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Biomedical subjects

A Wirth

Publications and source records attributed to A Wirth.

At least 19 recordsLinked to original sources
PubMed1992

Veratridine activates a silent sodium channel in rat isolated aorta.

To investigate the existence of silent Na+ channels, isolated rat aorta was treated with veratridine (0.1 mM) and the resulting Ca2+ uptake was determined. After 30-min incubation the total tissue uptake of Ca2+ and Ca2+ uptake increased from 2.325 +/- 0.017 to 2.614 +/- 0.080 nmol/mg wet weight (ww) and from 162.6 +/- 9.7 to 218.1 +/- 13.0 pmol/mg ww, respectively. The veratridine-induced Ca2+ uptake was blocked by tetrodotoxin (1 microM; to 17 +/- 5%) but not altered by amiloride (10 microM-1 mM). Activation of Na+/Ca2+ exchange by Na+ removal increased Ca2+ uptake from 74.2 +/- 4.5 to 97.3 +/- 5.3 pmol/mg ww, which was suppressed by amiloride (10 microM-1 mM). Nifedipine (10 nM) and verapamil (0.1 microM) at concentrations at which depolarization-induced Ca2+ uptake was diminished did not attenuate veratridine-induced Ca2+ uptake. Phenytoin at 0.1 mM reduced the Ca2+ uptake induced by veratridine or by depolarization. R 56865 (0.1 microM) and R 59494 (1 microM), novel anti-ischemic compounds inhibiting slowly inactivating Na+ channels, suppressed the veratridine-induced but not the depolarization-induced Ca2+ uptake. Guanidinium uptake was increased by veratridine (0.1 mM) from 371.2 +/- 7.2 to 574.8 +/- 45.9 pmol/mg ww. These results suggest that the rat aorta possesses a Na+ channel which is electrically silent under normal conditions but could be activated by veratridine.

Amiloride↗
PubMed1991

Veratridine-induced intoxication in the isolated left atrium of the rat: effects of some anti-ischemic compounds.

Veratridine-induced Na+ and Ca2+ uptake was used as a simulation of ischemia-induced Na+ and Ca2+ uptake. Therefore, electrically driven (1 Hz) isolated left atria of the rat were intoxicated with veratridine and the 45Ca2+ uptake was determined. Veratridine (10(-4) mol/l) increased the 45Ca2+ uptake from 575 +/- 13 to 2320 +/- 86 dpm/mg ww (n = 20). The total tissue content of 45Ca was elevated from 4328 +/- 132 to 5136 +/- 303 dpm/mg ww (n = 13). The veratridine-induced 45Ca2+ uptake was completely suppressed by tetrodotoxin (10(-7) and 10(-6) mol/l), whereas amiloride (6.10(-6) mol/l) and phentolamine (10(-6) and 10(-5) mol/l) exhibited no effect on the veratridine-induced 45Ca2+ uptake. Nifedipine (10(-7) and 10(-6) mol/l) was ineffective on veratridine-induced 45Ca2+ uptake. Verapamil (10(-5) mol/l) suppressed the veratridine-induced 45Ca2+ uptake, but the 45Ca2+ uptake in the absence of veratridine was also suppressed by verapamil (10(-6) and 10(-5) mol/l). The novel anti-ischemic compounds R 56865 (10(-8)-10(-5) mol/l) and R 59494 (10(-8)-10(-5) mol/l) totally abolished veratridine-induced 45Ca2+ uptake. It is speculated that Ca2+ enters the cell via a Na+ channel which changes its selectivity upon veratridine treatment. Consequently, R 56865 and R 59494 could display their protective effect by either inhibiting the modified Na+ channel or preventing the transition of the normal Na+ channel to its altered state.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Fatty acids in the portal vein of the rat regulate hepatic insulin clearance.

