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Biomedical subjects

N Brautbar

Publications and source records attributed to N Brautbar.

At least 37 records · Page 2Linked to original sources
PubMed1986

Effect of chronic renal failure on heart. Role of secondary hyperparathyroidism.

This study examined the effects of chronic renal failure in rats with and without parathyroid glands on myocardial energy production, transfer and utilization as well as on cardiac index. Chronic renal failure was produced by 7/8 nephrectomy in rats weighing between 240 and 350 g with intact parathyroid glands (CRF-control) and in parathyroidectomized (CRF-PTX) rats maintained normocalcemic. The data were compared to results obtained in intact rats and in normocalcemic parathyroidectomized rats with normal renal function. There were significant (p less than 0.01) decrements in myocardial content of ATP and creatine phosphate, mitochondrial oxygen consumption, and in the activity of both mitochondrial and myofibrillar creatine phosphokinase in CRF-control rats as compared to normal animals. The myocardial calcium content and the 45Ca uptake in CRF-control rats were significantly (p less than 0.01) higher than in normal rats. In CRF-PTX animals, the myocardial content of ATP, mitochondrial oxygen consumption, 45Ca uptake and calcium content were normal, but PTX did not normalize the activity of mitochondrial and myofibrillar creatine phosphokinase. Parathyroidectomy in rats with normal renal function was associated with a significant reduction in the activity of creatine phosphokinase of myocardial mitochondria and myofibrils. There was a significant (p less than 0.01) decrease in cardiac index in CRF-control rats as compared to normal animals, and cardiac index did not return to normal in CRF-PTX rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Effect of parathyroid hormone on energy metabolism of skeletal muscle.

Clinical states with primary or secondary hyperparathyroidism are associated with muscle dysfunction, suggesting that parathyroid hormone (PTH) may affect muscle metabolism. The present study examined the effect of 1-84 PTH and its amino-terminal fragment (1-34 PTH) on energy production, transfer, and utilization by skeletal muscle. Rats weighing 150 to 200 g were injected intraperitoneally with 1-84 or 1-34 PTH, 200 U/day, for 4 days, and control animals received vehicle only. The effect of the simultaneous administration of a calcium channel blocker, verapamil, was examined also. The muscle content of inorganic phosphorus, creatine phosphate, and adenine nucleotides were significantly (P less than 0.01) lower in the PTH-treated rats than in control animals. The hormone significantly reduced mitochondrial oxygen consumption without altering ADP:0 ratio, indicating reduced phosphorylation. Both 1-84 and 1-34 PTH produced significant (P less than 0.01) reduction in the activities of mitochondrial and myofibrillar CPK, and mitochondrial MgATPase. 1-84 PTH reduced the activity of myofibrillar CaATPase as well. There was a significant (P less than 0.01) increment in muscle uptake of 45Ca in the 1-84 PTH-treated rats. Verapamil abolished all the effects of PTH. Our data demonstrate that both 1-84 and 1-34 PTH impair energy production, transfer, and utilization. These biochemical derangements may, at least in part, underlie the myopathy observed in conditions associated with excess PTH.

Adenosine Diphosphate↗
PubMed1985

Effect of parathyroid hormone on myocardial energy metabolism in the rat.

This study examined the effect of parathyroid hormone (PTH) on myocardial energy production, transfer, and utilization. Rats (150 to 200 g) were injected with 1-84 PTH, 200 U/day i.p., or 1-34 PTH, 200 or 300 U/day i.p., for 4 days. Control animals received the vehicle only. The effect of the simultaneous administration of calcium channel blocker, verapamil, was also examined. Myocardial contents of Pi, ATP, and CP were significantly (P less than 0.01) lower in the 1-84 PTH-treated rats than in control animals. Both 1-84 PTH and 1-34 significantly (P less than 0.01) reduced mitochondrial oxygen consumption without altering ADP:O ratio indicating reduced phosphorylation. 1-84 and 1-34 PTH significantly (P less than 0.01) reduced the activities of mitochondrial and myofibrillar creatine phosphokinase and 1-84 PTH inhibited (P less than 0.01) the activities of mitochondrial Mg ATPase and those of myofibrillar Ca ATPase. There were significant (P less than 0.01) increments in myocardial 45Ca and in total calcium content in 1-84 PTH-treated rats. Verapamil abolished all the effects of 1-84 PTH. Similarly, inactivation of 1-84 PTH abolished its effects. Treatment with 1-84 PTH for 10 days was associated with a significant decrease in cardiac index and mean arterial pressure. Our data demonstrate that both 1-84 and 1-34 PTH impair energy production, transfer, and utilization. These biochemical derangements, if maintained, produce a decrease in cardiac index. It appears that the enhanced entry and the accumulation of calcium in the myocardium, either directly and/or indirectly, are responsible for the action of PTH on energy metabolism of the heart.

