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Biomedical subjects

U Gafter

Publications and source records attributed to U Gafter.

At least 109 records · Page 6Linked to original sources
PubMed1986

Inhibition of Ca absorptive flux by chlorthalidone in the rat duodenum and colon.

To evaluate the mode and intestinal sites of action of chlorthalidone on Ca transport, balance and flux studies by the Ussing technique were performed in rats fed a low Ca diet throughout the experiment to stimulate Ca absorption. Half of the rats received chlorthalidone (5 mg X kg-1 X day-1) orally for 18 wk, a duration of administration previously shown to yield consistent changes. Net Ca absorption was decreased by chlorthalidone (0.91 +/- 0.07 vs. 1.08 +/- 0.3 mg/day, P less than 0.05), which is similar to prior observations in rats fed a normal Ca diet. Ca balance was unchanged by chlorthalidone (0.34 +/- 0.08 vs. 0.36 +/- 0.05 mg/day) because of concomitant hypocalciuria of similar magnitudes. In the duodenum, chlorthalidone decreased mucosal-to-serosal flux (Jm----s) (96.7 vs. 111.5 nmol X cm-2 X h-1, P less than 0.05). Since serosal-to-mucosal flux (Js----m) was unchanged, net Ca flux (Jnet) was reduced (74.0 vs. 89.6 nmol X cm-2 X h-1, P less than 0.05). Similarly, chlorthalidone selectively inhibited Jm----s in the descending colon (27.0 vs. 36.2 nmol X cm-2 X h-1, P less than 0.01), reducing Jnet (14.3 vs. 23.2 nmol X cm-2 X h-1, P less than 0.005). Short-circuit current and tissue conductance were unaffected. These data suggest that chronic chlorthalidone treatment reduces Ca absorption by inhibiting active calcium transport in the small and large intestine.

Absorption↗
PubMed1986

Ca fluxes across duodenum and colon of spontaneously hypertensive rats: effect of 1,25(OH)2D3.

Calcium absorption by spontaneously hypertensive rats (SHR) was variably reported to be different from normotensive Wistar-Kyoto (WKY) controls. Furthermore, blunted responsiveness to the intestinal effects of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] has also been postulated. To evaluate this hypothesis, calcium fluxes were measured by the Ussing technique across duodenum and descending colon with or without prior 1,25(OH)2D3 treatment. Duodenal mucosal-to-serosal calcium flux (Jm----s) (44.9 vs. 52.4 nmol X cm-2 X h-1), serosal-to-mucosal flux (Js----m) (25.6 vs. 28.4 nmol X cm-2 X h-1), and net flux (Jnet) were comparable. 1,25(OH)2D3 increased duodenal Jm----s in both SHR and WKY groups (95.2 and 86.8 nmol X cm-2 X h-1). Js----m was lower in SHR (26.1 vs. 35.6 nmol X cm-2 X h-1, P less than 0.01), although the tendency for a higher Jnet in SHR (68.6 vs. 51.2 nmoles X cm-2 X h-1) was statistically insignificant. Short-circuit current was higher in the colon of SHR, both before and after 1,25(OH)2D3, suggesting increased sodium transport. Basal colonic Jnet was virtually zero in both groups but comparably increased by 1,25(OH)2D3 because of stimulation in only Jm----s. Prevention of hypertension by hydralazine since the 4th wk of age did not alter the findings compared with the hypertensive SHR, suggesting calcium transport rates were unaffected by hypertension. These data indicate that in vitro, duodenal, and colonic active calcium transport by the SHR is similar to WKY. Their normal responses to 1,25(OH)2D3 do not support the hypothesis of intestinal resistance.

Animals↗
PubMed1986

Parathyroid hormone effect on the fragility of human young and old red blood cells in uremia.

