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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of the Ca antagonist, verapamil, on the behaviour of parathyroid hormone was studied in normal and uraemic male Wistar rats. Parathyroidectomy was by cautery. Acute uraemia was induced by bilateral nephrectomy, and moderate uraemia by s.c. injection of gentamicin (200 mg/kg). Ethylendiamine tetracetic acid (50 mg/kg X d) was injected subcutaneously. Parathyroid hormone was determined by radioimmunoassay. The degree of uraemia was determined from plasma urea levels. Renal failure resulted in a significant increase in plasma parathyroid hormone (mean +/- SEM, ng/l) (84 +/- 6, n = 10, in the control; 277 +/- 39, n = 7, in the moderate uraemics and 667 +/- 128, n = 6, in the acute uraemics). Injection of verapamil significantly increased plasma levels of parathyroid hormone, ranging from 21% in the controls to 62% in the moderate uraemia group. In the acute uraemics, parathyroid hormone levels were very high and verapamil did not cause any further elevation of the hormone in the blood. Parathyroidectomy significantly lowered plasma parathyroid hormone, and verapamil resulted in a mean increase of 29%. EDTA caused an increase of 64%, compared with the control group.
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PMID:Effect of verapamil on plasma parathyroid hormone. 357 10

Extravascular lung water and vascular permeability-surface area products were measured with a multiple indicator dilution method in 6 premature lambs with hyaline membrane disease 1-5 hours following delivery by cesarean section. The indicators used were 51Cr-labelled erythrocytes, 125I-albumin, 3H-water, and 14C-urea. Results were compared with previously obtained data in newborn lambs without hyaline membrane disease also delivered by cesarean section. Extravascular lung water was significantly higher in lambs with hyaline membrane disease [23.2 +/- 1.0 (SEM) vs. 10.7 +/- 1.4 ml/kg body wt]. Vascular permeability-surface area products for 14C-urea were significantly lower in lambs with hyaline membrane disease (0.30 +/- 0.10 vs 0.78 +/- 0.11 ml/s per kg). It is concluded that extravascular lung water is high in lambs with hyaline membrane disease. Permeability-surface area products for 14C-urea is low in lambs with hyaline membrane disease, which probably indicates a decrease in detectable surface area for exchange due to derecruitment or hypoperfusion of pulmonary exchange vessels in edematous and hypoxic areas of the lungs.
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PMID:Lung water and vascular permeability-surface area in premature newborn lambs with hyaline membrane disease. 364 51

To evaluate whether the viscera contribute to the system of membranes used in peritoneal dialysis, dialysis rate studies were performed comparing control rats (n = 9, mean peritoneal area 509 +/- 38 cm2) with eviscerated rats (n = 12, mean peritoneal area 200 +/- 123 cm2). The mass transfer coefficient (MTC) and absorption from the peritoneal cavity were calculated for urea, creatinine, and inulin, which had been added to commercially available 1.5% hydrous dextrose dialysate. Rates of peritoneal blood flow to the peritoneal membranes remaining after evisceration were similar for both groups. Urea, creatinine, glucose, and inulin were used as markers to compare control and eviscerated animals. The MTC results were (in milliliters per minute, mean +/- SEM): urea 3.0 +/- 0.3, 4.1 +/- 0.5 (P less than 0.01); creatinine 1.4 +/- 0.2, 2.0 +/- 0.2 (P less than 0.05); glucose 1.2 +/- 0.3, 1.7 +/- 0.2 (P less than 0.09); inulin 0.3 +/- 0.02, 0.6 +/- 0.1 (P less than 0.01); and MTC inulin/MTC urea 0.16 +/- 0.01, 0.14 +/- 0.01. Absorption of urea, creatinine, glucose, and inulin from the peritoneal cavity was only 10% to 23% greater among control animals. Whether the results were caused by nonparticipation of the intestinal viscera or other mechanisms, such as improved contact between dialysate and membrane, awaits further study.
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PMID:Systems of membranes involved in peritoneal dialysis. 365 24

