinc deficiency (growth retardation, anemia, testicular atrophy, and impaired wound healing) are common in these patients. It remains unresolved whether these disease states are indicative of true symptomatic or asymptomatic zinc deficiency or merely reflect a decrease in available zinc binding proteins. The low serum zinc concentrations and high urinary zinc excretions in patients with nephrotic syndrome do not appear to be due to loss of zinc bound to urinary proteins. Studies in dogs indicate increased serum and urine concentrations of certain amino acids(cysteine, histidine) greatly increase urinary zinc excretions. Studies are now underway to determine if the hyperzincuria and hypozincemia of cirrhosis, nephrotic syndrome and hyperalimentation can be explained by an increase in these urinary amino acids.

Animals↗