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Biomedical subjects

P Silva

Publications and source records attributed to P Silva.

At least 163 records · Page 9Linked to original sources
PubMed1983

Socio-economic status and childhood injuries.

The hypothesis that there was an inverse linear relationship between childhood injuries and socio-economic status was tested. Four measures of socio-economic status were related to childhood injury records covering the first seven years of life. The results failed to show any significant relationship between history of injury and four measures of socio-economic status.

Child↗
PubMed1983

Features of gentamicin nephrotoxicity and effect of concurrent cephalothin in the rat.

Sprague-Dawley rats given gentamicin from 10 to 70 mg/kg/day for 9 days showed a linear decrease in glomerular filtration rate with increasing dose, paralleled by histologic changes of acute tubular necrosis and cast formation only at the higher doses. Nephrotoxicity was correlated with the peak, rather than trough, serum gentamicin levels in this study, suggesting that it is the mean level of gentamicin over time that determines renal injury. The polyuria caused by gentamicin resulted mainly from a tubular concentrating defect rather than enhanced sodium or osmolal excretion and may be explained by the finding of a predominance of casts in the medullary thin limbs of the loops of Henle. No effect of gentamicin on the activity of cortical or medullary sodium-potassium adenosine triphosphatase was found to account for the modest sodium wasting. Concurrent administration of sodium cephalothin decreased the renal toxicity of gentamicin at high doses, an effect not explained by the added sodium or nonreabsorbable anion.

Acute Kidney Injury↗
PubMed1983

Mechanism and control of hyperosmotic NaCl-rich secretion by the rectal gland of Squalus acanthias.

Secretion of chloride from blood to lumen is accomplished in the rectal gland of elasmobranchs by a process of secondary active transport involving the co-transport of Cl- with Na+ across the basolateral membranes of rectal gland cells. Energy is provided by ATP via membrane Na-K-ATPase, which establishes an electrochemical gradient favouring Na+ influx into the cell. The involvement of K+ in the co-transport mechanism, so as to provide a ratio of 1 Na+:1 K+:2 Cl- entering the cell, would increase the energetic efficiency of the process, and is consistent with the Cl/O2 ration of 27-30 observed in secreting rectal glands. Secretion is stimulated by cyclic AMP (cAMP) and by vasoactive intestinal peptide (VIP) and adenosine, which activate adenylate cyclase. Activation of the gland in vivo probably occurs via VIP-secreting nerves as well as circulating agents; it is inhibited by somatostatin. Cyclic AMP probably stimulates chloride secretion by at least three mechanisms: (1) increasing chloride conductance across the luminal cell membrane, (2) enhancing the co-transport pathway for transmembrane movements of Na+, K+ and Cl- and (3) activating Na-K-ATPase.

Animals↗
PubMed1982

Localization of renal vitamin K-dependent gamma-glutamyl carboxylase to tubule cells.

The renal vitamin K-dependent gamma-glutamyl carboxylase was present in microsomes prepared from the renal cortex as well as the inner and outer medulla of several species. When glomeruli were isolated from either dog or rat renal cortex, microsomes prepared from these glomeruli were devoid of carboxylase activity. Proximal tubules were isolated from rabbit renal cortex; microsomes derived from these tubules had easily measurable carboxylase activity. The experiments demonstrate that the vitamin K-dependent gamma-glutamyl carboxylase is located in renal tubule cells. Since the enzyme is found not only in cortex but also inner and outer medulla, its distribution is not restricted to specific tubule segments.

Animals↗
PubMed1982

Relationship among gluconeogenesis, QO2, and Na+ transport in the perfused rat kidney.

The relationship among sodium transport (TNa), oxygen consumption (QO2), and gluconeogenesis was studied in isolated perfused rat kidneys in which glucose formation was enhanced by providing pyruvate as a substrate and by prior treatment with methylprednisolone. TNa was increased abruptly by increasing perfusion pressure as to increase GFR or by lowering the albumin concentration of a hyperoncotic perfusate as to allow glomerular filtration to occur. Increases in TNa of 40% were accompanied by little or no increase in QO2, whereas gluconeogenesis decreased 55-80%. Conversely, a decrease in perfusion pressure that lowered TNa produced an increase in glucose formation without a change in QO2. When gluconeogenesis was blocked with 0.15 mM 3-mercaptopicolinate, an inhibitor of phosphoenolpyruvate carboxykinase, QO2 increased together with TNa as perfusion pressure was raised. The results suggest that the energy needed for ion transport by the kidney may under some circumstances be borrowed from nontransport functions and, therefore, that basal oxygen consumption may vary with the rate of reabsorptive transport.