Parathyroid hormone (PTH) is elevated in patients with chronic renal failure (CRF) and was suggested to be one of the factors responsible for the anemic syndrome of these patients because it raises the osmotic fragility of the red blood cells (RBC). In the present study, the youngest and oldest RBC were separated from circulating erythrocytes by high-speed centrifugation. The age distribution was described, and the effect of PTH on the different age groups was investigated. Median density (MD) and glutamic-oxaloacetic transaminase (GOT) activity were chosen as age markers. MD (1.0985 +/- 0.00087) and GOT activity (12.49 +/- 2.083 IU/g Hb) of the young uremic cells did not differ significantly from the values of young normal cells (1.0987 +/- 0.00046 and 10.36 +/- 1.174 IU/g Hb, respectively). The MD of the oldest cells, however, was lower (1.1048 +/- 0.00054) and GOT was higher (6.60 +/- 1.1019 IU/g Hb) in the uremic than in the control cells (1.1093 +/- 0.00175 and 3.77 +/- 0.233 IU/g Hb, respectively). These results indicate that the life span of RBC in uremics is shorter than normal and that an enrichment of circulating RBC by young cells occurs in uremic patients. The median osmotic fragility (MOF) of the young cells was lower in both uremic (0.376 +/- 0.006) and control patients (0.378 +/- 0.003) than the MOF of old cells (0.402 +/- 0.005 and 0.392 +/- 0.004, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Aspartate Aminotransferases↗
PubMed1986

Anterior uveitis, a presenting symptom in acute interstitial nephritis.

Two adult women with idiopathic acute interstitial nephritis (AIN) whose presenting symptom was anterior uveitis are described. On histologic examination of the renal biopsy, eosinophilic infiltrates and mononuclear cells were found. Immunofluorescence was negative. Immunological evaluation showed a slight decrease in the number of T cells with a normal subpopulation ratio. AIN responded to steroid treatment.

Acute Disease↗
PubMed1986

Evidence against the role of calcium deficiency in genetic hypertension.

Epidemiological studies suggest an association between reduced calcium uptake and hypertension, while clinical trials and rat experiments indicate a small but significant hypotensive effect with oral calcium supplements. These data imply that calcium deficiency has a role in genetic hypertension. We reasoned that if the hypothesis is correct, the hypertension should be aggravated by further reducing calcium balance but attenuated by augmenting calcium balance. We tested this hypothesis by evaluating the blood pressure response in spontaneously hypertensive rats (SHR) as calcium balance was decreased by dietary restriction of calcium or increased by supplementation with magnesium or 1 alpha, 25-dihydroxycholecalciferol (calcitriol). A low calcium diet within the physiological range did not accentuate the hypertension in SHR during the 11 weeks of treatment, even though calcium balance was reduced by half. Similar results were obtained with dietary calcium restriction in parathyroidectomized SHR, which excludes any offsetting effects of changes in parathyroid hormone levels. Conversely, 7 weeks of a high magnesium diet, which increased calcium balance without reducing PO4 balance, did not correct the hypertension of SHR. Similarly, long-term administration of calcitriol failed to reduce the blood pressure of parathyroidectomized SHR and normotensive Wistar-Kyoto (WKY) controls, despite the presence of increased serum calcium levels comparable to those produced by oral calcium loading. Finally, external calcium balance was measured directly in 25-day-old, prehypertensive SHR. As a result of the increased calcium absorption and reduced calcium excretion, SHR retained more calcium than did the normotensive WKY, which directly refutes the existence of calcium deficiency at this normotensive stage. These data do not support the role of calcium deficiency in genetic hypertension.

Animals↗
PubMed1986

Increased calcium absorption in prehypertensive spontaneously hypertensive rat. Role of serum 1,25-dihydroxyvitamin D3 levels and intestinal brush border membrane fluidity.

Changes in Ca absorption have been described in the spontaneously hypertensive rat (SHR) compared with Wistar-Kyoto (WKy) rats. In 3.5-wk-old SHR and age-matched WKy controls, we measured direct arterial blood pressure, Ca absorption, and serum 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] levels and small intestine brush border membrane (BBM) fluidity and lipid composition. The two objectives were (a) to define the nature of the absorptive changes before detectable hypertension and (b) to evaluate the potential mechanism(s). We found that even at this normotensive stage (106 +/- 4 vs. 107 +/- 2 torr for the female and 109 +/- 3 vs. 104 +/- 3 torr for the male), the SHR (a) absorbed more Ca (1.46 +/- 0.06 vs. 1.14 +/- 0.08 mmol/d and 1.53 +/- 0.06 vs. 1.28 +/- 0.06 mmol/d, respectively) and retained more Ca, (b) had higher serum 1,25(OH)2D3 levels (340 +/- 36 vs. 160 +/- 18 pg/ml and 230 +/- 25 vs. 150 +/- 16 pg/ml, respectively), and (c) possessed BBM with increased fluidity and with reduced fatty acyl saturation index owing to decreased stearic (32.2 +/- 2.6% vs. 38.2 +/- 0.9%) but increased linoleic acids (12.2 +/- 2.0% vs. 7.6 +/- 1.6%). These results demonstrate increased Ca absorption in prehypertensive SHR associated with increased serum 1,25(OH)2D3 levels, increased intestinal BBM fluidity, and reduced saturation index, which singly or in combination could produce the changes in intestinal Ca transport.