The effects of FFA on hepatic insulin clearance were studied in the in situ perfused rat liver. Clearance decreased with increasing body weight (age) of the rats. When FFA were added to the perfusate a 40% reduction of hepatic removal of insulin was found over the normal, physiological range (less than 1,000 mumol/liter), less pronounced in heavier rats. When perfusion was started with high concentrations of FFA, inhibition was rapidly reversible, a phenomenon again blunted in heavier rats. In contrast to FFA, different glucose concentrations in the perfusate did not affect the hepatic insulin uptake in the presence of FFA within physiological concentrations. Thus, hepatic clearance of insulin is proportional to rat weight (age) and portal FFA concentrations. Other studies have recently shown that fatty acids inhibit insulin binding, degradation, and function in isolated rat hepatocytes, and that hepatic clearance is inversely dependent on hepatic triglyceride concentrations, both inhibitions reversible by prevention of fatty acid oxidation. It is suggested that the diminished hepatic clearance of insulin in heavier (older) rats is at least partly due to their relative obesity and increased hepatic triglyceride contents. This effect as well as that of portal FFA is probably mediated via fatty acid oxidation in the liver. This mechanism may have implications for the regulation of hepatic metabolism, and peripheral insulin concentrations.

Animals↗
PubMed1979

Rapid development of immunoprecipitins in agarose gel.

A procedure for the rapid development of immunoprecipitins in agarose gels has been developed using polyanion precipitation after immunoelectrophoretical separations. Excellent results are obtained for serum apolipoproteins, immunoglobulins and other proteins. It is shown that quantitative determination of apolipoprotein B in hyperlipemic serum and isolated lipoproteins is affected by immunoprecipitated complexes when rocket immunoelectrophoresis is used. This effect can be avoided by addition of polyvinylpyrrolidone.

Apolipoproteins↗
PubMed1979

Metabolic adaptation to prolonged exercise.

A study was undertaken to evaluate and to examine the role of substrate supply in 50 healthy subjects after long distance events, such as 10 km, 25 km, and marathon races. The metabolic, variables of carbohydrate metabolism were greatest in 10-km runners, with the highest increase in glucose, lactate, and pyruvate, while in marathon runners only moderate changes were observed. Marathon competitors gave the greatest decrease in insulin concentration whereas glucagon and cortisol showed a contrary tendency. As for lipid concentrations, the most remarkable point was that after the marathon competition the best runners had the highest increase in free fatty acids; the longer the race, the higher were the beta-hydroxybutyrate and acetoacetate levels after the competition. It is important to emphasize that the limiting factor up to 90 min duration is the competitor's ability to deplete the stores of glycogen. Beyond 90 min (or 25 km) the decrease in insulin, the rise in cortisol and the higher concentration of ketnne bodies found indicate a change in metabnlic response.

Adaptation, Physiological↗
PubMed1979

Metabolic response to heavy physical exercise before and after a 3-month training period.

Twenty healthy athletes performed a heavy physical exercise before and after a controlled training period of 3 months. As a result of physical training there was a reduction in lactate concentration during and after exercise. Plasma free fatty acids and triglyceride levels were lower at rest as well as during and after exercise. Insulin concentrations decreased during exercise before the training period whereas they remained constant afterwards. The composition of individual free fatty acids changed in the same way during exercise before and after training: fatty acids with shorter hydrocarbon chains increased, those with longer chains decreased. Comparing the pattern of individual free fatty acids before and after training a higher percentage of saturated and a lower percentage of mono-unsaturated fatty acids was observed. It is concluded that changes in the plasma free fatty acid profile during heavy exercise reflect a preferential uptake and oxidation of certain individual free fatty acids. The significance of training-induced changes in the plasma free fatty acid pattern is discussed.

Adult↗
PubMed1979

Electroretinogram in general medicine.

The interest of the usage of the electroretinogram in various fields of general medicine is discussed, with particular regard to endocrinology, ionic changes and neurology. A review from the relevant literature and original contributions from the author's laboratory are reported in detail.

Adolescent↗
PubMed1978

Cardiopulmonary adjustment and metabolic response to maximal and submaximal physical exercise of boys and girls at different stages of maturity.

