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Biomedical subjects

E Kuhn

Publications and source records attributed to E Kuhn.

At least 109 records · Page 6Linked to original sources
PubMed1976

Changes of free amino acids in plasma of healthy subjects induced by physical exercise.

In eight healthy men a 20-min load of 1.5 W/kg body weight on a bicycle ergometer led to a significant increase of alanine and decline of leucine. Exhausting exercise caused in the same subjects a highly significant increase of alanine and decline of isoleucine, threonine, ornithine, leucine, serine, glycine, and asparasine and glutamine. The methionine and citrulline level declines also significantly. The total amino acids practically did not change. Physical exercise led furthermore to a marked increase of serum ammonia and uric acid. Urea nitrogen changed only little and on average had rather a declining tendency. The rise of alanine suggests the existence of a glucose-alanine cycle, the drop of ornithine and citrulline is most probably associated with the inhibition of ureogenesis in the liver. The reduction of leucine and isoleucine is probably the result of the entry of these amino acids into muscle and their deamination.

Adult↗
PubMed1976

Some adrenergic beta-blocking agents affecting lipolysis in human adipose tissue in vitro.

Antagonistic actions of beta-blocking drugs on isoproterenol-induced lipolysis were studied in human omental adipose tissue. Competitive interaciton characterized by the following pA2 values was found: propranolol 8.7; trimepranol 8.7; practolol 7.1; H 35/25 6.0. The plot of pA2 values of these drugs for human versus rat adipose tissue is linear with slope 2.0 indicating a higher differentiation of beta-antagonist actions in human than in rat adipose tissue.

Adipose Tissue↗
PubMed1976

Some adrenomimetic drugs affecting lipolysis in human adipose tissue in vitro.

In human adipose tissue in vitro, dose-response curves were followed for different adrenomimetics releasing free fatty acids and glycerol into an albumin-containing medium. Phenylephrine, salbutamol and t-butyl-norsynephrine produced lipolytic actions whose maximum did not exceed 20% of the maximal isoproterenol lipolysis. Phentolamine (1 x 10(-5) M) did not potentiate the effect of any of these drugs. When using salbutamol or t-butyl-norsynephrine for antagonizing isoproterenol actions, typical antagonism was found. The parallel shift of the isoproterenol curves showed pA2 values 5.8 for salbutamol and 5.7 for t-butyl-norsynephrine. Comparison of human and rat adipose tissue reactivity shows identical affinities of the drugs studied in both tissues, but related to isoproterenol, diminished intrinsic activities of salbutamol and t-butyl-norsynephrine in human adipose tissue.

Adipose Tissue↗
PubMed1975

Transport ATPases of cardiac sarcolemma in 20,25-diazacholesterol induced myopathy.

20,25-Diazacholesterol, known to induce myotonia in skeletal muscle, also affects cardiac muscle as can be concluded from the development of cardiomegaly. At the same time (Na+, K+) ATPase of cardiac sarcolemmal membranes of the 20,25-diazacholesterol treated rats showed an increased activity as compared with control animals (91 percent and 46 percent stimulation respectively). The Ca++ stimulated ATPase showed the same tendency (96 percent and 64 percent stimulation). In the plasma of the treated rats creatine phosphokinase activity was found to be elevated whereas the amount of protein-bound iodine was decreased, a finding that is common in myotonic dystrophy.

Adenosine Triphosphatases↗
PubMed1975

[Diastolic murmur caused by a phaeochromocytoma (author's transl)].

A protodiastolic murmur was noted in a 24-year-old man with phaeochromocytoma, the murmur disappearing three months after tumour resection. It was probably the result of pulmonary regurgitation, caused by reversible changes in the pulmonary vascular bed or pulmonary valve from the increased catecholamine production.

Adrenal Gland Neoplasms↗
PubMed1975

Adrenergic lipolysis in human adipose tissue in vitro.

In human adipose tissue in vitro, dose-response curves of lipolytic agents in releasing free fatty acids and glycerol into an albumine-containing medium were followed. Norepinephrine and adrenaline produced about 20% of the maximal effect of isoproterenol, isopropylnorsynephrine about 40%, theophylline more than 100%. Found pD2 values were approximately 7.4 for isoproterenol and norepinephrine, approximately 5.9 for isopropylnorsynephrine. Phentolamine (1 times 10-5 M) elevated the maximal norepinephrine effects up to the isoproterenol maxima. Phenoxybenzamine (1 times 10-5 M) had significantly lower potentiating effects. Phenylephrine depressed lipolytic actions of isoproterenol (1 times 10-6 M) showing the same pI2 value 3.0 as well in human as in rat adipose tissue and exerted per se weak lipolytic effects also. It is concluded neither potentiating actions of alpha-blockers nor depressing effects of phenylephrine in human adipose tissue seem related to affecting adrenergic alpha-receptors. The existence of antilipolytic actions of adrenergic alpha-receptors is questioned.

Adipose Tissue↗
PubMed1975

Ammonia and uric acid formation after rapid intravenous fructose administration to healthy subjects and patients with compensated cirrhosis of the liver.

To seven healthy volunteers, 12 and 24 g i.v. fructose were administered in the form of 20% solution at a rate of 4 g/min. After both doses, during the 10th min after the completed intravenous administration, a statistically significant increase of serum ammonia and serum uric acid occurred. After 24 g, the rise of the uric acid level remains significant during the 40th min after administration, while ammonia values return to the basal level. Increments of ammonia and uric acid are higher after a larger fructose dose. Under the same set-up and at the same rate, 24 g fructose were administered to eight patients with compensated cirrhosis of the liver. The rise of uric acid was practically the same as in healthy subjects similar to the rise of the ammonia level during the 10th min after administration. 40 min after administration, however, the ammonia level in cirrhotic patients remained significantly raised, as compared with the initial level.

Adult↗
PubMed1975

Desmosterol accumulation in rats with experimental myotonia.

Desmosterol is found in various organs of rats that show signs of myotonia in their skeletal muscle as a result of treatment with 20.25-diazacholesterol. The amount of desmosterol depends on the time of treatment, and is different in different organs and different kinds of muscle. The increase in desmosterol is much lower and the rats do not show any signs of myotonia when fed a cholesterol rich diet in addition to treatment with 20.25-diazacholesterol. Treatment with triparanol also causes desmosterol accumulation but in these rats myotonia is rarely observed. Our results suggest that in the experimental animals myotonia becomes manifest when every second cholesterol molecule of the muscle cell membrane is replaced by desmosterol. This is easily achieved in animals fed with 20.25-diazacholesterol but rarely occurs with triparanol.

Animals↗