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Biomedical subjects

W Jubiz

Publications and source records attributed to W Jubiz.

At least 55 records · Page 3Linked to original sources
PubMed1977

Potassium-renin-aldosterone relationships during the first year of life.

In order to gain insight into factors controlling aldosterone secretion during the first year of life, we studied the relationships between PRA, serum potassium, sodium, and serum aldosterone levels. While we found a dissociation during the early neonatal period, there was a high degree of correlation between serum aldosteron, PRA, and serum potassium by 3 to 12 months of age. This suggests that aldosterone secretion in the 3- to 12-month-old child, as in adults, is regulated by the circulating levels of potassium and angiotensin II.

Aldosterone↗
PubMed1977

Plasma prostaglandin E concentrations from birth through childhood.

The prostaglandins are synthesized in a variety of tissues and participate in an extensive number of physiologic processes. As prostaglandin concentrations have not been reported in infants and children, we measured PGE levels from birth through childhood. PGE levels in cord blood were significantly higher than those in adults. By 48 to 72 hours of age, however, they had fallen to levels that were significantly lower than those in adults. Although PGE concentrations increased with age, they remained significantly lower than did adult levels. These low levels may be related to some of the functional pecularities of the immature kidney.

Adolescent↗
PubMed1977

The role of iodine in the pathogenesis of thyroid enlargement in rats with chronic renal failure.

In rats with mild renal failure produced by a 2/3 nephrectomy on one side followed by a total nephrectomy on the other, ingestion of a high (10 mg/kg) iodine diet for two months resulted in thyromegaly, high serum iodine levels and a good correlation between thyroid weight and serum iodine (r = 0.75, P less than 0.01) or thyroid weight and blood urea nitrogen (r = 0.745, P less than 0.01). Iodine may potentiate the effects of unidentified gointrogens that accumulate in rats with renal failure. Since the serum iodine levels were higher in the animals with renal failure, it is also possible that iodine alone may have been responsible for the observed differences in thyroid weight.

Animals↗
PubMed1977

Serum thyrotropin and thyroid hormone levels in humans receiving chronic potassium iodide.

Serum thyroxine (T4), triiodothyronine (T3) and thyrotropin (TSH) concentrations were measured in 13 patients with chronic obstructive pulmonary disease receiving saturated solution of potassium iodide (SSKI). All had a low serum T4 and a high serum TSH concentration. However, serum T3 levels were normal in eight. Recovery of normal thyroid function was observed in each of the seven patients in whom the iodide was discontinued. The same hormones were measured in four normal subjects who received 30 drops of SSKI daily for 11 weeks. An increase in serum TSH levels was preceded by a fall in serum concentrations of T4 and to some extent, T3. Upon SSKI withdrawal subsequent increases in the serum concentrations of both thyroid hormones, but particularly T3, resulted in the return of serum TSH to baseline levels. None of the subjects developed clinical hypothyroidism. It is not apparent why the normal subjects did not exhibit clinical or laboratory evidence of hypothyroidism while the patients with chronic pulmonary disease did. A younger age and the shorter duration of iodide administration in the normal subjects may have played a role.

Adult↗
PubMed1977

Plasma 1,25-dihydroxyvitamin D levels in patients receiving anticonvulsant drugs.

Recent evidence has linked altered plasma vitamin D metabolite levels to the reported occurrence of hypocalcemia and other metabolic abnormalities in patients receiving anticonvulsant drugs. We have measured plasma levels of 25-hydroxyvitamin D (25-(OH)D) and 1,25-dihydroxyvitamin D (1,25-(OH)2D) in institutionalized patients on diphenylhydantoin (Dilantin) and/or phenobarbital therapy. Values were compared with those obtained in institutionalized patients receiving no drugs and with normal ambulatory subjects. Although plasma 25-(OH)D levels were lower in the patients on drugs, a deficiency of 1,25-(OH)2D, the tissue active metabolite of vitamin D, was not present. These results indicate that in patients taking anticonvulsant drugs, the serum calcium, phosphorus, alkaline phosphatase and parathyroid hormone (PTH) abnormalities are not caused by a defective formation of 1,25-(OH)2D.

Adult↗
PubMed1977

Abnormalities in the regulation of prolactin in patients with chronic renal failure.

We have investigated the hypothalamic-hypophyseal regulation of prolactin secretion in patients with chronic renal failure treated with chronic hemodialysis. When compared to control subjects, baseline serum prolactin levels were elevated in the renal failure patients (range 11 to 16 mmicrogram/ml for renal failure patients, 6 to 9 mmicrogram/ml for controls, P less than 0.05). In addition, serum prolactin levels in the renal failure patients failed to suppress significantly following the administration of L-dopa, and did not increase in response to chlorpromazine or thyrotropin releasing hormone. These findings suggest an abnormal regulation of prolactin secretion and appear to be another example of the endocrine dysfunction that occurs in uremic subjects.

Adult↗
PubMed1976

Changes in serum thyroxine, triiodothyronine, and thyrotropin induced by lithium in normal subjects and in rats.

