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Biomedical subjects

G Raberger

Publications and source records attributed to G Raberger.

At least 91 records · Page 5Linked to original sources
PubMed1980

[Animal model for testing the influence of drugs on partially ischaemic and normal myocardial regions (author's transl)].

Blood flow was measured both in the circumflex and descending branch of the left coronary artery of anaesthetized dogs. Venous blood was sampled from the areas supplied by these vessels and arterial blood from the aorta for determination of oxygen-saturation, haemoglobin content, pCO2, glucose, lactate, and free fatty acids (FFA). The coronary blood flow in both branches, heart rate, aortic blood pressure, LVEDP and LVdp/dtmax were registered continuously. After taking control values, resting blood flow in the circumflex branch was mechanically reduced by 40% and the changes in haemodynamics and myocardial metabolism were measured 30 min thereafter. Heart rate, blood flow in the descending branch and LVEDP rose, whilst arterial blood pressure and LVdp/dt were not significantly changed. The partially ischaemic myocardium showed a decrease in lactate, FFA and oxygen uptake and CO2 release. The simultaneously determined metabolic parameters for the non-ischaemic region showed significant increases in lactate and oxygen uptake and CO2 and H-ion release. The overall balance (partially ischaemic and normal regions) showed a significant decrease in lactate and FFA uptake, which was, however, of very small magnitude. These results show that the antianginal action of drugs should not be assessed by determination of arterio-coronary venous balances for the whole heart, but for partially ischaemic and normal regions separately, as is possible in the presented experimental model. Moreover, sympathetic or direct stimulation can be used to stimulate increased effort of the heart such as occurs in angina pectoris.

Animals↗
PubMed1979

L-cysteine hydrazide--its pharmacological and immunosuppressive activity.

The authors investigated the immunological and pharmacological activity of l-cysteine hydrazide. It was found, that the preparation exhibited an interesting immunosuppressive and anti-inflammatory effect, which was evoked by the interference of the drug in nucleic acids and by stabilization of the cell membranes. Moreover it diminished the number of T lymphocytes. L-cysteine hydrazide showed no significant side effects. The authors discussed the possibility of its application in clinical therapy.

Analgesia↗
PubMed1979

Effect of a 5'-substituted adenosine analogue (744c96) on insulin and glucagon release in isolated rat islets of Langerhans.

The effect of adenosine-5'-(N-ethylcarboxamide) (744-96), a highly vasoactive adenosine analogue, was investigated on insulin and glucagon release from isolated rat islets of Langerhans. The compound inhibited glucose-induced insulin release in a dose-dependent manner (concentration range 10(-8) to 10(-5 M). No effect of 744-96 was observed on basal or on arginine-induced glucagon release. By contrast, 744-96 (5 microgram/kg i.v.) produced a significant increase in plasma glucagon and glucose levels in normal as well as in reserpinized rats. The observed failure to promote glucagon release from isolated islets may be attributable to the isolation procedure, to a release of glucagon in vivo from non-pancreatic stores, or to a non-specific effect of 744-96 on glucagon secretion.

Adenosine↗
PubMed1978

Evidence for glucagon-releasing activity of vasoactive adenosine analogues in the conscious dog.

An investigation was carried out in conscious dogs concerning the effects of three adenosine derivatives substituted at the 5'-(744-96) or 2'-, 3'-, and 5'-positions (744-98, 744-99), with pronounced and long-lasting coronary dilator activity, on glucagon release. All three compounds (10 microgram/kg i.v.) induced a sustained increase in plasma glucose and a decrease in plasma FFA concentration; concomitantly, plasma glucagon levels rose 2--3 fold. Changes in plasma insulin concentration were relatively small and of no statistical significance. A simultaneous fall in arterial blood pressure was also observed. A lowering of blood pressure of similar magnitude by sodium nitroprusside infusion in control experiments failed to show any significant effect on plasma glucagon level. These results point to a specific effect of vasoactive adenosine derivatives on glucagon release.

Adenosine↗
PubMed1978

Influence of aminophylline or beta-adrenoceptor blockade on glucagon release by a vasoactive adenosine analogue.

The glucagon-releasing activity of adenosine-5'-ethyl-carboxamide (744-96) was studied in conscious dogs pretreated either with aminophylline or with bupranolol, a beta-adrenoceptor blocking drug. The adenosine antagonist, aminophylline, inhibited both the glucagon-releasing and the blood pressure lowering effects of 744-96 (10 microgram/kg i.v.). The actions of the adenosine analogue on glucagon release and haemodynamics were not affected by bupranolol pretreatment. These results indicate that the adenosine analogue mediates glucagon release by interaction with so-called adenosine receptors. A beta-adrenoceptor mediated release secondary to 744-96-induced hypotension and baroreceptor-activation can be excluded.

Adenosine↗
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

Haemodynamic and coronary actions of ouabain during coronary infusion.