Animals↗
PubMed1982

Stimulation of renin release by hyperoncotic perfusion of the isolated rat kidney.

Renin release was measured in the isolated rat kidney perfused with a recirculating artificial medium containing bovine serum albumin at 6.7 g per 100 ml of 11 g per 100 ml. At the higher concentration of albumin, glomerular filtration ceased and the rate of renin release over 70 minutes of perfusion was increased 6-fold. The addition of ouabain to the perfusate containing 11 g per 100 ml inhibited the release of renin, suggesting that inhibition of Na-K-ATPase or the related changes in cellular volume or composition prevented renin release. Lowering the osmolality of the perfusate by reducing the concentration of sodium chloride also prevented the increase in renin secretion produced by perfusion with 11 g per 100 ml albumin. Increasing the osmolality of the perfusate with mannitol restored the augmented renin release. These results are consistent with the hypothesis that alterations in the volume of certain cells, perhaps in the juxtaglomerular apparatus itself, can control renin release.

Animals↗
PubMed1981

Sodium-chloride transport in the thick ascending limb of Henle's loop. Oxygen consumption studies in isolated cells.

Isolated cells were prepared from the medullary thick ascending limb of Henle's loop (TALH) and the response of oxygen consumption was correlated with the active chloride transport system found in these cells. Oxygen consumption was 31.6 microliters O2/mg protein . h and inhibited 50% by the absence of either sodium or chloride in the incubation medium. The absence of both sodium and chloride produced no further inhibition of oxygen consumption. Ouabain (10(-4) M) inhibited oxygen consumption by 50% and the inhibitory effect depended on the presence of both sodium and chloride in the incubation medium. Further, furosemide inhibited oxygen consumption by a maximum of 50% at 10(-3) M and also had no inhibitory effect if either sodium or chloride were absent. Furosemide had no effect on the Na, K-ATPase activity or ATP levels of the TALH cells. Thus, the data suggest or ATP levels of the TALH cells. Thus, the data suggest that 50% of the oxygen consumption of the TALH cells is related to the movement of sodium and chloride into the cell and that the ions may be transported in a coupled manner. In addition the effect of various diuretics on oxygen consumption in the isolated TALH cells was tested. The diuretics could be grouped in three categories: (1) highly effective in inhibiting chloride-dependent oxygen consumption with an apparent inhibitory constant (Ki) of around 10(-6) M, including the diuretics furosemide, bumetanide, ethacrynic acid-cysteine and piretanide, (2) diuretics which were less effective in inhibiting oxygen consumption with an apparent Ki of around 10(-4) M, HOE 740 and ethacrynic acid, and (3) diuretics which were ineffective in inhibiting chloride-dependent oxygen consumption, amiloride and hydrochlorothiazide.

Adenosine Triphosphate↗
PubMed1981

Role of the malate--aspartate shuttle in renal sodium transport in the rat.

1. Experiments were designed to establish the relationship between renal gluconeogenesis and sodium transport. Six inhibitors of gluconeogenesis, with different sites of action, were tested in the isolated perfused rat kidney in which renal function, and in particular Na+ reabsorption, was followed. 2. In kidneys from fed or starved rats specific inhibitors of gluconeogenesis neither inhibited nor stimulated Na+ reabsorption; gluconeogenesis and sodium reabsorption are therefore independent of one another under these conditions. 3. Inhibitors of transaminase or malic dehydrogenase inhibited gluconeogenesis from lactate and pyruvate respectively; the transaminase inhibitor significantly inhibited oxidation of lactate and glucose. 4. Sodium reabsorption was inhibited by a transaminase inhibitor when glucose or lactate was the sole substrate, and by inhibition of malic dehydrogenase when pyruvate was the substrate. 5. These results indicate that the malate--aspartate shuttle controls Na+ reabsorption in the intact kidney by regulating substrate oxidation (and the provision of energy) rather than by any direct involvement of gluconeogenesis in Na+ transport.

Aminooxyacetic Acid↗
PubMed1981

Sympathetic system in potassium homeostasis.

The extrarenal disposal of potassium was studied in nephrectomized and adrenalectomized rats by measuring the rise in serum potassium produced during an infusion of 3 meq KCl/kg over 90 min. Adrenalectomy alone did not alter the volume of distribution of infused potassium in nephrectomized animals. When nephrectomy and adrenalectomy were combined with either insulin deficiency produced by streptozotocin or chemical sympathectomy induced by injection of 6-hydroxydopamine, potassium tolerance was significantly impaired. Hyperkalemia produced in chemically sympathectomized animals by potassium infusion was minimized by simultaneous infusion of epinephrine, an effect blocked by the beta-antagonist propranolol but not by the alpha-blocker phenoxybenzamine. These results suggest that extra renal uptake of potassium, in addition to being influenced by insulin and circulating catecholamines, is modulated by peripheral sympathetic activity.

