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Biomedical subjects

I Balogh

Publications and source records attributed to I Balogh.

At least 127 records · Page 7Linked to original sources
PubMed1982

Changes in myosin isozyme distribution induced by low doses of isoproterenol.

The Ca2+-activated myosin ATPase activity in isoproterenol-induced hypertrophied left ventricle increased by 20-30% while in Goldblatt rats hypertrophy occurred with a decreased myosin ATPase activity. In non-dissociating (pyrophosphate) gel electrophoresis isoproterenol treatment showed decreased V2 and V3 myosin isozymes; at the higher dose of isoproterenol (0.5 mg/kg body weight) only V1 was present. In contrast a shift toward the V3 isozyme is present in the ventricles of Goldblatt rats. One group of rats was treated with toxic doses of digitoxin: no hypertrophy occurred but there was a disappearance of V1 and V2 isozymes and a 50% decrease in Ca2+-activated ATPase activity. Thus low doses of isoproterenol produce hypertrophy with an isozyme pattern similar to that found in young (approximately 4-6 weeks old) rats. The results with digitoxin show that shifts in the cardiac isozyme distribution can occur without hypertrophy.

Adenosine Triphosphatases↗
PubMed1982

Topographical patterns of ultrastructural changes in the rat brain during methionine sulphoximine convulsions.

Ultrastructure of the cerebral and cerebellar cortex, hippocampus and nucleus facialis was examined in albino rats during MSO convulsions. Three, 6 and 12 h after peritoneal injection of the drug (600 mg/kg) perfusion and dissection were done. Convulsions appeared 4-5 h, status epilepticus 8-9 h after drug administration. Following the onset of clinical seizures, the mitochondria of the neurons became severely damaged. The vesicles and cisterns of the Golgi complex and the endoplasmic reticulum dilated considerably. In the synapses the vesicles were packed together, their number gradually decreased. The astroglia became highly oedematous. During status epilepticus, dark cells and a thickening of the synaptic membranes could be seen beside the above alterations. The morphological changes were most prominent in the cerebellar cortex and in the h1 area of the hippocampus. The neuronal structure of the cerebral cortex was the least damaged.

Animals↗
PubMed1982

Cytochemical detection of nickel in the myocardium after acute carbon monoxide intoxication.

The dimethylglyoxim cytochemical method was used for detecting endogenous nickel (Ni) in the canine and human myocardium. Electrondense deposits were observed in the myocardial cells and the wall and lumen of capillaries of the dog heart when after CO-intoxication the blood COHb level exceeded 30%. Energy-dispersive microanalysis proved the presence of Ni in the reaction product. Detection of the Ni-reaction product in the myocardium of human cadavers may be of forensic importance, since the reaction is resistant to post mortem autolysis and may help to identify the cause of death.

Animals↗
PubMed1981

New findings concerning the pathogenesis of acute carbon monoxide (CO) poisoning.

The pathomechanism of carbon monoxide (CO) poisoning was studied by means of cardiopathological and neuropathological investigations in experimental CO intoxication. It has been shown that besides CO-hemoglobin association, the binding of CO to cytochromes is a significant factor. The latter is thought to be responsible for the cytotoxic phenomena. Combined ultrastructural and cytochemical studies have enabled differentiation between toxic, hypoxic, and mixed alternations.

Acute Disease↗
PubMed1981

Electroncytochemical studies on changes of the adenylcyclase activity following experimental hypoxia and ischaemia in perfused rat hearts.

Changes in activity and localization of adenylcyclase were studied in rat heart perfused according to LANGENDORFF after N2-and CO-hypoxia and ischaemia. Under hypoxic conditions an increase of adenylcylase activity was found in the first minutes. Following 3 h nitrogen or 30 min CP perfusion the intensity of reaction was diminished. This later decrease of reaction intensity was not encountered under ischaemic conditions. Changes in localization were not observed either in hypoxia or in ischaemia. After reserpine or propranolol pre-treatment the posthypoxic/ischaemic initial activity-increase did not occur. It is assumed that the early increase in adenylcyclase activity (reaction intensity) following hypoxia/ischaemia is due to endogenous catecholamine release.

