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Biomedical subjects

M Hohenegger

Publications and source records attributed to M Hohenegger.

At least 55 records · Page 3Linked to original sources
PubMed1988

Inhibition of calcium release from skeletal muscle sarcoplasmic reticulum by calmodulin.

The effect of calmodulin on calcium release from heavy sarcoplasmic reticulum isolated from rabbit skeletal muscle was investigated with actively and passively calcium loaded sarcoplasmic reticulum vesicles and measured either spectrophotometrically with arsenazo III or by Millipore filtration technique. The transient calcium-, caffeine- and AMP-induced calcium release from actively loaded sarcoplasmic reticulum vesicles was reduced to 29%, 51% and 59% of the respective control value by 1 microM exogenous calmodulin. Stopped-flow measurements demonstrate that calmodulin reduces the apparent rate of caffeine-induced calcium release from actively loaded sarcoplasmic reticulum. The rate of calcium uptake measured in the presence of ruthenium red, which blocks the calcium release channel, was not affected by calmodulin or calmodulin-dependent phosphorylation of sarcoplasmic reticulum vesicles with ATP[S]. The rate of the calcium-, caffeine- and AMP-induced calcium release from passively loaded sarcoplasmic reticulum vesicles was reduced 1.4-2.0-fold by 1 microM exogenous calmodulin, i.e. the half-time of release was maximally increased by a factor of two, whilst calmodulin-dependent phosphorylation of a 57 kDa protein with ATP[S] had no effect. The data indicate that calmodulin itself regulates the calcium release channel of sarcoplasmic reticulum.

Adenosine Monophosphate↗
PubMed1988

Effect of some uremic toxins on oxygen consumption of rats in vivo and in vitro.

In rats, oxygen consumption is reduced by about 40-50% 24 h after bilateral nephrectomy. This is also the case when the animals are pretreated with triiodothyronine, 3 x 0.75 mg/kg body weight orally, for 2-3 days. Indole, cresol, putrescine, methylguanidine or acetoine was given intraperitoneally to normal rats at doses of between 5 and 300 mg/kg body weight. Only low single doses of indole (5 mg/kg) reduced oxygen consumption significantly. Single doses of the other substances studied were ineffective even at tenfold higher doses. Some combinations of these substances, however, (10 mg/kg each), reduced the metabolic rate significantly. In contrast to the results in vivo, plasma of uremic rats, as well as the uremic toxins, dissolved in Krebs-phosphate buffer pH 7.4 at concentrations of 30 mg/dl each, had no influence on respiration of rat diaphragma or liver slices in vitro (single substances and different combinations).

Acetoin↗
PubMed1988

Toxicity in uremia. 1. Correlation between PTH levels and depressed cell proliferation.

Cell proliferation is significantly depressed in uremia; to assess the influence of PTH on it, normal lymphocytes were cultured in presence of uremic patients' serum with low or high plasma PTH levels (Group A; PTH less than 2.5 ng/ml; Group B: PTH greater than 12 ng/ml), and serum of normal subjects (Group C). Cell proliferation was lowered by serum from both groups (p A vs C less than 0.004; p B vs C less than 0.001). However, the depressing effect was more evident when group B serum was employed (p A vs B less than 0.002).

Cell Division↗
PubMed1988

Toxicity in uremia. 2. Correlation between PTH levels and impaired aspecific immunity.

The role of PTH in depressing polynuclear leucocyte (PMN) phagocytosis in uremia was investigated. The hydrophobicity and phagocytic activity of normal PMN was tested in presence of uremic patients' serum with low (Group A) or high (Group B) levels of plasma PTH. The PMN phagocytic index was lowered by serum of both groups, but more in presence of Group B serum (p A vs B less than 0.002). Similarly, the contact angle of cells was affected more in presence of serum of patients with high PTH levels (p B vs A less than 0.003; p B vs C less than 0.002).

Cytotoxins↗
PubMed1987

Influence of some uremic toxins on oxygen consumption of rats in vivo and in vitro.

According to our present knowledge hypometabolism and hypothermia in uremia are most probably due to direct actions of toxic substances at the cellular level. A cardiovascular etiology seems less possible. A similar reduction of oxygen consumption as observed in uremia can be produced by 5 mg/kg body wt. indole i.p. Acetoine, m- and p-cresol, methylguanidine and putrescine do not reduce oxygen consumption even at tenfold higher doses. Some combinations of these substances, however, are effective when given only 10 mg/kg body wt. each. The effects in vivo cannot be reproduced by employing in vitro systems.