Adrenalectomy↗
PubMed1981

Indomethacin impairs water diuresis in the DI rat: role of prostaglandins independent of ADH.

The mechanisms by which endogenous renal prostaglandins regulate water excretion were investigated in these studies. Inhibition of prostaglandin synthesis slowed water diuresis in water-loaded unanesthetized Sprague-Dawley rats and in Brattleboro rats with hereditary diabetes insipidus owing to absence of endogenous vasopressin. In both strains, treatment with indomethacin or meclofenamate increased the osmolality of the renal papilla by raising sodium and urea content, and also increased the osmolality of the urine. Endogenous creatinine clearance and solute excretion were unchanged. The data are consistent with an effect of prostaglandins on solute transport by renal tubules and demonstrate that endogenous prostaglandins influence water excretion by a mechanism independent of the presence of antidiuretic hormone.

Animals↗
PubMed1981

Sodium orthovanadate diuresis in rats.

The renal actions of differing doses of sodium orthovanadate were studied in conscious and anesthetized female Wistar rats. In conscious rats, sodium orthovanadate was given by i.v. or i.p. injections or by mouth. The most pronounced renal effects were seen after a 5 mg/kg i.p. injection of sodium orthovanadate. Urine flow and sodium excretion increased approximately 400% and urine osmolality fell from 1108 to 549 mOsmol/kg . H2O. Higher doses of sodium orthovanadate (20, 30 and 50 mg/kg) injected i.p. did not cause diuresis and were toxic. In anesthetized rats undergoing a 0.9% NaCl diuresis, i.v. infusion of sodium orthovanadate at a dose of 5 mg/kg/hr significantly increased urine flow and the excretion of sodium, calcium, phosphorus, sulfur, magnesium and chlorine, whereas glomerular filtration rate was unaltered. In anesthetized rats undergoing a water diuresis, i.v. infusion of sodium orthovanadate (5 mg/kg/hr) markedly reduced free-water clearance, indicating that this compound inhibits tubular reabsorption of sodium and chloride in diluting nephron segments. Blood and renal tissue levels of vanadium, measured using emission spectrographic analysis, in rats infused with sodium orthovanadate were 4 times higher than the concentration of sodium orthovanadate (1--10 microM) needed to inhibit 50% of the Na-K-adenosine triphosphate activity of rat renal homogenates in vitro. These data suggest that sodium orthovanadate produces diuresis at least in part by inhibiting Na-K-adenosine triphosphatase and solute transport in the distal nephron, likely the ascending limb of the loop of Henle.

Administration, Oral↗
PubMed1981

Behavioral and psychiatric assessment of preterm and full-term low birth weight children at 9-11 years of age.

Preterm (N = 33) and full-term (N = 18) low birth weight subjects were compared at age 9 to 11 years to 52 full-term normal birth weight subjects of similar age and socioeconomic levels. All groups were evaluated by a psychiatrist who was not aware of prenatal or perinatal histories at the time of the interview. Mothers completed various standardized questionnaires designed to elicit information about the children's behaviors. There were no significant differences among the groups in the numbers of subjects with diagnoses of psychiatric disorders or in scores on ratings of hyperactivity, general behavioral maladjustment, and specific behavioral factors. These results indicate that low birth weight per se does not portend serious psychiatric sequelae during middle childhood.

Child↗
PubMed1980

Adrenergic modulation of extrarenal potassium disposal.

We studied the role of catecholamines in the regulation of potassium homeostasis in nine healthy subjects given intravenous potassium chloride (0.5 meq per kilogram of body weight) in the presence and absence of propranolol. Potassium infusion elevated serum potassium 0.6 +/- 0.09 meq per liter (mean +/-S.E.M.). Addition of propranolol augmented the rise (0.9 +/- 0.05 meq per liter) and prolonged the elevation in serum potassium without decreasing urinary potassium excretion. In a separate study, the same potassium load was administered with a concomitant infusion of epinephrine in five subjects. Epinephrine markedly blunted the increment in serum potassium (0.1 +/- 0.06 meq per liter) while reducing renal potassium excretion. Plasma aldosterone was not altered by the experimental procedures. Serum insulin fell minimally in the presence of propranolol but was unaffected by epinephrine. beta-Adrenergic blockade impairs and epinephrine enhances extrarenal disposal of an acute potassium load. These findings suggest that in patients with impaired potassium disposal, the risk of hyperkalemia may be increased when sympathetic blockade is induced.

Adrenergic beta-Antagonists↗