Adenine Nucleotides↗
PubMed1985

Effect of phosphate depletion on blood pressure and vascular reactivity to norepinephrine and angiotensin II in the rat.

Phosphate depletion (PD) adversely affects myocardial function but its influence on blood pressure is not well elucidated. In this study we evaluated whether PD influences blood pressure and/or affects its hormonal regulation or the peripheral vascular response to pressor agonists. Mean arterial pressure (MAP) in PD rats was lower than in normal animals, whereas heart rate was not significantly different between the two groups. Cardiac index (CI) in PD rats was lower and systemic vascular resistance (SVR) was higher than in controls. Plasma norepinephrine (NE) in the resting state and during the stress of immobilization was significantly greater in PD rats than in controls. Base-line plasma renin activity was also significantly higher in PD rats and increased similarly in the two groups of rats after administration of isoproterenol. Bolus injections of NE or angiotensin II produced a smaller rise in MAP in PD rats than in controls. Reduced responsiveness to NE was also demonstrated in isolated hind-limb preparation from PD rats. When NE was infused to achieve a rise in MAP of 30 mmHg, the dose required in PD was higher than in controls. Treatment with indomethacin did not affect the response in MAP to NE. The content and affinity of both alpha- and beta-receptors in PD hearts were not different from those of control hearts. The contents of PiATP, and AMP in the mesenteric vessels of PD rats were significantly lower than in control animals. These data show that PD leads to reductions in MAP, arteriolar response to pressor agents, and CI with appropriate compensatory rise in NE but with inadequate compensatory increase in SVR.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1985

Calcium, parathyroid hormone and phospholipid turnover of human red blood cells.

PTH enhances entry of calcium into RBC, stimulates their Ca ATPase and increases osmotic fragility. The effect on the latter occurs only in the presence of calcium. The mechanisms of action of PTH and those mediating their increased calcium influx into RBC are not evident. It is possible that calcium, PTH or both affects phospholipid turnover of RBC and results in production of ionophoric compounds such as phosphatidic acid which in turn allows calcium movement. The present study examined the effect of calcium (1 mM), 1-84 PTH (50 U/ml) and calcium and PTH on phospholipid contents and 32P incorporation into phosphoinositides of human RBC and RBC ghosts. Calcium produced significant decrements in 32P incorporation into phosphatidylinositol, di- and triphosphatidylinositol and an increase into phosphatidic acid. PTH decreased the 32P into phosphatidylinositol only. Both PTH or calcium caused a significant increase in RBC content of phosphatidylserine. The data show that calcium alone alters phospholipid turnover of RBC and such an effect may mediate the PTH-induced calcium influx. Alternatively, PTH may enhance entry of calcium into RBC independent of the effect of calcium on phospholipid turnover and the increase in cytosolic calcium would then alter phospholipid turnover which in turn would further facilitate the effect of PTH on calcium influx. The increase of phosphatidylserine by PTH may increase rigidity of RBC membrane and enhance osmotic fragility.

Calcium↗
PubMed1984

Impaired myocardial lipid metabolism in phosphate depletion.

This study examines the effects of phosphate depletion on myocardial carbohydrate, lipid, and phospholipid metabolism. Rats were studied after 4 (short-term) and 8 to 12 weeks (long-term) of selective dietary phosphate restriction. Myocardial biopsy samples were examined for glucose-6-phosphate and glycogen to evaluate carbohydrate pathways, and for glycerol phosphate and mitochondrial fatty acid oxidation and phospholipid contents to evaluate lipid and phospholipid turnover. The fall in cellular inorganic phosphorus was associated with a fall in myocardial glycogen, glucose-6-phosphate, glycerol phosphate, and cytidine triphosphate, as well as the contents of phosphatidylcholine, phosphatidylethanolamine, and total phospholipid phosphorus. These observations demonstrate impaired phospholipid metabolism, probably at the biosynthetic level. The oxidation of long-chain and short-chain fatty acids is also impaired in phosphate depletion, further demonstrating impaired lipid metabolism. The abnormal phospholipid metabolism may be compatible with the changes in cellular membrane described in phosphate depletion.

Animals↗
PubMed1984

The possible role of magnesium in hypercalcemic hypertension.