Serum thyroxine (T4), triiodothyronine (T3), and thyrotropin (TSH) were measured in 4 normal subjects before, during, and 2 wk after administration of lithium carbonate (1,200 mg/day) for 6 wk. All subjects developed thyroid enlargement associated with increase in TSH. Serum T3 and T4 did not change significantly. In 3 hypothyroid maintained on thyroxine replacement, lithium administration did not alter circulating levels of T4 or T3, suggesting no effect of lithium on the extrathyroidal metabolism of the thyroid hormones. In rats fed a low iodine diet containing 122 mg/kg/day lithium carbonate, goiter, increased 131I uptake, and a decrease in intrathyroidal T3 and T4 with an increase in MIT, DIT, and MIT/DIT were observed at 3 wk. Serum T3 fell significantly only during the third week, while T4 did not change. Thyroid enlargement, secondary to a rise in TSH, appears to play a role in the adaptation of the thyroid gland to lithium carbonate. The exact mechanism for the elevation of TSH has not been elucidated.

Adult↗
PubMed1976

Effects of aspirin on gastric prostaglandin E (PGE) and acid output in normal subjects.

Aspirin administration to normal subjects resulted in a reduction in gastric prostaglandin E (PGE) output. Both PGE concentration and gastric juice volume were decreased. Gastric acid output also decreased, although the difference was not statistically significant. An increased sensitivity of the PGE system to inhibition by aspirin at 11 p.m., midnight, and 1am was observed.

Adult↗
PubMed1976

Degradation of prostaglandin E2 and F2alpha by the canine liver.

Degradation of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha) by the liver was determined in 16 dogs. PGE2 (8 dogs) or PGF2 alpha (8 dogs) was infused into the left ventricle at rates of 3.75, 7.5, 15, 37.5, and 75 mug/min. Blood samples obtained simultaneously from the portal vein (PV), hepatic vein (HV), and abdominal inferior vena cava (IVC) at each infusion rate were tested for PGE or PGF concentration by radioimmunoassy. During PGE2 infusion the mean PGE concentrations in the PV were 0.60, 1.05, 1.40, 2.29, 4.80, and 7.29 ng/ml at each infusion rate, Corresponding concentrations in the HV were 0.51, 0.62, 0.71, 0.96, 1.94, and 2.62 ng/ml, and in the IVC 0.51, 0.95, 1.31, 1.96, 4.31, AND 5;18 NG/ML. During PGF2 alpha infusion, the mean PGF concentrations in the PV were 0.32, 0.59, 0.73, 1.73, 4.11, and 7.11 ng/ml at the respective infusion rates; Corresponding concentrations in the HV were 0.26, 0.24, 0.33, 0.48, 0.49, and 0.96 ng/ml, and in the IVC 0.32, 0.50, 0.61, 1.10, 2.40, and 4.17 ng/ml. Thus, these data indicate that the canine liver has substantial, but not unlimited, capacity for degradation of PGE2 and PGF2 alpha in the portal circulation. Whether or not PGE or PGF levels in the PV may exceed this capacity during periods of stress or whether this enzymatic mechanism may be suppressed by either physiological or pharmacological factors is not known.

Animals↗
PubMed1976

Prostaglandin E release in the dog: effect of sodium.

Renal arterial injections (20 ml) of 4 M NaCl in 8 dogs and of 0.5 M NaCl in two dogs were followed by significant but delayed increases over 60 min in renal venous prostaglandin E (PGE) concentrations as measured by radioimmunoassay. Perfusion pressure increased significantly only at 5 min but plasma sodium concentration remained above base line for 60 min. In two dogs in which renal artery blood flow was maintained at a constant rate, comparable increases in PGE concentrations were observed. Injections of 1 M mannitol in three dogs and 5% dextrose in water in two dogs did not result in significant changes in PGE concentrations. In four dogs, administration of 50 mg indomethacin 15 min prior to injection of 20 ml of 4 M NaCl abolished the changes of PGE concentration. Sodium appears to have an effect on stimulation of PGE release by the canine kidney. This phenomenon may be of physiologic significance.

Animals↗
PubMed1976

Enhanced erythropoietin and prostaglandin E production in the dog following renal artery constriction.

Renal artery constriction (RAC) to 30% of normal flow for 12 hr in the unilaterally nephrectomized dog produced a marked increase in both erythropoietin titers and prostaglandin E (PGE) levels in the blood. In dogs pretreated prior to RAC with indomethacin, a potent inhibitor of prostaglandin synthetase, there was no significant increase in either PGE or erythropoietin levels as compared to zero-time control values. These data suggested an involvement of renal PGE in the generation of erythropoietin following RAC.

Animals↗
PubMed1976

Thyroid dysfunction in uremia: evidence for thyroid and hypophyseal abnormalities.

