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Biomedical subjects

F K Assadi

Publications and source records attributed to F K Assadi.

33 records · Page 2Linked to original sources
PubMed1986

Effect of tolazoline on renal function in newborn puppies.

Tolazoline is used in pulmonary hypertension and hypoperfusion syndrome during the neonatal period. Some of the side effects of tolazoline are hypotension, bleeding disorders and renal dysfunction. The present study was designed to investigate the effect of hypoxia and tolazoline on renal function in newborn puppies. The data in normal animals administered tolazoline alone did not reveal any statistically significant changes in blood pressure or in renal function. In the hypoxia group changes in renal function were noticed in spite of normal blood pressure. When tolazoline was administered to the hypoxic animals, a marked decrease in blood pressure resulted. Indeed, changes in renal function were more profound in the hypoxic animals receiving tolazoline than in hypoxic animals not receiving tolazoline, even though some of the renal functional values did not reach statistical significance.

Animals↗
PubMed1986

Zinc status of infants with fetal alcohol syndrome.

Plasma and urinary zinc levels were examined in 6 infants with fetal alcohol syndrome to determine whether zinc deficiency, if present in fetal alcohol syndrome patients, is secondary to an increased urinary zinc excretion. Six infants born to nonalcoholic mothers served as controls. There was no significant difference in creatinine clearance, urine flow rate, or plasma albumin concentrations between the two groups. Plasma concentrations of zinc were significantly lower in fetal alcohol syndrome patients (62.5 +/- 2.8 micrograms/dl) in comparison to controls (71 +/- 1.8 microgram/dl), (p = 0.0001). Urinary excretion of zinc in fetal alcohol syndrome patients averaged 646 +/- 125 micrograms/24 h, significantly higher than in control subjects (76.6 +/- 22 micrograms/24 h), (p = 0.0001). Thus (1) lower plasma zinc levels are present in infants with fetal alcohol syndrome and (2) increased urinary zinc excretion appears to be responsible for decreased plasma zinc concentrations.

Creatinine↗
PubMed1985

Beta 2-microglobulin clearance in neonates: index of tubular maturation.

Serum and urinary beta 2-microglobulin (beta 2M) were studied by enzyme immunoassay in 28 normal neonates at day 1 and day 4 of life in relation to gestational age (GA) and postnatal age (PNA). The infants were grouped according to GA; 10 with GA ranging from 32 to 35 weeks (mean 33.5 weeks) and 18 with GA ranging from 36 to 41 weeks (mean 38.3 weeks). Serum beta 2M varied directly with both GA and PNA. When values for serum beta 2M were related to conceptional age (CA), a significant positive correlation was present for all the infants studied (r = 0.68, P less than 0.01). Fractional excretion of beta 2M (FE beta 2M) decreased as a function of both GA and PNA. When a comparison of FE beta 2M was made in infants of all CA, a significant inverse correlation was noted for infants with CA less than or equal to 35 weeks (r = -0.89, P less than 0.001). The fall in FE beta 2M reached a plateau by 36 weeks. The highest FE beta 2M (33%) was observed in infants of 32 weeks CA who had the lowest filtered beta 2M (F beta 2M). No statistically significant relationship between changes in FE beta 2M and fractional urine flow rate was observed within each of the CA categories (infants less than or equal to 35 weeks, r = 0.21, P = 0.28; infants greater than or equal to 36 weeks, r = 0.25, P = 0.18).(ABSTRACT TRUNCATED AT 250 WORDS)

Gestational Age↗
PubMed1985

Effect of ultrafiltration on peritoneal dialysis drug clearances.

To determine the effect of dialysate osmolarity on peritoneal dialysis drug transfer, peritoneal dialysis clearances of theophylline, phenobarbital, and tobramycin were determined in 10 rabbits using dialysate containing 1.5 and 4.25% glucose. Urea and creatinine clearances were also obtained for comparison. Under similar dialysis conditions, the peritoneal clearances of the three drugs remained unchanged for the two types of dialysate. In contrast, the peritoneal clearances of urea and creatinine were significantly higher with the use of 4.25% glucose dialysate (p less than 0.001). Thus, peritoneal dialysis clearances of theophylline, phenobarbital and tobramycin are not significantly affected by hypertonicity-induced ultrafiltration during acute peritoneal dialysis.

Animals↗
PubMed1985

Hypouricemia in neonates with syndrome of inappropriate secretion of antidiuretic hormone.

