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Biomedical subjects

S Solomon

Publications and source records attributed to S Solomon.

At least 361 records · Page 20Linked to original sources
PubMed1977

Body water distribution after operation.

The effect of a major surgical procedure on the distribution of body water was investigated in two groups of patients. The first group of four patients did not receive any salt during the first 24 hours following operation, while the second group of five patients received a moderate amount of isotoric saline solution during this period. For seven days prior to operation, the patients were maintained by bed rest and a daily intake of 100 milliequivalents of sodium and 100 milliequivalents of potassium. A multiple isotope dilution technique was used, before and after operation, to measure red cell mass, plasma volume, extracellular water, total body water and total exchangeable sodium. In addition, the aldosterone secretion rate was measured, both before and after operation, to assess the physiologic control of the extracellular water volume. In the patients who did not receive any salt, the mean extracellular water volume decreased following operation from 39.7 to 37.5 per cent of the total body water; a mean decrease of 0.9 liter while the aldosterone secretion rate increased significantly, p less than 0.02, by 101 per cent from 206 to 414 micrograms per day. In the second group of patients who received an average of 1.3 liters of isotonic saline solution during the first 24 postoperative hours, the extracellular water increased from 37.9 to 42.8 per cent of total body water; a mean increase of 1.1 liters p less than 0.02. The mean aldosterone secretion rate in this group of patients increased by only 13 per cent from 167 to 188 micrograms per day. The blood volume did not change in either group as a result of operation. These data support the hypothesis that, following operation, sequestration of extracellular water occurs within the injured tissues, necessitating the postoperative infusion of a moderate amount of a balanced salt solution.

Adult↗
PubMed1977

Reduction in severity of acute renal failure (ARF) in rats by dopamine.

Dopamine was administered to rats at the time of initiation of anoxic acute renal failure. Dopamine partially reduced the severity of ARF as evidenced by a reduction in blood urea, serum creatinine as well as an increase in glomerular filtration rate (GFR). (UNaV) in dopamine treated ARF was similar to sham operated animals and both were significantly lower than control ARF.

Acute Kidney Injury↗
PubMed1976

Maturation of the renal response to hypertonic sodium chloride loading in rats: micropuncture and clearance studies.

1. The ability of maturing rats to excrete a sodium load was studied by micropuncture and clearance procedures. 2. During control conditions, no change of glomerular filtration rate or sodium excretion was observed for the time period of the entire procedure (P greater than 0-20). During the infusion of hypertonic (4%) sodium chloride, fractional sodium excretion was 0-08 +/- 0-01 in rats 21-30 days old and 0-14 +/- 0-01 (P less than 0-01) in adults. However, the depression of proximal tubular water re-absorption was equal in both groups (P greater than 0-20). 3. Proximal glomerulotubular balance for water re-absorption was similar in all groups (P less than 0-20). Since end proximal tubular water excretion and depression of fractional water excretion were the same in all animals, differences of urinary sodium excretion during development are probably due to differences of function of segments beyond the proximal tubule during development. 4. Fractional potassium excretion was reduced in young rats (0-17 +/- 0-04) during hypertonic sodium chloride infusion, compared to adults (0-24 +/- 0-01, P less than 0-05). 5. Passage time of fast green through cortical segments in seconds is prolonged in young rats during control conditions. Similar decreases of passage time were seen in all groups during hypertonic sodium chloride infusion. No segmental differences of passage time were seen during developmental. 6. No difference in the relationship between fractional sodium and water excretion was seen during development of the renal response to hypertonic sodium chloride infusion. Thus, altered sensitivity to sodium chloride osmotic diuresis does not exist during maturation in rats.

Age Factors↗
PubMed1976

Development of the renal response to blood volume expansion in normal and fast-growing rats.

Male rats from reduced (fast-growing) litters between 14 and 50 days of age were studied. Standard renal clearnce techniques were employed. After a 60-min control period, the animals were infused (2.3% body wt) with heparinized donor blood obtained from lillermates of the same age. Renal function was followed for an additional 60 min. The efficiency of the diuretic response, the percent infused volume excreted above control levels, and the sodium efficiency, the percent infused Na excreted, were calculated. Results indicate that both efficiencies develop in a discontinuous pattern and that they are comparable. This pattern of development, as well as the magnitude of the mature response, is comparable to that previously reported for rats from intact (normally growing) litters. The onset and attainment of the mature response is, however, shifted in time, such that reduced-litter animals achieve the mature response 10-15 days earlier than intact-litter rats. Results exclude chronological age or body weight alone as principal determinant of the mature response and suggest that some function of growth rate is responsible for the maturation of this regulatory function.

Aging↗
PubMed1976

Amino acid uptake by fetal kidney slices.