Absorption↗
PubMed1986

Metabolic acidosis enhances 1,25(OH)2D3-induced intestinal absorption of calcium and phosphorus in rats.

The effect of metabolic acidosis on the intestinal absorption of calcium (Ca) and phosphorus (P), plasma vitamin D metabolites and urinary excretion of Ca in adult rats treated with a small dose of 1,25(OH)2D3 were investigated. The rats in the experimental group received 1.8% ammonium chloride (NH4Cl) and a commercial chow, and their pair-fed controls received 0.45% NaCl. Both groups were given subcutaneously 1,25(OH)2D3. Intestinal absorption of Ca and P was measured by gut sac uptake of 45Ca and 32P. In the acidotic rats, duodenal, jejunal and ileal 45Ca uptake as well as jejunal and ileal 32P uptake were significantly increased. Plasma 1,25(OH)2D, 25(OH)D and 24,25(OH)2D were similar in both groups. 1,25(OH)2D3 treatment induced a greater calciuria in acidotic rats and increased their fractional excretion (FE) of Ca. An additional experiment showed increased 45Ca uptake by duodenum at a pH of 7.0 compared to pH 7.4. The present study suggests that NH4Cl-induced metabolic acidosis may enhance the effect of 1,25(OH)2D3 on intestinal absorption of Ca and P in the rat. However, the data from the study cannot exclude the possibility that acidosis may have a direct, vitamin D-independent effect on the intestine.

Acidosis↗
PubMed1985

Effect of bicarbonate feeding on intestinal absorption of calcium and vitamin D metabolism in rats.

The effect of bicarbonate (NaHCO3) feeding on intestinal absorption of calcium and phosphorus and vitamin D metabolism was investigated. Gut sac uptake of 45Ca and [32P]phosphate in vitro, as well as the plasma level of vitamin D metabolites, was determined in rats fed with NaHCO3 for 9 days and their pair-fed controls. Duodenal uptake of 45Ca and [32P]phosphate by alkalotic rats was less than duodenal uptake by controls. 1,25(OH)2D plasma level was much higher in alkalotic rats than in their controls, and 25(OH)D slightly higher than in controls. These data suggest that NaHCO3 feeding causes a substantial increase in 1,25(OH)2D plasma level, but interferes with calcium and phosphorus absorption in the duodenum.

24,25-Dihydroxyvitamin D 3↗
PubMed1985

Intraocular pressure in uremic patients on chronic hemodialysis.

Intraocular pressure (IOP) was measured before and after hemodialysis in 30 uremic patients receiving regular treatment. Osmolality, blood pressure and weight before and after dialysis were also determined. Low IOP of 11.4 +/- 2.7 and 11.5 +/- 3.1 mm Hg was found in the left and right eye, respectively. Following hemodialysis osmolality, blood pressure and body weight decreased significantly but IOP did not rise significantly. This study suggests that there is only a remote possibility for severe IOP increase following hemodialysis in uremic patients on chronic treatment.

Adolescent↗
PubMed1985

Sialic acid content of erythrocytes in uremic patients. Correlation with the age distribution of erythrocytes as assessed by glutamic oxaloacetic transaminase determination.