As manifest by tubular collapse and the virtual absence of flow into the glomerulotubular junction (GTJ), filtration in most nephrons (SNGFR) of rats poisoned with 9 mg/kg body wt HgCl2 16 to 28 hours earlier was virtually absent. Arterial colloid osmotic pressure (COPA) and Bowman's space pressure (PBS) were modestly depressed (P less than 0.05 or below), and mean blood pressure was reduced from 115 +/- 2 mm Hg (SEM) to 97 +/- 1 mm Hg (P less than 0.001). Glomerular capillary hydraulic pressure (Pg), 25.6 +/- 1.3 mm Hg was some 24 mm Hg lower than control (P less than 0.001) and yielded a net afferent effective filtration pressure (Pnet) of 4.1 +/- 1.2 mm Hg. Excluding three rats with values greater than 10 mm Hg, Pnet averaged 2.0 +/- 0.9 mm Hg (N = 17 rats) versus 20.0 +/- 1.8 mm Hg in controls (N = 10, P less than 0.001), the former being statistically almost indistinguishable from 0 mm Hg and barely able to support any filtration. This decrease in Pg was caused by a major increase in preglomerular resistance (RA) and a reciprocal fall in efferent arteriolar resistance (RE), the RA/RE ratio of 7.2 +/- 0.8 being fourfold higher than control (P less than 0.001). Renocortical blood flow was not different from control (P greater than 0.2). A wide spread of Pg values in individual glomeruli and the absence of tubular flow despite the appearance of i.v. injected lissamine green in a quadrant of surface glomeruli suggested the possibility of a greatly increased, glomerular capillary resistance. It is concluded that reciprocal changes in RA and RE are the immediate cause of filtration failure in this form of ARF and that, in the virtual absence of filtration, tubular leakage can play no important role. Since PBS was depressed in both the developmental and established phases of ARF, tubular obstruction appears to play no direct role in the pathogenesis of this particular model of murine acute renal failure.
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PMID:Glomerular hemodynamics in mercury-induced acute renal failure. 365 37

We have studied the efficacy of urea in the treatment of hyponatremia and hydrosaline retention in cirrhotic patients with ascites resistant to diuretics. In 5 patients with hyponatremia and ascites resistant to a major diuretic treatment (200-400 mg spironolactone combined with 40-160 mg furosemide/day for 4 of them), urea intake (30-90 g/day) induced the following changes: the daily weight changed from a gain of 0.01 +/- 0.06 kg/day to a loss of 1.03 +/- 0.12 kg/day (p less than 0.001) (mean +/- SEM), serum sodium concentration rose from 128 +/- 1.3 to 133 +/- 1.4 mmol/l (p less than 0.01), sodium output increased from 24 +/- 4 to 82.5 +/- 11 mmol/day, diuresis increased from 1.05 +/- 0.10 to 2.24 +/- 0.24 liters/day (p less than 0.01). Despite an important weight loss, the creatinine clearance did not change significantly (53.6 +/- 4.5 ml/min before and 70.0 +/- 8.2 ml/min during urea). In patients responding to classical diuretics, urea as a monotherapy was less effective. From the 6 patients with resistant ascites, only 1 developed prerenal uremia after urea treatment. In order to enhance urea efficacy, it is important to take it together with a long-loop diuretic. Intermittent urea intake seemed to be useful in cirrhotic patients with hyponatremia associated with ascites resistant to diuretics and with low or normal blood urea concentrations.
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PMID:Treatment of hyponatremic cirrhosis with ascites resistant to diuretics by urea. 379 73