Kidney slices of 7-17-week-old human fetuses were incubated for 90 min or less in Krebs-Ringer solution containing aminoisobutyric acid (AIB). Cell to medium ratios of AIB decrease with increasing fetal age. Uptake rate is slower than for mature human tissue. Both water content and extracellular space is high in embryonic tissue as compared to adult.

Age Factors↗
PubMed1976

Function and structure in the diphenylamine-exposed kidney.

Standard micropuncture and microdissection techniques were used to examine the function and structure of nephrons in rats whose kidneys were made cystic by dietary exposure to diphenylamine. Heterogeneity characterized the lesion, with dilation and frank cyst formation occurring in 5-30% of nephrons. Elevated intraluminal hydrostatic pressures, occurring in the absence of increased glomerular filtration or decreased net water reabsorption, were recorded in dilated, but not in nondilated nephrons. Structural studies demonstrated communication of dilated nephrons with cysts, concretions of debris within tubular lumens, evidence of extrinsic pressure by cysts on adjacent tubules, and apparent luminal narrowing of some proximal tubules. These observations were used to explain prolonged loop of Henle transit times and occasional failure to detect [3H]inulin excretion after microperfusion into dilated tubules. It was concluded that the elevated hydrostatic pressures in the dilated nephrons of diphenylamine-exposed kidneys were the consequence of variably severe and frequently incomplete tubular occlusion. These findings support the hypothesis that cyst formation is a consequence of partial obstruction and elevated intratubular pressure in this model and perhaps in other susceptible mammalian kidneys.

Aniline Compounds↗
PubMed1976

In vitro sensitivity of enteric bacteria to epicillin, chloramphenicol, ampicillin and furazolidone.

Strains of Salmonella typhi (148) and Salmonella paratyphi A (27) isolated from the blood of patients with clinical features of enteric fever were tested in vitro for their sensitivity to epicillin, ampicillin, chloramphenicol and furazolidone. Results from both the disc and tube dilution methods showed that greater percentages of the two strains were sensitive to epicillin than to the other antibiotics.

Adolescent↗
PubMed1976

Cytoplasmic glucocorticoid receptors in the developing small intestine of the rabbit fetus.

Glucocorticoid binding and alkaline phosphatase activity in the small intestine of the fetal rabbit were studied to investigate the relationship of glucocorticoid receptors and the development of the tissue. In the cytosol fraction, the binding of (3H)dexamethasone involves a macromolecule with high affinity (Kd = nM) for the hormone and a limited number of binding sites (saturable at a hormone concentration of 10 nM). That the binding reaction involves a protein and sulfhydryl groups was demonstrated by the absence of binding of the steroid in the presence of Pronase and sulfhydryl blocking reagents. In sucrose density gradients, the complexes have sedimentation coefficients of about 4S and 7S at low ionic strength, but only 4S at high ionic strength (0.4m KCl). The binding protein is thermolabile, and is stabilized by complexing with the hormone. The ability of different steroids to compete with (3H)dexamethasone for the binding sites correlates well with their glucocorticoid potency. During development of the fetal rabbit small intestine, the total number of glucocorticoid-binding sites in the cytosol increases in parallel with the increases in the tissue weight until term. However, the concentration of the binding sites (pmol/mg cytosol protein) is maximum at day 25 of gestation, followed by a decrease to the adult level within a few days after birth. Alkaline phosphatase activity is first detectable on day 25 of gestation and increases rapidly thereafter. These observations suggest that there may be a temporal relatioship between the development of the fetal rabbit small intestine, as reflected in the alkaline phosphatase and the levels of glucocorticoid receptors in the cytosol.

Alkaline Phosphatase↗
PubMed1976

Chronic saline loading in anoxic renal failure in rats.

The effect of saline loading was compared in two types of experimental acute renal failure--due to i.m. administration of glycerol or to anoxia. In the glycerol model, chronic saline loading for about three weeks prior to the experiment achieved almost complete prevention of the uremia. The blood urea and serum creatinine levels 24 h after the experiment were 44 +/- 2 and 1.3 +/- 0.3 se) mg/dl, respectively. The values for the water-drinking rats were 292 +/- 23 and 3.7 +/- 0.4 mg/dl, respectively. In the anoxic model of acute renal failure, produced by uninephrectomy and contralateral renal artery clamping, chronic saline loading reduced the severity of the resultant uremia, although less impressively than in the glycerol model. The blood urea and serum creatinine 24 h after the experiment were 148 +/- 15 and 1.8 +/- 0.2 mg/dl, respectively. The values for the water-drinking rats were 237 +/- 15 and 2.3 +/- 0.2 mg/dl, respectively. Plasma renin activity was similar in the saline-loaded rats in both the toxic and anoxic models. It seems, therefore, that all known models of acute renal failure have at least a common pathogenic mechanism, which can be influenced by chronic saline loading prior to onset of the disease, and which is most probably not renin dependent. In the anoxic model additional factors, which cannot be counteracted by chronic saline loading, are active in the development of uremia.

