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Biomedical subjects

O Kraupp

Publications and source records attributed to O Kraupp.

At least 37 records · Page 2Linked to original sources
PubMed1978

Effects of a 2',3',5'-substituted adenosine derivative on systemic and coronary hemodynamics and on cardiac metabolism in the anesthetized dog.

Hemodynamic and metabolic effects of 2',3'-O-methoxyethylidene-adenosine-5'-(Nethyl-carboxamide) (744-98), an adenosine analogue with long-lasting coronary dilator activity, were studied in the anesthetized, closed-chest dog. The coronary sinus outflow increased 5fold following administration of the compound (5 microgram/kg i.v.) and still remained three thimes higher than the control level after 4 h. Total peripheral resistance decreased markedly, accompanied by a baroreceptor-mediated increase in heart rate, left ventricular dp/dtmax and myocardial oxygen consumption. Blood glucose levels and glucose uptake by the heart increased concomitantly, whereas plasma free fatty acid (FFA) levels decreased markedly, without consistent changes in myocardial FFA balance. These effects are explained by antilipolytic and glucagon-releasing activities of the adenosine analogue. The myocardial oxygen extraction ratio for glucose greatly exceeded the aerobic metabolic requirement, a finding already previously obtained with coronary dilators.

Adenosine↗
PubMed1978

Cardiovascular and metabolic actions of an adenosine analogue (2'3'-o-methoxy-ethyliden-adenosine-5'-ethylcarboxamide) in the conscious dog.

The haemodynamic and metabolic actions of 2'3'-o-methoxyethyliden-adenosine-5'-ethylcarboxamide (744-98) were investigated in conscious dogs after i.v. and oral administration. 744-98 led to a marked dose-dependent increase in coronary blood flow, together with a slight increase in renal blood flow. In the standing position high doses of the drug revealed an adenosine-like negative chronotropic action, together with marked hypotension. Metabolic effects were observed with the higher coronary-active doses only. The increase in arterial glucose and decrease in free fatty acid levels are considered to be caused by a glucagon-releasing and adenosine-like action of 744-98. The haemodynamic and metabolic changes were observed both after i.v. and oral administration, showing a ratio of approximately 3:1 in favour of the parenteral route.

Adenosine↗
PubMed1977

Effects of glucagon on liver metabolism in intact dogs.

Chloralose-anaesthesized dogs, starved for 24 hours, were used to determine the effects of 10 microgram/kg glucagon, administered i.v. as a single bolus injection, on liver substrates in situ (glycogen, glucose-1-phosphate, glucose-6-phosphate, glucose, fructose-6-phosphate, fructose-1,6-diphosphate, triose phosphates, glycerol-3-phosphate, phosphoenolypyruvate, pyruvate, lactate, citrate, malate, ATP, ADP, and AMP). liver samples were obtained by instant deep-freezing with Wollenberger clamps on four consecutive occasions at 10-minute intervals. Heart rate and blood pressure were continuously monitored. Serial liver sampling per se had no significant effects on liver metabolism or systemic haemodynamics in a group of control animals. In a second group glucagon, administered after the initial freeze-clamp sampling to obtain baseline values, led to a marked activation of the glycogenolytic pathway resulting in glucose release from the liver.

Animals↗
PubMed1977

Relaxation of coronary artery strips by adenosine and acidosis.

Cumulative dose-response curves of Ca2+-induced tension increments were studied in K+-depolarized helical strips of dog coronary arteries. Adenosine 10(-4) M reduced the Ca2+ sensitivity of the strips without altering the maximal tension with full Ca2+ activation. In contrast, acidosis of pH 7.05 significantly diminished the maximal tension with full Ca2+ activation. The relaxing effect of acidosis was almost completely abolished by 10(-4) M adenosine. It is concluded that adenosine inhibits Ca2+ influx, whereas acidosis depresses the contractile process of vascular smooth muscle directly.

Acidosis↗
PubMed1977

[Effect of the beta-adrenergic blocking agent bupranolol on the plasma renin activity in normotensive rats].