Serum osteocalcin (BGP), a vitamin K-dependent gamma-carboxyglutamic acid (GLA) containing bone protein, provides an index of bone turnover in patients with a variety of metabolic bone diseases. BGP increases with increasing age in both sexes, but more so in women. BGP rises above normal when the glomerular filtration rate falls below 30 ml/min. Because of its importance in bone disease, its low mol wt, and the effect of uremia, we measured BGP by RIA in serum and dialysate fluid in patients on hemodialysis (HD) or peritoneal dialysis (PD). In 32 HD patients (22 women and 10 men), serum BGP was not different pre- and postdialysis [67.5 +/- 4.4 (+/- SEM) ng/ml vs. 67.7 +/- 5.2), but was significantly elevated compared to the level in normal subjects (7.3 +/- 0.8 ng/ml). The sex difference previously reported in normal subjects was not found in patients with renal failure. The serum BGP level in 8 PD patients was 49.4 +/- 6.9 ng/ml, with a peritoneal fluid concentration of 27.6 +/- 9.3 ng/ml. The hemodialysate fluid concentration of BGP was 1.7 +/- 0.4 ng/ml, which was significantly lower than the serum BGP levels in the HD patients, the PD patients, and peritoneal fluid (P less than 0.01). A significant correlation existed among BGP, alkaline phosphatase, immunoreactive PTH, creatinine, and blood urea nitrogen. We conclude that BGP is markedly elevated in patients with renal failure, not altered in the serum by HD or PD, but very low in HD dialysate fluid. These findings may reflect a combination of impaired clearance and increased skeletal production. The difference in clearance between the peritoneal and hemodialysis fluid is compatible with the mol wt of BGP. In 15 patients who had successful kidney transplantation, serum BGP was normal despite an elevated serum PTH level.
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PMID:Serum and dialysate osteocalcin levels in hemodialysis and peritoneal dialysis patients and after renal transplantation. 388 31

The peritoneal generation of arachidonic acid metabolites was studied in eight patients with end-stage renal disease undergoing continuous ambulatory peritoneal dialysis (CAPD) during infection-free periods and during bacterial peritonitis. The prostacyclin metabolite 6-keto-PGF1 alpha was found to be the major prostanoid generated by human peritoneal mesothelium (1090 ng (6h)-1, SEM 86, n = 8) followed by lesser amounts of PGE2 (142 ng (6 h)-1, SEM 26, n = 8), PGF2 alpha (162 ng (6 h)-1, SEM 27, n = 8) and TXB2 (59 ng (6 h)-1, SEM 5, n = 8). During peritonitis a significant increase of all prostaglandins and TXB2 occurred (P less than 0.001). The ratio of the vasodilating prostaglandins and their metabolites (PGE2 and 6-keto-PGF1 alpha) to the vasoconstrictors and their metabolites (PGF2 alpha and TXB2) increased from 6.6 to 10.5 during peritoneal inflammation. Augmented peritoneal clearances of creatinin and urea and increased losses of proteins during peritonitis as well as the enhanced peritoneal generation of prostanoids were reduced to basal values by adequate antibiotic therapy. The present results suggest that the increased peritoneal blood flow during peritonitis, probably responsible for the observed changes of peritoneal transport properties, may be induced by a change in the ratio of vasoactive prostaglandins generated by peritoneal mesothelial cells.
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PMID:Stimulation of peritoneal synthesis of vasoactive prostaglandins during peritonitis in patients on continuous ambulatory peritoneal dialysis. 392 79