Animals↗
PubMed1986

Metabolism of free fatty acids (FA) and triacylglycerol (TG) in acute and subacute fluoride intoxication of the rat.

In rats acute intoxication with 100 mg sodium fluoride/kg body wt. orally has the following metabolic consequences. Oxygen consumption is reduced by about 30-50%. Plasma free FA decrease in fed as well as in starved rats. Hepatic FA synthesis is enhanced, but TG secretion to the blood is not altered. Intravenously injected Intralipid 20% is removed at a normal rate. In subacute intoxication (30 mg sodium fluoride/kg body wt given orally per day over 1 week) oxygen consumption is not affected. TG secretion and removal of Intralipid remain in the normal range whereas hepatic FA synthesis is increased as in acute intoxication. TG concentration in the liver, however, increases by about 30% after 1 week.

Animals↗
PubMed1986

Fatty acyl-CoA oxidase in rat kidney and liver after application of thyroxine.

Male rats were fed a standard diet containing 2.5 mg% L-thyroxine. After 10 and 20 days, in postnuclear fractions of the kidney the specific activity of fatty acyl-CoA oxidase, the enzyme responsible for the rate-limiting first step of peroxisomal fatty acid beta-oxidation, was increased by 100 and 160%, respectively. A similar effect was found in the liver. It is suggested that thyroxine essentially affects only this step of the fatty acid beta-oxidation sequence. Presumably the elevation of fatty acyl-CoA oxidase is one reason for the beneficial action of thyroid hormones in toxic lesions of the kidney.

Acyl Coenzyme A↗
PubMed1986

Metabolic effects of water deprivation.

Under the conditions of pair feeding, water-deprived rats predominantly use fat as a metabolic fuel, whereas total energy turnover as measured by oxygen consumption is not altered. Plasma free fatty acids are elevated in dehydrated rats, indicating enhanced lipolysis. Reduced hepatic fatty acid synthesis and reduced triacylglycerol secretion into the blood seem to be the main factors for the decrease of plasma triacylglycerol, observed 48 hours after the onset of water deprivation. Enhanced plasma levels of corticosterone (about 100%) and glucagon (about 50%) may contribute to the metabolic situation observed in water deprivation.

Animals↗
PubMed1985

The key role of sex dependency on kidney citrate metabolism in the rat.

An evaluation of the potential role of the kidney in the regulation of the blood citrate level under different acid-base statuses and various diets was performed. Twenty-four hours after bilateral nephrectomy there was a highly significant increase in the blood citrate concentrations in female rats, whereas the blood citrate levels either remained unchanged or decreased in bilateral nephrectomized male animals. Our data clearly indicate a key role of sex dependency on kidney citrate metabolism in the rat.

3-Hydroxybutyric Acid↗
PubMed1985

Increased serum triacylglycerol and cholesterol binding reserve in acute uremic rats.

In acute uremic rats (24 h after bilateral nephrectomy, serum urea 280-300 mg/dl) the interface tension of the serum is significantly reduced. Serum levels of triacylglycerol are significantly elevated in uremia, whereas cholesterol levels do not show a significant alteration. The in vitro serum binding reserve for both, triacylglycerol and cholesterol is considerably enhanced. These results let suppose the presence of tenside-like substances in uremic serum which may be involved in disturbed triacylglycerol transport from the serum to the tissues and in development of uremic hypertriglyceridemia.

Acute Disease↗
PubMed1985

Lipolytic activity of renal cortex during ontogenetic development in rats.

The lipolytic activity of rat kidney cortex was investigated in newborn and adult rats. Two peaks of lipolytic activity could be detected at pH 5.0 and 8.4, respectively. Lipase activity at pH 5.0 is completely inhibited by 0.2 M sodium fluoride and can be stimulated by norepinephrine (10 micrograms/ml). Full activity is already present in 5-day-old rats. The response to sodium fluoride and norepinephrine is identical in newborn and adult animals. Lipase activity at pH 8.4 is inhibited up to 85% by 0.6 M sodium chloride. Activity is very low in 5-day-old rats and increases during maturation. This lipase can be stimulated by heparin (100 micrograms/ml) by about 10-25% in newborn and adult animals.