The effects of the beta-adrenergic blocking agent 3-tert.-butyl-amino-1-(6'-chloro-3'-methylphenoxy)-propan-2-ol hydrochloride (bupranolol; KL 255; Betadrenol) on the plasma renin activity (PRA) of normotensive rats were studied in comparison to propranolol. Bupranolol (10--100 microgram/kg) reduced basal PRA and inhibited the isoproterenol as well as dihydralazine induced increase of PRA in a dose dependent fashion. Bupranolol exhibited an effect 2--4 times stronger than that of propranolol. The PRA inhibiting effects of bupranolol seem to be linked to its beta-receptor blocking properties.

Adrenergic beta-Antagonists↗
PubMed1977

Coronary dilatory action of adenosine analogues: a comparative study.

The coronary dilatory action of 23 adenosine analogues was investigated on a comparative basis after i.v. administration in anaesthetized dogs. Substitution of adenosine in position 5' with a COOH group and esterification led to a 50- to 100-fold increase in coronary efficacy (flow increase integrated over the time of action). Amidation of the carboxylic acid analogue further enhanced the coronary efficacy. The most effective analogue, adenosine-5'-ethyl-carboxamide, showed 20000 times greater activity than adenosine. Additional substitution in positions 2' and 3' with NO2, O-methoxy-methyliden or O-methoxyethyliden resulted in a delayed onset and prolonged duration of action.

Adenosine↗
PubMed1976

[Risks of long-term administration of drugs (author's transl)].

A short review is given of the side effects of drugs during long-term treatment and the possible mechanisms involved. The possibilities and causes of interactions occurring with simultaneous administration of two or more drugs are discussed. The pharmacokinetical basis of cumulation phenomena of the control of long-term treatment either by means of blood-level monitoring or by the observed effect is briefly outlined.

Adenosine Triphosphatases↗
PubMed1975

[The place of ultrasound diagnosis in internal medicine].

The applications of ultrasound diagnosis within the framework of general medicine are discussed on the basis of case reports. Ultrasonic equipment with manual moving of the probe is used in this department for the investigation of the abdomen in cases of occult neoplasms and metastases to differentiate between cysts and solid tumours and to determine the situation and size of parenchymatous organs like liver and kidney and spleen. Special fields of application are: follow up of patients after renal transplantation, investigation of systemic haematological diseases such as lymphogranuloma, or the demonstration of abnormal fluid masses such as haematomata in haemophilic patients, ascites or pericardial effusions.

Diagnosis, Differential↗
PubMed1975

Blood histamine levels and arteriovenous concentration differences after the intravenous administration of the basic compounds l-3 and 48/80 in the anaesthetized dog.

The effects of the i.v. administration of inulin trinicotinate-monomethochloride (L-3) on haemodynamics, airway pressure and blood histamine levels were studied in chloralose-anaesthetized dogs and compared with the effects of compound 48/80. The control arterial histamine level was 0.041 plus or minus 0.002 mug/ml (mean plus or minus SEM) as determined by a fluorometric assay. L-3 (0.15 mg/kg) released high amounts of histamine, as indicated by a peak level in arterial histamine of 0.212 plus or minus 0.027 mug/ml within 3 min, which was not futher enhanced on increasing the dosage of L-3 to 1 mg/kg. After the i.v. injection of 0.15 mg/kg of 48/80 the peak level in arterial histamine was 0.146 plus or minus 0.008 mug/ml, and the level was further markedly elevated to 0.918 plus or minus 0.068 mug/ml after the administration of 1 mg/kg of 48/80. The concomitant fall in systemic blood pressure and the rise in airway pressure can be satisfactorily explained on the basis of histamine liberation. Whereas these parameters as well as the blood histamine concentration gradually returned to control values, the heart rate remained elevated during the observation period of 2 h. The arteriovenous differences in blood histamine across various tissues and organs following L-3 and 48/80 administration indicated histamine release mainly from skin and muscle and histamine uptake by the kidney, the digestive tract and to a lesser extent the lungs. The portal-hepatic vein differences revealed no consistent changes in liver histamine balance. As regards the lungs and liver, the present results suggest a dynamic equilibrium between histamine release and uptake in these organs in the intact animal. Both, L-3 and 48/80 elicited a similar pattern of histamine release and uptake. The extreme histamine releasing capacity of 1 mg/kg of 48/80 may be explained by an additional non-selective mechanism of histamine liberation.

Airway Resistance↗