Cardiopulmonary and metabolic variables were investigated at maximal and submaximal bicycle ergometer exercises in 41 swimmers of both sexes, 8--18 years old. VO2 max and VO2 max . HR-1 were higher in boys than in girls and increased with maturity, while VO2 max. kg-1 and HVE were not influenced by this. The HV increased clearly during this growth period, the pubertal and postpubertal subjects showing 16 and 17% higher values for HV and HV . kg-1 than those reported in normal schoolchildren populations. During the submaximal exercise at 70% VO2 max the highest HR values were found in the prepubertal group, whilst the lowest were observed in the postpubertal subjects. These findings suggest that a given percentage of VO2 max as a reference unit, is more reliable than a certain HR to obtain comparable results in subjects with different ages. Blood samples were collected before, during, and after the submaximal exercise. Blood glucose and FFA did not differ in relation to the stages of maturity. During exercise, insulin decreased in prepubertal children, did not alter in pubertal adolescents, and increased in postpubertal subjects. The lactate concentration, during exercise, increased in relation to maturity. The same results were found for HGH, but no differences were found with regard to sex. Since the pattern of HGH secretion during exercise is similar to that found after arginine and insulin administration it is assumed that the same mechanism (i.e., sex hormones) triggers the HGH release.

Adolescent↗
PubMed1978

Hyperlipoproteinemia in experimental chronic renal insufficiency in the rat.

Lipid metabolism was studied in experimental uremia. Uremic (U) rats were compared with sham-operated, pair-fed (PF) controls and with ad-lib-fed (AL) controls. In U animals, fasting glucose concentrations were normal, immunoreactive serum insulin (IRI) levels were decreased, and immunoreactive glucagon levels were increased. A significant increase in the serum concentration of all lipid classes was observed: triglycerides were elevated 10-fold above the values in PF and AL controls; phospholipids, twofold; total cholesterol, threefold; and free cholesterol, sixfold. Cholesterol concentration was increased in beta- and pre-beta-lipoproteins and even more so in alpha- and pre-alpha-lipoproteins. There was an increase in the ratio of free cholesterol/total cholesterol. The fatty acid composition of serum lipoproteins was unchanged. Concomitantly, in liver tissue, there was no change in lipid content (triglyceride, cholesterol) and fatty acid composition. These findings argue against glucose- or insulin-mediated changes in hepatic de novo fatty acid synthesis, chain elongation, or poly-desaturation. In U animals, the HMG-CoA-reductase activity of liver microsomes was slightly, but not significantly, reduced as was tritiated water incorporation into cholesterol in isolated perfused liver preparations. In adipose tissue, there was a decrease in triglyceride content. The results provide evidence against insulin-mediated hepatic overproduction as a major cause of hyperlipoproteinemia in this model of experimental renal insufficiency and point to peripheral under-utilization of lipoproteins.

Animals↗
PubMed1977

Effect of prolonged glucose infusion on total serum fatty acids and free fatty acids in the rat.

This investigation evaluates the effect of prolonged glucose infusion on triglycerides and the composition in total serum fatty acids and free fatty acids in the rat. Glucose infusion over a period of 4 days leads to the following changes: serum triglyceride concentrations are two to three times elevated and serum insulin levels rise 10 times after 12 hours, followed by a steady decrease. Chain elongation is depressed in serum free fatty acids and even more in total serum fatty acids. In serum free fatty acids monodesaturation is unaltered whereas it is highly stimulated in total serum fatty acids. These alterations correlate with the changes of hepatic total fatty acids and do not correlate with changes of fatty acids from epididymal fat pads. The alterations reflect a specific carbohydrate-induced effect on hepatic fatty acid desaturation and chain elongation. They do not support the idea that serum free fatty acids are mainly secreted from the storage pool of adipose tissue; yet, they may have been newly synthesized in fat cells or even in the liver.

Animals↗