A survey was carried out in a steel foundry in Brisbane to evaluate the nature and frequency of respiratory symptoms and to assess ventilatory function. The foundry used many moulding processes including the Furane, Isocure, Shell, carbon dioxide, and oil sand systems. Nasal symptoms and wheeze were often reported, particularly by workers in the general foundry and core shop, and on a semiautomated line. By contrast, workers in the aftercast section not exposed to fumes or vapours from the various moulding processes reported these symptoms less often. Of 46 workers exposed to moulding fumes and vapours, 11 had developed a wheeze while working at the foundry. Wheeze and other respiratory tract symptoms were often attributed by the workers to exposure to substances at work, particularly from the Shell process which uses phenol formaldehyde resin and hexamethylenetetramine. Symptoms were reported also, but less often, on exposure to materials used in the Furane process (urea formaldehyde and furfuryl alcohol) and the Isocure process (methylene diphenyl diisocyanate, phenol formaldehyde, and dimethylethylamine). Ventilatory function studied over Monday and Friday showed a small and inconsistent changes. The six subjects working on the semiautomated line showed a small decrease in FEV1 (+/- SEM) (208 +/- 70 ml) only on Monday; this differed significantly from that in 17 aftercast workers (9 +/- 50 ml, p less than 0.05). Ventilatory function recorded before work on Monday morning showed no evidence of chronic airway obstruction in any group. Most environmental measurements were below the threshold limit values (TLV) except in the general foundry, where furfuryl alcohol was detected at concentrations of up to 50 ppm and formaldehyde at 4 ppm. The onset of symptoms in relation to exposure to various fumes and vapours suggests that both irritant and hypersensitivity mechanisms are present. As environmental modifications had occurred recently the apparent hypersensitivity may relate to past exposure levels above the TLV.
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PMID:Respiratory disease in foundry workers. 397 Aug 67

Cortisol was infused, intravenously, for 4 h continuously into 5 chronically cannulated ovine fetuses at 111-120 days of gestation (term is 142-152 days). The dose used was 100 micrograms/h, and raised fetal blood cortisol concentrations from 8.2 +/- 4.0 to 56.5 +/- 19.0 nmol/l (values are mean +/- SEM). The effects observed were a 4-5 fold increase in sodium and chloride excretion, a doubling of potassium excretion and free water clearance, no significant changes in urine pH, urea and creatinine excretions, and an increase in urine osmolality from 129 +/- 7.5 to 154.4 +/- 11.3 mosmol/kg water. There were no significant changes in any of the measured parameters in 5 fetuses infused with 0.9% NaCl for 4h. It is suggested that the hyponatremia and inability to retain sodium observed in many premature or very low birth weight babies may be due to the fact that their kidneys are behaving as fetal rather than neonatal organs and responding to the high plasma cortisol concentrations found in such babies with a natriuresis.
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PMID:Cortisol is natriuretic in the immature ovine fetus. 402 Mar 17

To study the potential contribution of glycine toxicity in the transurethral resection syndrome, we evaluated hemodynamic and visual evoked potential responses to glycine infusion (1 g/kg) in 22 dogs anesthetized with halothane (1.0-1.2% end tidal. Three dogs received 5% glucose in normal saline without glycine; three received arginine (4 mg/kg) in normal saline without glycine; three received arginine (4 mg/kg) in normal saline without glycine; 10 received glycine (1 g/kg), then arginine (4 mg/kg) 120 min after the completion of glycine infusion; and six received arginine 30 min after the completion of glycine infusion. Arginine was infused to evaluate potential antagonistic effects of glycine toxicity. Blood levels of glycine, ammonia, arginine, urea, and formate were determined after infusions of glycine or arginine. All animals received about 5 ml X kg-1 X hr-1 of normal saline during the 2-4 hr of study. Immediately after glycine infusion, cardiac output increased 57%, whereas systemic vascular resistance and mean arterial pressure decreased 32% and 8%, respectively. Later cardiac output and mean arterial pressure were 41% and 18% less than control levels, whereas systemic vascular resistance returned to control levels. Both amplitude and latency of visual evoked potential waveforms were altered in the animals receiving glycine infusion but not in the control animals. These responses were associated with elevations of blood glycine (149 +/- 5 to 9591 +/- 809 microM/L, mean + SEM) and blood NH3 (10.5 +/- 2.8 to 100.0 +/- 13.6 microM/L), but not with formate levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of glycine on hemodynamic responses and visual evoked potentials in the dog. 405 Dec 5


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