Disturbances in thyroid function and a high prevalence of goiter develop in patients on chronic hemodialysis. This study shows that in patients on dialysis, mean serum thyroxine and triiodothyronine levels are lower than normal. Patients with chronic renal failure not on dialysis, have mean serum thyroxine levels similar to normal subjects and low mean serum triiodothyronine levels. However, both serum thyroxine and triiodothyronine concentrations decrease as the renal failure worsens. In addition, both groups of patients with renal failure have a decreased serum thyroxine response to oxogenous thyrotrophin and a diminished serum thyrotrophin response to thyrotrophin-releasing hormone. These data suggest the presence of an intrathyroidal and an hypophyseal defect in uremic patients. Although serum iodide concentrations are elevated, there is no correlation between the level of serum iodide and the degree of renal failure. Therefore, we have no direct evidence that iodide excess is responsible for the abnormalities observed.

Adolescent↗
PubMed1975

Prostaglandin F2alpha (PGF2alpha) and prolactin secretion in rats.

Plasma prolactin and F-prostaglandins (PGF) were measured anesthetized male Sprague-Dawley rats before and at 15, 30, 45 and 60 minutes following i.v. injection of either PGF2alpha (4 mg/kg), chlorpromazine, 1 mg/kg or chlorpormazine (1 mg/kg) after pretreatment with i.p. indomethacin (2 mg/kg). Following PGF2alpha administration, plasma prolactin levels increased significantly only at 15 and 30 minutes in spite of extremely high PGF levels throughout 60 minutes. Besides the expected rise in plasma prolactin, chlorpromazine caused a transient but statistically significant increase in PGF. Indomethacin blocked the chlorpormazine-induced PGF rise but not prolactin increase. Animals stressed with ether anesthesia showed elevation of plasma prolactin, which was not blocked by indomethacin although PGF concentration fell. Theese results indicate that PGF2alpha can stimulate prolactin release. This effect does not appear to be physiologic since very high PGF levels are required. Furthermore, blockade of prostaglandin synthesis by indomethacin does not prevent the release of prolactin in response to chlorpormazine or stress. Our findings do not support a possible role of PGFs as intermediaries in prolactin release. However, it is possible that PGFs may work through other mechanisms not investigated in our study.

Animals↗
PubMed1975

Endotoxin-induced prostaglandin E and F release in dogs.

Prostaglandin E and F (PGE and PGF) levels in sequential blood samples obtained simultaneously from the renal and portal veins and aorta during endotoxin shock in dogs were determined by radioimmunoassay. Four groups of dogs were studied. In five control dogs in which no endotoxin was given, PGE and PGF levels did not change significantly at 0, 15, 30, 60, and 90 min. In eight dogs given endotoxin alone, PGE and PGF levels did not change in the aorta. In samples taken from the portal vein there was a significant rise in PGE and PGF 15 min after endotoxin, whereas renal vein PGE and PGF did not become significantly elevated until 60 and 90 min after endotoxin. In six dogs pretreated with acetylsalicylic acid and six dogs pretreated with indomethacin, PGE and PGF levels did not change after endotoxin. Indomethacin modified the delayed hemodynamic effects of endotoxin whereas acetylsalicylic acid did not. Neither drug blocked the immediate hemodynamic effects of endotoxin. Endotoxin-induced PGE and PGF release is probably due to increased synthesis. The mechanism whereby synthesis is stimulated and the extent to which vasomotor tone is influenced by PGE and PGF during endotoxin shock cannot be determined from our data.

Animals↗
PubMed1975

Prostaglandin F and E levels during endotoxin-induced pulmonary hypertension in calves.

Prostaglandin F and E (PGF and PGE) concentrations in sequential blood samples obtained simultaneously from the pulmonary artery (PA) and pulmonary vein (PV) during endotoxin-induced pulmonary hypertension in calves were determined by radioimmunoassay. Three groups of calves were studied. In nine control calves in which no endotoxin was given PA pressure and PGF and PGE concentrations in four pairs of samples taken at 0, 5, 15, and 45 min did not change. In 17 calves given 1 mg E. coli endotoxin, PGF concentrations were increased significantly in the PV and to a lesser degree in the PA in the 15-and 45-min samples. The increased PGF concentration in the 15-min sample corresponded to an increased PA pressure of 74 plus or minus 4 mmHg (mean plus or minus SE). In three of the endotoxin-treated calves studied a second time and three separate calves indomethacin pretreatment completely blocked the hemodynamic effect of endotoxin as well as PGF release. PGE concentrations did not change in either group. These data suggest that endotoxin-induced pulmonary hypertension may be mediated by PGF, a known pulmonary pressor agent in the bovine, and that blockade of this effect by indomethacin may be due to inhibition of prostaglandin synthesis and/or release.

Animals↗
PubMed1975

Hypertension in primary hyperparathyroidism: the role of the renin-angiotensin system.

In four out of seven patients with primary hyperparathyroidism, we have found elevated plasma renin activity (PRA) and blood pressure, both of which returned to normal following surgical correction of the hyperparathyroidism. However, PRA was normal in nonmotensive patients with primary hyperparathyroidism, those with hypercalcemia of other etiologies, and those with secondary hyperparathyroidism. These findings suggest that the renin angiotensin system may play a role in the etiology of the hypertension in primary hyperparathyroidism.

Adult↗