Adenylyl Cyclases↗
PubMed1981

Protection of functional and structural integrity of the rat myocardium by dexamethasone in hemorrhagic shock.

Rat hearts were isolated from control animals (C), following 2.5 hours of hemorrhagic hypotension (Sh) and from rats pretreated with 10 mg/kg dexamethasone (Sh + D), and they were perfused by the modified Langendorff technique. Dexamethasone pretreatment prevented the development of depression of left ventricular mechanical performance and increase of coronary resistance, but the reduction of O2 consumption observed in Sh hearts was not influenced by the synthetic glucocorticoid. Sh animals exhibited elevation of blood inorganic phosphate level, which was significantly diminished in Sh + D rats. Zonal lesions of myofilaments and mitochondria were not seen in electron micrographs of Sh + D hearts, but there was an increase in the number of cellular glycogen particles following dexamethasone pretreatment. The protection of contractile function and coronary circulation during shock cannot be the result of direct inotropic or coronary dilating action, since addition of dexamethasone (10 mg/liter) to the perfusate of C hearts did not alter contractility and coronary resistance. It is assumed that systemic hemodynamic and local cellular effects lead to the protection of myocardial integrity, which may contribute to the general beneficial action of dexamethasone in hemorrhagic shock.

Animals↗
PubMed1981

Multilamellar bodies in rat cerebellar Purkinje cells.

Multilamellar bodies appearing in the rat's cerebellar Purkinje cells were studied ultrastructurally in methionine sulphoximine convulsions, hypovolaemic shock and carbon monoxide poisoning. It is concluded that multilamellar bodies are pathological formations due to toxic hypoxic factors.

Animals↗
PubMed1980

Extracranial spreading of glioblastoma multiforme.

On the basis of 4 observations, the formation of extracranial metastases of multiform glioblastomas is dealth with which complied with all the criteria established by Weiss (histological identification of a primary brain tumour, connection of clinical data between cerebral tumour and metastases, ruling out of another primary tumour not belonging to the neuraxis by a complete autopsy). All 4 patients were--in some cases several times--trephined, subjected to postoperative irradiation and some of them were also treated with chemotherapeutics. The postoperative survival time was between 16 and 24 months, the average age of the patients was 35 years which was strikingly low. 3 patients showed infiltrations of bones and neighbouring soft parts, in one case the tumour penetrated into the sinus, in one patient paranasal sinuses and orbitae were affected, two cases showed metastases in the vertebral column and in one case metastases were found in the cervical gland nodes. One glioblastoma accompanied by a fibrosarcoma showed a particularly extensive extracranial formation of metastases. As regards the reasons for the formation of extracranial metastases of intracranial tumors many hypotheses have been established which are critically discussed by the authors.

Adult↗
PubMed1980

[Effect of calcium-free perfusion on the myocardium].

Authors studied the effect of the perfusion free of calcium on the myocardium. It was performed on the Langendorff cannula. Ultrastructural alterations were described in detail. The severity of the damage to the cells could be correlated with the duration of the perfusion. This study suggests that in the pathogenesis of these lesions lack of the membrane stabilizing effect of calcium ions may play a role.

Animals↗
PubMed1980

[Morphological study of the adenyl cyclase activity of the rat heart in experimental hypoxia and ischemia].

Alteration of the activity and localization of the reaction of adenylcyclase after perfusion of the rat heart with nitrogen, carbon monoxide and after ischaemia was studied by electronmicroscopy. In the first minutes of hypoxia increase of the activity of the adenylcyclase was revealed. After perfusion with nitrogen during three hours and with carbon monoxide during 30 minutes intensity of the reaction was observed to be decreased. In ischaemia decrease of the intensity of the late reaction could not be observed. Alteration of the localization of the reaction in ischaemia and hypoxia was not significant. Administration of reserpine and propanol did not cause any alteration. Authors believe, that increase of the activity of the adenylcyclase may be caused by accumulation of an endogenous catecholamine.

Adenylyl Cyclases↗