The investigations were carried out on 24 mongrel dogs which were anaesthetized with chloralose or sodium pentobarbital. Ouabain was added to the coronary blood (50, 100 and 200 ng/ml coronary blood or 0.7, 1.4 and 2.8 X 10(-7) M) over periods of 30 or 60 min by intracoronary infusion of the glycoside. Under chloralose anaesthesia, ouabain at concentrations of 100 and 200 ng/ml coronary blood augmented left ventricular dp/dt significantly. No significant changes were observed in coronary resting flow and flow per beat at the same time. Likewise, the maximum reactive hyperaemic blood flow remained constant, indicating the absence of any changes in the tone of the large extramural arteries. Under sodium pentobarbital anaesthesia small decreases in heart rate and increases in left ventricular dp/dt were seen only at the highest ouabain concentration (200 ng/ml). All flow parameters remained unchanged. These experiments provide evidence that concentrations of ouabain which 100- and 200-fold exceed therapeutic maintenance levels and 10- and 20-fold exceed the concentrations that produce constriction of helically cut pig and rabbit coronary arteries in vitro, do not diminish the coronary blood supply of the anaesthetized dog in vivo.

Animals↗
PubMed1977

Effect of aminophylline on coronary reactive hyperaemia following brief and long occlusion periods.

The effects of an intracoronary aminophylline infusion, adjusted to give a constant concentration of 25 microgram.cm-3 coronary blood, on the reactive hyperaemic responses following coronary occlusion for 4, 10, and 25 heart beats were investigated in anaesthetised, open-chest dogs. The vasodilator effect of intracoronarily-administered adenosine and the hyperaemic response after coronary occlusion for 10 and 25 heart beats were both significantly diminished under the influence of aminophylline. However, the decrease in the coronary dilator effect of adenosine amounted to 80%, whereas the hyperaemic response was diminished by only 20%. The hyperaemic response following a coronary occlusion for only 4 heart beats remained unchanged. The present results obtained with aminophylline suggest at least a partial involvement of adenosine in mediating reactive hyperaemia after sufficiently long periods of coronary artery occlusion.

Adenosine↗
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

Blood flow in intact and constricted coronary arteries under the influence of ouabain.

The effects of ouabain on intact and experimentally constricted coronary arteries were investigated in anaesthetized, thoracotomized dogs. Ouabain decreased the blood flow in the intact artery without changing the flow per beat values and increased flow in the constricted artery. Since ouabain decreased left ventricular enddiastolic pressure, it is proposed that the drug-induced augmentation of flow in the constricted artery is related to an elevation of driving pressure to the endocardial layers of the myocardium which are supplied by the constricted artery.

Animals↗
PubMed1976

Haemodynamic effects of adenosine-5'-carboxylic acid-amide in the anaesthetized dog during normal respiration and hypercapnic acidosis.

Adenosine-5'-carboxylic acid-amide (1 mug/kg/min) and adenosine (500 mug/kg/min), given in a 10-min infusion to anaesthetized dogs, produced qualitatively and quantitatively comparable cardiovascular effects, namely a marked increase in coronary blood flow and a generalized vasodilation, concomitantly with an increase in heart rate, left ventricular dp/dt, heart work, myocardial oxygen consumption, and pulmonary blood pressure; the pulmonary vascular resistance remained unchanged. Hypercapnic acidosis enhanced the coronary dilator effect of both compounds. These results indicate that adenosine and adenosine-5'-carboxylic acid-amide act at the same receptor sites.

Acidosis↗
PubMed1975

[Partial parenteral nutrition in acute myocardial infarction (author's transl)].

The influence of partial parenteral nutrition (PPN) was compared with the effect of a calorie-free solution in 2 groups of patients (n = 10) with acute myocardial infarction. Both groups received the same daily diet of 800 to 1000 Cal. The control group was given, in addition, a calorie-free electrolyte solution and the PPN group was given a nutritious solution consisting of 1000 Cal carbohydrate and 26.5 g 1-amino acids daily by means of a subclavian catheter. The exact monitoring of the water balance indicated that patients with acute myocardial infarction can safely be given parenteral nutrition. Neither haemodynamic nor metabolic complications occurred in the group with PPN due to the small infusion volume and the continuous administration of the infusion volume and the continuous administration of the infusion. The control group was in negative nitrogen, potassium and phosphorus balance in comparison with the PPN group. This demonstrates that a hypocaloric diet is insufficient in the acute phase of myocardial infarction and causes catabolism, which can be prevented by PPN. Stimulation of healing of the myocardial infarct can be expected through the improvement of protein metabolism by PPN.

Diet↗
PubMed1975

[Fatal self-poisoning with the tetracyclic antidepressive drug, ludiomil (author's transl)].

The clinical and analytical data are presented of a case of severe Ludiomil self-poisoning (assumed total ingested dose: 3000 mg). Ludiomil resembles the tricyclic antidepressive drugs in regard to its toxic effects. Two essential observations made in Ludiomil poisoning are: 1) the limited therapeutic possibilities due to delayed elimination and 2) the severe degree of respiratory distress.

Adult↗
PubMed1975

[Acute pancreatitis with shock and acute renal failure (author's transl)].

Acute pancreatitis is discussed from the viewpoint of a medical intensive care unit, with particular reference to the early and late complications. The measures which must be promptly implemented in order to successfully combat the grave early complications of shock and acute renal failure are stressed. Continuous monitoring ensures that prompt surgical management is undertaken in cases of late complications-abscess formation, sequestration and sepsis. A review of the characteristic clinical and laboratory data of patients with acute pancreatitis treated in our unit is presented in table I.

Acid-Base Equilibrium↗