Aging↗
PubMed1985

Reduced hepatic fatty-acid synthesis and lowered plasma triacylglycerol (TG) in potassium deficient rats.

Potassium deficiency was induced in rats by feeding a potassium- free synthetic diet containing 5% Resonium A. Feeding this diet for 1 week resulted in a decrease of plasma potassium by about 50% vs. pair fed controls. In hypokalemic rats hepatic fatty-acid synthesis and TG secretion by the liver were significantly reduced. In contrast the removal of an intravenous lipid load occurred optimally under this condition. As a consequence plasma TG levels were reduced in potassium-deficient rats.

Animals↗
PubMed1984

Oligomycin toxicity in intact rats.

Intraperitoneal injection of oligomycin into the rat (0.5 mg per kg, corresponding to the LD33 dose) reduces the oxygen consumption by about 50%, whereas the arterial pO2 remains normal. The large extent of this decrease points to an involvement of liver and muscle tissue. Triiodothyronine pretreatment (3 doses of 0.075 mg/100 g body weight) is not able to prevent this effect. From the blood metabolites measured glucose, pyruvate and the parameters of lipid metabolism remain unchanged; only lactate is significantly increased, causing compensated metabolic acidosis. Heart rate, systolic blood pressure and electrocardiogram are essentially unchanged. Oliguria, reduced renal excretion of urea and increase of plasma urea also indicate a nephrotoxic action. The results are discussed in comparison with some effects of experimental uremia.

Animals↗
PubMed1984

Triacylglycerol secretion and fatty acid synthesis by the liver in acute uremic rats.

In bilaterally nephrectomized rats fatty acid synthesis (incorporation of 3H from 3H2O into fatty acids by the liver) and triacylglycerol (TG) secretion by the liver (Triton method) were investigated 24 h after surgery. Starved and fed rats were employed. In uremic rats fatty acid synthesis occurs at a normal rate; prevention of acidosis during uremia by bicarbonate treatment has no influence on lipid synthesis. Following intravenous injections of Triton WR 1339 the TG plasma levels are considerably lower in uremic rats than in corresponding controls. As the plasma volume is significantly higher in uremic animals, there is only an insignificant decrease in the absolute TG secretion rate in these animals. The removal of TG from the blood to the tissues in severely reduced in uremia with acidosis. The normal rates of fatty acid synthesis and nearly normal rates of TG secretion may, therefore, be considered as permissive factors for the development of uremic hypertriglyceridemia. The lesser degree of hypertriglyceridemia in uremia without acidosis is only caused by the better removal of TG from the blood (as could be demonstrated earlier). Fatty acid synthesis and TG secretion do not play any role in this case.

Acidosis↗
PubMed1984

The influence of permanent adrenalin application on the triacylglycerol concentration and fatty acid synthesis in various tissues of the rat.

Adrenalin tablets (15 mg) or placebos were implanted into the neck of male Sprague-Dawley rats weighing between 150 to 250 g. 18 hours after implantation a significant lipolysis as well as enhanced concentrations of triacylglycerol in liver, kidney cortex and skeletal muscle can be observed in adrenalin treated rats. Measurements of fatty acid synthesis (3H method) in these tissues indicate that in kidney cortex and liver there is no contribution of local synthesis to elevated triacylglycerol content. In skeletal muscle local synthesis seems to be efficient to some degree. The main cause for lipid deposition in adrenalin supplied rats is, therefore, uptake of free fatty acids from the blood and following esterification with glycerol.

Animals↗
PubMed1984

Some aspects of renal energy and lipid metabolism in newborn rats.

Some aspects of renal energy and lipid metabolism were studied in the postnatal period of rats. Oxygen consumption, RQ values, stimulation of oxygen consumption by exogenous substrates (8 mM glucose, 8 mM acetate, 1 mM palmitate), and conversion of acetate or palmitate to CO2 were measured in slices of cortex and inner medulla. The results obtained in 5-day-old rats are not essentially different from those observed in adults. On the other hand, the phenomenon of triacylglycerol storage in kidney cortex during starvation (well known in adult animals) is absent in the newborn rat. It can be demonstrated first in 30-day-old rats. At the same age renal arteriovenous concentration differences for total glycerol indicate a significant uptake during starvation and a release in the fed state.

Animals↗