A prospective study of serum levels of uric acid in 23 hyponatremic neonates was performed. Infants on diuretic medications or with renal failure were excluded. The infants were separated into two groups: group I consisted of 11 neonates with clinical evidence of syndrome of inappropriate secretion of antidiuretic hormone (SIADH), (mean +/- SD serum sodium 127 +/- 1.36 mEq/liter). Group II included 12 infants with hyponatremia (mean serum sodium 128 +/- 1.10 mEq/liter) associated with decreased effective vascular volume manifest by a fractional sodium excretion less than 1%. The groups were similar for gestational and postnatal ages, birth weight, clinical conditions, and concurrent use of drugs. The serum urate concentration in neonates with SIADH was 2.46 +/- 0.54 mg/dl; serum urate concentration in group II infants was 8.49 +/- 2.45 mg/dL (p less than 0.001). Water restriction in the group I infants with SIADH resulted in a rise in mean serum urate concentration (p less than 0.001). Fractional excretion of urate was elevated during hyponatremia in the group I infants (to 78 +/- 0.13%) and fell to 51 +/- 0.08% after correction (p less than 0.001). In group I infants, a direct correlation was found between fractional excretion of urate and sodium (r = 0.7667, p less than 0.001). These results indicate that hypouricemia is common in infants with suspected SIADH and seems to be due to increased urate clearance secondary to volume expansion.

Humans↗
PubMed1985

Impaired renal acidification in infants with fetal alcohol syndrome.

Urinary acidification was studied in six unrelated infants with fetal alcohol syndrome and eight healthy age-matched infants. Creatinine clearance, fractional sodium excretion, plasma renin activity, and plasma aldosterone were normal in all patients but fractional potassium excretion was lower in the patients than in the controls (p = 0.0001). After ammonium chloride loading, minimum urine pH was significantly higher in FAS patients than in control subjects (5.5 +/- 0.1 and 4.7 +/- 0.1, respectively, p = 0.00005). Net acid excretion was also lower in the patients (24.5 +/- 1.7 Eq/min) than in the controls (27.8 +/- 2.1 Eq/min, p = 0.008). Following sodium bicarbonate loading, fractional bicarbonate excretion was significantly higher (p = 0.00005) and fractional potassium excretion significantly lower (p = 0.002) in the patients than in the controls with comparable blood pH and bicarbonate levels. Treatment with chlorothiazide lowered plasma potassium and raised plasma bicarbonate to normal levels (p = 0.05). Concomitantly, fractional sodium excretion, fractional potassium excretion, and urinary net acid excretion increased significantly (p = 0.01). We conclude that patients with fetal alcohol syndrome have a defect in distal acidification and potassium excretion which cannot be attributed to abnormal aldosterone secretion.

Acidosis, Renal Tubular↗
PubMedDate not supplied

Evaluation of the reproductive and developmental safety of cysteamine in the rat: effects on female reproduction and early embryonic development.

Cystinosis is an autosomal recessive metabolic disease in which the amino acid cystine accumulates in lysosomes due to a defect in lysosomal cystine transport. Cystinosis in infancy is associated with poor growth, muscle wastage, and death at about age 10 due to kidney failure. Treatment with cysteamine and kidney transplantation enables cystinotic girls to reach reproductive age and to be healthy enough to permit pregnancy. It is not known whether exposure to cysteamine will have adverse effects on reproduction in the human. It is also possible that some of the complications seen in cystinotic children could be avoided if a pregnant woman carrying a cystinotic fetus were given cysteamine. However, this treatment is not likely to occur until therapeutic exposures to cysteamine are judged to present no increased risk to the human fetus. As part of a larger investigation assessing the reproductive and developmental safety of cysteamine (as phosphocysteamine) using the rat, the two studies reported herein were performed. The first, a dose-finding study, led to the selection of 150 mg/kg/day as the highest dose of cysteamine used for the second and primary focus of this report. The second study involved the exposure of female rats to cysteamine from premating through day 6.5 postconception and assessment of female fertility and early embryonic development. Cysteamine was administered orally in doses of 0, 37.5, 75, 100, or 150 mg/kg/day. There were no clinical signs of maternal toxicity during the exposures of 2 to 5 weeks before successful mating. Animals in the 150 mg/kg/day group experienced a nonsignificant decrease in body weight gain during pregnancy to day 6.5 postconception, a significant increase in liver and spleen weights, and a significant increase in days to coitus--suggesting that a low level of toxicity was manifested. However, there were no adverse effects on reproductive performance with respect to conception and early embryonic development.

Animals↗
PubMedDate not supplied

Developmental toxicity of cysteamine in the rat: effects on embryo-fetal development.

The reproductive and developmental safety of cysteamine has become an important issue to children with cystinosis because renal transplants and treatment with cysteamine reduce the complications associated with cystinosis and increase the lifespan of the affected children. In addition, there is the potential to decrease the severity or the incidence of renal Fanconi syndrome with administration of cysteamine to pregnant women carrying fetuses with cystinosis, and to ease significantly the burden of this disease throughout their lives. If cysteamine increases significantly the risk of fetal death, growth retardation or birth defects at doses used to treat women with cystinosis, treatment of the affected female should cease during pregnancy and would not be considered for fetal treatment. The goal of this study was to assess the developmental safety of exposure in utero to cysteamine in the rat. Pregnant rats were given cysteamine (as phosphocysteamine) from day 6.5 through day 18.5 postconception and fetuses were assessed for survival, growth, and structural abnormalities on day 20.5. Cysteamine was administered orally in doses of 0, 37.5, 75, 100, or 150 mg/kg/day. Cysteamine produced dose-dependent developmental toxicity with an apparent no adverse effect observed level of 75 mg/kg/day. Specific malformations were associated with this effect (cleft palate, kyphosis), as well as intrauterine growth retardation and fetal death at 100-150 mg/kg/day, without signs of maternal toxicity. Investigations continue into the mechanism for the developmental toxicity of cysteamine.

