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Biomedical subjects

J Stepanek

Publications and source records attributed to J Stepanek.

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

[Broncholytic therapy--beta 2 stimulation and vagolysis from an animal experimental viewpoint].

Continuous recordings of heart rate, respiration rate, minute volume and bronchial resistance were made over a period of altogether 3 h in spontaneously breathing dogs anesthetized with chloralose. At hourly intervals, before and 1 and 2 h after the administration of bronchodilators, bronchial spasm was induced by inhalation of an acetylcholine solution. Terbutaline, a beta-stimulant, was administered by inhalation in doses of 0.5, 0.16 and 0.05 mg/kg. For comparison, an atropine derivative, ipratrapium bromide, was given in doses of 0.04 and 0.01 mg/kg. Controls received normal saline. Terbutaline caused an increase in heart rate, respiration rate and minute volume. Acetylcholine-induced bronchial spasm was inhibited to the extent of 10-70% for 2 h after the administration of terbutaline. The acetylcholine antagonist ipratropium bromide caused only transient changes in heart rate, respiration rate and minute volume. Acetylcholine-induced bronchial spasm was inhibited by 95% and 80% for 2 h after doses of 0.04 and 0.01 mg/kg respectively. Terbutaline had a slight stimulant effect; ipratropium bromide displayed no stimulant activity.

Acetylcholine↗
PubMed1978

[Experimental hyperammoniemia].

The effect of chloralose anesthesia and of hypoxia or hypercapnia of altogether 40 minutes' duration on the concentrations of ammonia in the arterial blood was investigated in mongrel dogs. The NH3 values increased marginally as a result of chloralose anesthesia and only slightly as a result of severe (Pao2=32 mm Hg), acute hypoxia. Hypercapnia (Paco2=75 or 111 mm Hg) induced with a mixture of gases was accompanied by an increase of commensurate degree in the blood ammonia levels which was presumably attributable to an augmented protal-to-systemic shunt circulation.

Ammonia↗
PubMed1978

Haemodynamic effects of the beta-receptor blocking agents metoprolol and propranolol in the anesthetized dog.

The haemodynamic effects produced by intravenous infusions of the beta-blocking agents metoprolol and propranolol in doses of 0.3 and 1 mg/kg/10 min were compared in anaesthetized dogs. When administered in a dose of 0.3 mg/kg/10 min, metoprolol caused a longer-lasting increase in pulmonary-arterial pressure and total pulmonary resistance, a greater increase in pulmonary capillary pressure and a more marked decrease in O2 partial pressure in the arterial blood than propranolol. These differences are probably due to differences in the pharmacokinetics of the two drugs. The effects of the two beta-blockers in a dose of 1 mg/kg/10 min were similar. At neither of the dose-levels tested were the changes induced by the compounds in the various parameters studied clearly dose-related.

Animals↗
PubMed1978

Bronchial spasmolytic action of terbutaline and fenoterol compared with that of ipratropium bromide in the anaesthetized dog.

Continuous recordings of heart rate, respiration rate, minute volume and bronchial resistance were made over a period of altogether three hours in spontaneously breathing dogs anaesthetized with chloralose. At hourly intervals, before and 1 and 2 hr after the administration of bronchodilators, bronchial spasm was induced by inhalation of an acetylcholine solution. Two beta2-stimulants, terbutaline and fenoterol, were administered by inhalation in doses of 0.5, 0.16 and 0.05 mg/kg and 0.1, 0.3 and 0.01 mg/kg respectively. For comparison, an atropine derivative, ipratropium bromide, was also given by the same route in doses of 0.04 and 0.01 mg/kg. Controls received normal saline. Terbutaline and fenoterol caused an increase in heart rate, respiration rate and minute volume. Acetylcholine-induced bronchial spasm was inhibited to the extent of 10--70% for 2 hr after the administration of terbutaline, and by 15--70% after fenoterol. The acetylcholine antagonist ipratropium bromide caused only transient changes in heart rate, respiration rate and minute volume. Acetylcholine-induced bronchial spasm was inhibited by 95% and 80% for 2 hr after doses of 0.04 and 0.01 mg/kg, respectively. Fenoterol had a slightly greater central stimulant effect than terbutaline; ipratropium bromide displayed no stimulant activity.

Acetylcholine↗
PubMed1977

[Metabolic effects of acute experimental hypoxia and hypercapnia].

Hypoxia and the hypercapnia were produced in anesthetized dogs by artificial respiration with appropriate gas mixtures, and a study was conducted of the effects of these conditions on various metabolic parameters, viz. catecholamines, renin activity, lactate, pyruvate, cortisol, non-esterified free fatty acids (FFA), and ammonia, in the plasma of the arterial blood. Hypercapnia caused a distinct increase in catecholamine concentrations, renin activity and ammonia, and a decrease in lactate and pyruvate; cortisol and FFA levels were only slightly altered. Hypoxia increased lactate, pyruvate and--though only to a slight extent--FFA, cortisol and NH3. The changes induced by hypercapnia were chiefly attributable to activation of the sympathico-adrenal system; those induced by hypoxia were not.