Hypercalcemic conditions are commonly associated with hypertension and with abnormal magnesium homeostasis. The mechanism by which the hypertension of hypercalcemia is mediated is not clear, and the role that magnesium may play in its generation has not been examined. We review here the available clinical and experimental data and propose a role for abnormal magnesium metabolism in the mediation and generation of the hypertension of hypercalcemia.

Animals↗
PubMed1984

Skeletal myopathy and magnesium depletion: cellular mechanisms.

Muscle weakness and abnormal electrical activity of muscle cells have been described in magnesium-depleted patients and animals. The cellular mechanisms by which magnesium depletion causes the skeletal myopathy are not known. We review here the available clinical and experimental data on the effects of magnesium on: skeletal muscle cellular bioenergetics; excitation-contraction coupling, and biochemical and functional integrity of the cellular membrane. The data suggest that abnormalities in one or more of the above pathways may mediate the myopathy of magnesium depletion.

Adenosine Triphosphate↗
PubMed1983

Application of chromatography to the analysis of phosphate compounds in small biopsy tissue samples in different experimental conditions.

Biochemical analysis of tissue biopsy samples for evaluation of the phosphate compounds of metabolism has been limited to a large tissue sample size, and thus, repeated biopsies on the same animal or patient are too difficult to obtain. We report here the use of the Bessman analyzer: anion exchange chromatography followed by automatic phosphorus analysis on small tissue samples. The method described here enables the repetitive measurement of high-energy phosphate compounds (ATP, ADP, AMP, creatine phosphate (CP], inorganic phosphorus (Pi), sugar phosphorus (glucose 6-phosphate and fructose 6-phosphate), and inosine monophosphate (IMP), an indicator of adequate biopsy processing and sample preparation. The data also emphasize the importance of adequate oxygenation of the experimental animal or patient. This method is easy to apply in almost any clinically oriented research laboratory for the study of needle biopsies from human and animal tissues and permits a more convenient and complete investigation of the high-energy phosphate compounds of intermediary metabolism than do the methods of firefly luminescence or the multiple, NAD-linked enzymatic systems required for the necessary sensitivity.

Biopsy↗
PubMed1983

Impaired energy metabolism in skeletal muscle during phosphate depletion.

The effects of phosphate depletion (PD) of 4, 8, and 12 weeks on skeletal muscle energy metabolism were studied in rats fed a phosphate deficiency diet and compared with rats pairfed with a normal phosphate diet. Skeletal muscle biopsy specimens were examined for energy production, transport, and utilization. The results show that already by 4 weeks of PD, the concentration of inorganic phosphorus of the skeletal muscle was significantly reduced and remained low thereafter. There was significant (P less than 0.01) and direct correlation between the cellular inorganic phosphorus and that of serum phosphorus. Adenine nucleotides, ATP, ADP, AMP, and creatine phosphate levels did not change. Mitochondrial respiration and oxidative phosphorylation were impaired by PD. Total cellular mitochondrial and myofibrillar creatine phosphokinase activities were significantly reduced at 4 weeks of PD and fell further at 8 and 12 weeks. There was a significant (P less than 0.01) and direct correlation between the activity of total extractable creatine phosphokinase and both serum and cellular levels of inorganic phosphorus. These data show that chronic PD is associated with a decrease in energy production, transfer, and utilization by skeletal muscle and provides information on the molecular events responsible for the myopathy of PD.

Animals↗
PubMed1982

Impaired energy metabolism in rat myocardium during phosphate depletion.

The effects of phosphate depletion (PD) of 4, 8, and 12 wk duration on myocardial energy metabolism were studied in rats fed a phosphate-deficient diet and compared with rats pair-fed a normal phosphate diet. Myocardial biopsies were examined for high-energy phosphate bonds. The results show that PD causes a significant reduction in myocardial concentration of inorganic phosphorus at 4 wk of PD and creatine phosphate at 8 wk of PD, while adenine nucleotides were significantly reduced only after 12 wk of PD. The changes in cellular inorganic phosphorus and creatine phosphate displayed a significant correlation with serum phosphorus levels. Mitochondrial respiration was impaired early in PD. Total cellular, mitochondrial, and myofibrillar creatine kinase activities were significantly reduced at 4 wk of PD and fell further at 8 and 12 wk. These data show that chronic PD is associated with reduced mitochondrial capacity to produce ATP, impaired transport via the creatine phosphate shuttle, and reduced myofibrillar ability to utilize ATP. These abnormalities indicate that all steps of myocardial energetics are impaired in PD and provide the molecular basis for the altered myocardial function seen in PD.

Animals↗