Acute Kidney Injury↗
PubMed1976

High renin activity accompanying angiotensin II inhibition in rats with ischemic renal failure.

Acute renal failure was produced in rats by right nephrectomy and total occlusion of the left renal artery for 70 min. Angiotensin II competitive inhibitor, P113 (1-sar-8-ala-angiotensin II), was administered intravascularly for 100 min, starting 15 min before the clamping of the renal artery. A marked rise in plasma renin activity was observed 15 min after declamping and was significantly higher in the P113-treated rats than in saline-treated animals. The rise in plasma renin activity was observed 15 min after declamping and was similar in the two groups, indicating that P113 does not prevent the development of acute renal failure in this experimental model. It is suggested that the marked rise in plasma renin activity may be due to interruption of the normal feedback mechanisms which suppress renin release, as a result of occupation of the angiotensin II receptor sites by P113.

Acute Kidney Injury↗
PubMed1976

beta-Adrenergic blockade reduces the severity of acute renal failure in rats.

Propranolol administration in the hypoxic model of acute renal failure (ARF) in rats has reduced plasma renin activity (PRA) and uraemia as compared to untreated controls. P113 has no effect on uraemia but increased PRA in ARF. A combination of both drugs is no more effective in reducing uraemia than propranolol alone. These results support the view that beta-adrenergic blockade by propranolol reduces the severity of ARF by preventing the post-hypoxic release of renin.

Acute Kidney Injury↗
PubMed1975

Reduction in severity of acute renal failure in rats by beta-adrenergic blockade.

The effectiveness of beta-adrenergic blockade in preventing acute renal failure (A.R.F.) in rats was studied in the hypoxia model produced by unilateral nephrectomy and clamping of the contralateral renal artery for 70 minutes. Beta-adrenergic blockade effectively reduced the severity of A.R.F. in this experimental model. Treatment with a combination of propranolol and a synthetic angiotensin-II competitive inhibitor (P113) produced no further improvement. These results are consistent with the view that intrarenal release of renin is to some extent involved in the pathogenesis of A.R.F.

Acute Kidney Injury↗
PubMed1975

Testosterone stimulation of a rapidly labeled, low-molecular-weight RNA fraction in human hepatic erythroid cells in culture.

The addition of erythropoietin to cell cultures of erythroid cells of human fetal liver resulted in an increased incorporation of thymidine, adenine, and uridine into trichloroacetic acid-insoluble cell fractions and in an increased uptake of adenine and uridine into the cell. Although the effects of testosterone and erythropoietin on heme synthesis in these cells are known to be very similar, there was no effect of testosterone on the total incorporation of radioactive precursors into DNA or RNA. The RNA synthesized after short pulses of radioactive uridine, when analyzed on sucrose gradients containing 1% sodium dodecyl sulfate, consisted of a homogeneous peak sedimenting at 10 plus or minus 2 S, which is quite different from the heterogeneous, high-molecular-weight RNA synthesized under identical conditions in primary cultures of human fetal lung, kidney, or liver parenchymal cells. Addition of testosterone to liver erythroid cells in cultures for 5 hr followed by a 1-hr uridine pulse resulted in a 3-fold increase of RNA species with an average sedimentation coefficient of 14 plus or minus 3 S. The similarity with the sedimentation coefficient of the globin mRNA described in other systems and the high degree of specialization of the erythroid cells suggest that this RNA may be a stable intermediate involved in the synthesis of hemoglobin.

Adenine↗
PubMed1975

Suppressive action of prolactin on renal response to volume expansion.

The effects of prolactin on rat renal sodium and water handling during volume expansion were studied using clearance techniques. Both control and experimental adult male Wistar rats were prehydrated with an oral water load of volume equal to 2.5% body weight (BW). At least 3 h later, a continuous intravenous infusion of ovine prolactin (NIH-P-S8), 7.1 mug/h per 100 g, was started in the experimental group. After a 1-h steady-state period, the rats were given an intravenous expansion infusion of either hypotonic saline (2.5% BW), isotonic saline (2.5% and 7.5% BW), or blood (2.5% BW). In all control hypotonic and isotonic saline-expanded animals, within 1 h the rats excreted a volume of urine equal to over 50% of the volume of saline infused. The diuretic and natriuretic responses to saline expansion of prolactin-treated rats were significantly smaller than controls. In contrast to the effects of prolactin on the renal response to saline infusions, it did not alter the natriuretic or diuretic response to blood infusion. Prolactin may be counteracting the effects of physical factors on the regulation of sodium reabsorption in the proximal tubule.

Animals↗