Ammonia↗
PubMed1977

[Experimentally induced alterations in wedge pressure and O2-partial pressure during acute hypoxia].

Suprarenal occlusion of the aorta by means of a balloon catheter results in an increase in wedge pressure, alterations in blood flow in the pulmonary circulation, and an increase in O2 partial pressure in the arterial blood. It is demonstrated that these changes take place after occlusion of the aorta during normoxia or hypoxia (Pao2:43 mmHg) in anaesthetized normotensive or spontaneously hypertensive mongrel dogs.

Acute Disease↗
PubMed1976

[Increasing the bronchial resistance by means of aortic occlusion in the dog].

In 11 spontaneously breathing, anesthetized dogs, suprarenal occlusion of the aorta was produced by means of a ballon-tipped catheter and maintained for 20 min. The obstruction led to an increase in O2 saturation in arterial blood (the rise in wedge pressure alters pulmonary perfusion), in aortic pressure and in bronchial resistance. Bronchial resistance could be partially diminished by inhalations of atropine or terbutalin.

Airway Resistance↗
PubMed1976

[Hemodynamic concomitant effects of experimentally increased pulmonary capillary pressure].

An acute suprarenal occlusion of the aorta was produced in anaesthetized dogs by means of a ballon-tipped catheter. The resultant increase in wedge-pressure led to changes in pulmonary perfusion and raised O2 partial pressure in the arterial blood. The additional, simultaneous occlusion of the left subclavian artery by means of a second balloon-tipped catheter aggravated the haemodynamic manifestations of the pressure-load on the heart; but did not cause a proportionate increase in wedge pressure and O2 partial pressure.

Animals↗
PubMed1975

[Proceedings: Experimentally induced effects on the plasma renin activity].

In dogs, plasma renin activity (PRA) was increased by anesthesia, by hypercapnia and by extreme hypoxia (paO2 47.6 mm Hg). Relatively moderate hypoxia (paO2 47.6 mm Hg) and artificial respiration had no appreciable influence on PRA. It appears that the sympathomimetic stimulus of CO2 has an important bearing on PRA.

Anesthesia↗
PubMed1975

[Cardiopulmonary effects after i.v. administration of maprotiline in the dog].

The cardiopulmonary effects of the antidepressive agent maprotiline were investigated in the dog. In ventilation experiments on dogs anaesthetized with chloralose, respiratory minute volume decreased by 5-10% shortly after intravenous injection of 1 and 3 mg/kg; acid-base-balance variables remained unchanged. After an intravenous dose of 10 mg/kg ineffective hyperventilation was observed, associated with a transient decrease of P-O2 and a slight increase in P-CO2 in the arterial blood. In cardiac-catheterization experiments on dogs anaesthetized with chloralose and morphine and receiving artificial respiration, an intravenous dose of 3 mg/kg maprotiline had no appreciable effect on the cardiovascular system, apart from a transient and slight, but statistically significant increase in pulmonary capillary pressure immediately after the injection. Anaesthesia was slightly deeper and more prolonged after the intravenous administration of maprotiline.

Animals↗
PubMed1975

[Two-year peroral administration of aminorex in the dog. 2].

In an attempt to develop an experimental model of pulmonary hypertension, five mongrel dogs were treated with 1 mg/kg p. o. and five with 1.5 mg/kg p. o. of Aminorex base five days a week for two years. A control group was given empty capsules by months. The following effects of treatment with Aminorex were noted: 1. Anorexia and central stimulation, 2. Natriuresis, 3. an increase in respiration rate, heart rate and body temperature, 4. a tendency towards usually compensated metabolic acidosis, 5. an increase in pulmonary arterial pressure, total pulmonary resistance and right ventricular work, and, in the group given the higher dose, a slight increase in mean aortic pressure and peripheral resistance. 6. Only slight histopathological changes were detectable, e.g.: perivascular oedema; increase in the number of muscle arteries, occasionally with hypertrophy of the tunica media and slight, focal fibro-elastoid thickening of the intima in some elastic arteries. These changes were present in about 60% of the treated dogs. Only one dog that died after 91 weeks' treatment also showed moderate, focal phlebosclerosis of large pulmonary veins and focal, fibro-elastoid thickening in the coronary artery. Serious morphological changes in the pulmonary vessels such as are observed in the human pulmonary hypertension were not seen in our laboratory animals. Two dogs in each dosage group died in the course of the experiment. The results of this experiment show that it is, in general, possible to induce pulmonary hypertension by administering Aminorex orally. In two dogs, however, pressure in the pulmonary artery (measured under anaesthesia) was below 20 mm Hg (controls: 13.8 +/- 1.3 mm Hg). One possible pathogenetic mechanism underlying the pulmonary hypertension would appear to be precapillary vasoconstriction induced by Aminorex, which can lead to transient, persistent or, for some unknown reason, even permanent fixation of pulmonary resistance.

Adrenal Glands↗