In a previous study we suggested that an enrichment in young red blood cells (RBC) should occur in the erythrocyte population of uremic-anemic patients. This change in RBC age distribution together with the fact that young cells were reported to be richer in sialic acid would provide an explanation for the observed lack of difference in sialic acid content between patients' and controls' whole erythrocyte populations in spite of an increased neuraminidase activity found to be present in patients' serum. To verify this assumption glutamic oxaloacetic transaminase (GOT) activity, which is an erythrocyte age index, and sialic acid were determined in low and high density fractions separated by centrifugation of packed cells representing young and old RBC, respectively, from two groups of 8 individuals with chronic renal failure and two groups of controls. GOT was determined also in whole erythrocyte populations. Mean GOT activity was significantly higher in the young fractions compared to the old of both patients' and control RBC (14.9 vs. 7.8 and 12.4 vs. 7.5 IU/g Hb). Activity of the whole RBC population was significantly higher in uremics as compared to controls (11.7 vs. 5.6 IU/g Hb) which is compatible with a lower median erythrocyte age. Mean sialic acid was higher in the young fractions as compared to the old (42.7 vs. 35.3 nmol/10(9) cells in controls and 48.9 vs. 43.0 nmol/10(9) cells in patients). These differences together with an enrichment in young cells would compensate for the eventual loss of sialic acid in the whole population resulting from an increased neuraminidase-like activity in patients' serum.

Aspartate Aminotransferases↗
PubMed1985

Effect of hyperparathyroidism on cardiac function in patients with end-stage renal disease.

Heart studies were carried out in 7 patients with end-stage renal disease (ESRD) who underwent parathyroidectomy for secondary hyperparathyroidism. The studies, which included echocardiography and equilibrium radionuclide angiography (ERNA), were performed prior to parathyroidectomy and 2 weeks, 3 months, and 6 months following it, on a nondialytic day. Heart rate decreased from 89.3 +/- 1.3 to 81.4 +/- 1.5 min-1 (p less than 0.001) following parathyroidectomy and returned to the initial level at 3- and 6-month examination. Cardiac output decreased from 3170 +/- 68 to 2943 +/- 57 ml/min (p less than 0.01) following parathyroidectomy and returned to basal level on 3 and 6-month determinations. End-diastolic dimension (EDD), end-systolic dimension (ESD), septal and posterior wall thickness and shortening fraction (SF) as measured by echocardiography were normal prior to parathyroidectomy and remained unchanged following it. Left ventricular ejection fraction (LVEF), end-diastolic and end-systolic volumes measured by ERNA did not change following parathyroidectomy. This study suggests that hyperparathyroidism has little effect on cardiac performance and, except for a short-lived decrease in heart rate and cardiac output, parathyroidectomy does not affect cardiac performance when performed in patients with preoperatively normal cardiac output.

Adult↗
PubMed1985

Hypercalcemia associated with transitional cell carcinoma without bone metastases: description of two cases.

Two cases of hypercalcemia associated with transitional cell carcinoma and negative bone scan are described. In both cases hypercalcemia appeared while there was evidence of tumor spread. Although hypercalcemia was controlled, both patients died shortly thereafter. Hypercalcemia rarely occurs in transitional cell carcinoma and its appearance may suggest spreading of the tumor and poor prognosis.

Aged↗
PubMed1984

Hypophosphatemia accompanying blastic crisis in a patient with malignant lymphoma.

A patient with malignant lymphoma showed severe hypophosphatemia during a blastic crisis. x-Ray microprobe analysis of the cells at this stage revealed a high phosphorus content. Following treatment and a decline in the white cell count the serum phosphorus increased, whereas the cellular phosphorus decreased. The potential prognostic value of serum and cellular phosphorus determinations during the course of malignant disorders of the hematopoietic system is discussed.

Adult↗
PubMed1984

Neuraminidase-like activity in sera of uremic anemic patients.

A shortened life of erythrocytes in uremia has been suggested as one of the causes of anemia in this condition. Since partially desialylated erythrocytes are promptly removed from the circulation, we examined whether sera from renal failure patients would exhibit increased neuraminidase activity which could be held responsible for this phenomenon. Sera of 22 patients with end stage renal failure were examined for neuraminidase activity by assessing their effect on desialylation upon incubation at 37 degrees C for 2 and 1 h, respectively, of erythrocytes of healthy donors matched for blood group and of fetuin as substrate. As deduced from the residual content of sialic acid of erythrocytes and of the amount of sialic acid released from fetuin, the results showed a statistically higher neuraminidase-like activity of patients' sera as compared to sera of healthy individuals. It is suggested that increase in neuraminidase activity could be one of the factors involved in the mechanism of generation of anemia in uremia by acting on erythrocytes, rendering them more prone to sequestration by the liver and spleen.

Adult↗