Administration, Oral↗
PubMedDate not supplied

Acute effect of ethanol on renal electrolyte excretion in rats.

The purpose of this study was to investigate the renal handling of sodium and potassium in rats during an acute ethanol (ETOH) administration and to relate any observed changes to alterations in renin-aldosterone secretion. Eight male Wistar rats, 7 to 8 weeks of age, were injected intraperitoneally (IP) with 1.0 g/kg body wt. ETOH (15% v/v, 95% ETOH in saline, pH 6.98, osmolality 284 mOsm/kg). Blood ETOH levels were 159 +/- 16 (Mean +/- SEM) and 120 +/- 12 mg/dl, 10 and 30 min after the ETOH injection respectively (p less than 0.05). Control animals were given either an equal volume (1.77 ml/100 g body wt.) of 0.9% saline (n = 6) or 5% dextrose solution (n = 4) with similar pH and osmolality. Following ETOH administration blood pH, urine pH, plasma bicarbonate (HCO3) concentration declined significantly (p less than 0.01) while glomerular filtration rate (GFR) and hematocrit (Hct) remained unchanged (p = 0.1). Mean fractional sodium excretion (FENa), fractional potassium excretion (FEK), and osmolar clearance (Cosm) fell significantly despite an increase in plasma sodium (p less than 0.01), potassium (p less than 0.05) and osmolality concentrations (p less than 0.05). There was no significant change in plasma aldosterone concentration (PA) or plasma renin activity (PRA) following the ETOH administration. No difference in GFR, FENa, FEK, Cosm, blood pH, urine pH, plasma electrolytes, PA, or PRA was observed following the saline or dextrose injections. In conclusion, acute ETOH administration in rats alters renal sodium and potassium excretion independent of changes in GFR, PA, PRA or plasma volume as reflected by Hct.

Aldosterone↗
PubMedDate not supplied

Effects of prenatal ethanol exposure on postnatal renal function and structure in the rat.

Effects of prenatal ethanol exposure on postnatal renal function and structure in the rat. Renal function and morphology were studied in 90-day-old offspring of ethanol-fed (E) rats and were compared to pair-fed control (C) animals. Compared to C rats, E rats were smaller at birth, had higher fractional sodium excretion (p less than 0.01) and lower fractional potassium excretion (p less than 0.01). In E rats, sodium (Na) restriction resulted in a significant increase in urine flow and Na wastage, whereas C rats remained in Na balance. E rats developed hyperkalemia, when potassium (K) intake was increased from 2.8 to 14 mEq/day. Baseline creatinine clearance, urine and blood osmolalities and pH, plasma electrolytes and aldosterone concentrations were similar in both groups. There was no significant difference in wet or dry kidney weight, renal water content, or renal tissue concentrations of Na or K between the two groups. No difference was found in gross morphology or light microscopic appearances of the kidneys between E and C rats. Thus rats exposed to ethanol during fetal life have a defect in urine concentration and Na conservation when fed a low Na diet and a defect in K excretion when given a K load without evidence of any gross or light microscopic renal structural abnormalities at 90 days of age.

Animals↗
PubMedDate not supplied

Ultrastructural changes in the rat kidney following fetal exposure to ethanol.

Previous studies have implicated renal ultrastructural abnormalities in the pathogenesis of tubular dysfunction in fetal alcohol syndrome. Scanning electron microscopic studies were performed to examine the role of glomerular and tubular structural changes in this syndrome. Pregnant Sprague-Dawley rats were fed a liquid diet in which ethanol constituted 35% of the total caloric content or pair-fed an isocaloric control diet from gestational day 8 to the day of birth. After delivery, offspring were housed with the dam and left undisturbed until 18 days of age when they were weaned and given free access to standard chow diet and water. At random, kidneys from 11 offspring of ethanol-fed (E) rats and 7 pair-fed control (C) rats were fixed by in vivo retrograde perfusion at 90 days of age for ultrastructural studies. The E rats showed cytoplasmic mitochondrial atrophy and vacuolar structures of the epithelial cells of the distal tubules and collecting ducts not seen in C rats. No obvious difference was found in the glomerular, proximal tubule, or loop of Henle architecture between the two groups. These findings suggest that rats prenatally exposed to ethanol have renal ultrastructural abnormalities that may be important in the genesis of functional disturbances.

Animals↗