Biomedical subjects

B Broniszewska-Ardelt

Publications and source records attributed to B Broniszewska-Ardelt.

17 recordsLinked to original sources

PubMed1981

Prevention of adrenaline-induced metabolic systemic and myocardial alterations by the beta-blocking agent metipranolol in the dog.

We investigated the effectiveness of the beta-blocking agent metipranolol in preventing detrimental systemic and myocardial alterations induced in healthy dogs by adrenaline (AD) infused at a rate which mimics spontaneous secretion after coronary occlusion. Metipranolol (0.3 mg/kg) was infused intravenously concurrently with AD (1.2 micrograms/kg/min) for 4 h and blood values of free fatty acids (FFA) and triiodothyronine(T3) were measured initially, after 2 and 4 h of infusion and compared with those obtained in dogs infused with AD alone and with saline. Metipranolol suppressed a rise in free fatty acid, reversed AD-induced histoenzymatic changes in succinic dehydrogenase and ATPase activity and considerably inhibited the development of mitochondrial alterations detected in dogs infused with AD alone. A tendency to attenuate AD-induced fall in serum T3 was also detected in metipranolol-treated dogs. Results suggest that this drug might be of value in preventing consequences of increased adrenergic activity in the acute stage of myocardial infarction.

Adenosine Triphosphatases↗

PubMed1979

High-energy phosphate compounds and some glycolytic substrates in the rat brain during hypoxia.

The influence of acute and prolonged (with resuscitation) hypoxia, upon some glycolytic substrates and high energy phosphate compounds in the rat brain, was studies. Acute hypoxia decreased the content of glucose and glucose-6-phosphate as well as of high energy phosphate compounds. Stimultaneously, an increase of lactic level was recorded. Some adaptation features could be observed, when 30-minute hypoxia with resuscitation was studied. Brain content of high energy compounds returned to the normal value, while that of glucose increased twice over control. However, the level of lactic acid was still increased.

Adenosine Diphosphate↗

PubMed1979

Beneficial effect of practolol in preventing adrenaline-induced systemic and myocardial metabolic changes.

The aim of the study was to investigate whether the beta blocking agent, practolol, is able to modify some of the metabolic and hormonal responses and the local myocardial changes evoked by an excess of adrenaline similar to that seen after acute coronary occlusion. Adrenaline (1.2 micrograms/kg/min) and practolol (1 mg/kg) were infused concurrently to anaesthetized intact dogs for 5 h. Blood free fatty acid and triiodothyronine levels were measured initially and after 2, 4 and 5 h of infusion. At the end of the infusion the myocardium was subjected to biochemical, histoenzymatic and electron microscopic examination. The results were compared with those obtained in dogs infused with adrenaline alone and with saline alone. Practolol reduced the adrenaline-induced increase in free fatty acids and a fall in triiodothyronine in the blood. Myocardial acetate accumulation and ATP decrease were both reduced by practolol. Histoenzymatic and electron microscopic changes were less. These effects of practolol upon systemic and myocardial disturbances induced by the excess of adrenaline indicate that it might be effective in modifying any excessive adrenergic response which may occur in acute myocardial infarction.

Adenosine Diphosphate↗

PubMed1978

Evidence for the detrimental effect of adrenaline infused to healthy dogs in doses imitating spontaneous secretion after coronary occlusion.

We have previously shown that acute coronary occlusion in the dog is often accompanied by increased adrenaline release into the blood. In the present study the consequences of this humoral reaction were studied in anaesthetised healthy mongrel dogs subjected to adrenaline infusion administered at a rate relevant to spontaneous release of this amine in coronary occlusion. Adrenaline was infused in a dose of 1.2 microgram.kg-1.min-1 for 4 h. Dogs receiving saline served as the control. Adrenaline administration led to the decrease in insulin/glucose ratio, to a significant fall in serum triiodothyronine and in blood pH. Free fatty acid levels doubled. Histochemically, a diminution in succinic dehydrogenase and ATPase activity in adrenaline-treated hearts was found. A significant fall in the activity of mitochondrial hexokinase in these hearts was detected spectrophotometrically. Electron microscopic study revealed alterations in the mitochondrial structure. These findings indicate that an excess of adrenaline in ammounts similar to that seen in experimental infarction leads to profound metabolic and hormonal disturbances and exerts a detrimental effect upon myocardium.

Animals↗

PubMed1978