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Biomedical subjects

I Balogh

Publications and source records attributed to I Balogh.

At least 109 records · Page 6Linked to original sources
PubMed1985

Endogenous nickel release in injured patients: a possible cause of myocardial damage.

Atom absorption spectrophotometry was used for the study of serum nickel levels in 58 injured patients. From 27 autopsies an electron cytochemical examination of the myocardium was performed in 19 patients. In patients with severe burns and cerebral injury, the serum nickel content showed a significant increase in the early period after injury. In these cases direct traumatic or toxic damage to the central nervous system and, in cases of early death, cerebral oedema, were present. The ECG tracings revealed disturbances in repolarization in a large majority. Nickel-dimethylglyoxim complex precipitates were found in the myocardium of all patients who died. In addition to disorientation, increased serum nickel levels and abnormal ECG records were observed in septicaemia. On the basis of these observations and the experimental data, we suggest that one of the causes of posttraumatic myocardial damage may be endogenous nickel release as part of the homeostatic disequilibrium arising as a direct or indirect effect of the injury.

Adolescent↗
PubMed1985

Post-mortem examination of the heart in cases of sudden death.

Sudden unexpected death is an important topic of forensic medicine. Several papers have been published on the morphological changes of the coronary arteries and the myocardium in sudden cardiac death. Forensic pathology demands more and more accurate methods of postmortem diagnosis of early ischaemic lesions of the heart muscle that occur shortly before death and which, in the absence of other explanations, may presumably be related to the cause of death. The cause of death is often evident from post-mortem findings, still in a number of cases the diagnosis may be doubtful. The application of electron microscopy has increased rapidly over recent years and the electron microscopic investigation of post-mortem biopsy material may be useful in narrowing down the cause of death. This report presents the results of electron microscopic and cytochemical studies of the myocardium in cases when death had occurred at a precisely recorded time.

Calcium↗
PubMed1985

[Ultrastructural analysis of viral and bacterial lesions in human sudden cardiac death].

Sinoatrial node, perinodular working myocardium of the right atrium and subendocardial muscle fibers of the left ventricle of 8 persons who died suddenly at the age of 23-69 years were studied ultrastructurally. In 1% of working cardiomyocytes, in 2 out of 5 cases of sudden cardiac death, viruses were detected. Myofibrils were destroyed in the damaged myocytes but the contact zones with undamaged myocytes remained intact. Rod-like bacteria were observed in the interstitium of the subendocardial myocardium of the left ventricle in one case. Destructive changes of the mitochondria, myofibrils and intercalated discs were found in the myocytes adjacent to bacteria. Viruses and bacteria were absent in 3 control cases. The possible role of viruses and bacteria in the development of sudden cardiac death is discussed.

Adult↗
PubMed1984

Diabetic myocardial alterations in ultrastructure and function.

Myocardial samples taken from six healthy and six alloxan-diabetic dogs by means of percutaneous needle-biopsy were investigated electronmicroscopically. Specific increase in the number of collagen fibers and that of mitochondria were demonstrated beside the widening of Z bands. In the same experimental animals, a close, inverse correlation was detected (y = 0.0068x + 0.1680; r = 0.8648; F = 29.6705; n = 12) between the values of the left ventricular passive elastic modulus and those of the plasma glucose disappearance rate determined immediately before the haemodynamic investigation. On the basis of the ultrastructural findings, the proliferation of collagen fibers can be made also responsible for functional disorder of the diabetic myocardium.

Animals↗
PubMed1984

Contributions to the mechanism of action of beta-adrenergic stimulants.

Subcellar localization of ionic Ca was investigated by the Pb-acetate cytochemical method in rat myometrium on the 21st day of pregnancy, following oxytocin and Bricanyl treatment. Following Oxytocin treatment the amount of ionic Ca increased in the muscle cells of the uterus and decreased in the plasma membrane and mitochondria as compared with the control. Tocolytics given in the last four days of pregnancy caused a decrease in the cytoplasmic concentration of ionic Ca and increased the Ca++ content of Ca++ pools (plasma membrane, mitochondrium). The change in the intracellular distribution of Ca++ may be involved in the mechanism of action of tocolytics and in the development of the relaxation of smooth muscle.

Animals↗
PubMed1983

Electron-cytochemical detection of endogenous nickel in the myocardium in acute carbon monoxide poisoning. Applicability of a new cytochemical technique in forensic medicine.

After acute carbon monoxide poisoning (inhalation, dogs; perfusion, rats; postmortem, humans) endogenous nickel was cytochemically detected in heart muscle by dimethylglioxime reaction. Dimethylglioxime cytochemical reaction, in each case at the COHb level, was always positive in experiments and in postmortem samples. A nickel ion accumulation in the heart muscle above 30 rel.% of COHb was suggested. A possible role of nickel ion in the pathomechanism of the acute carbon monoxide poisoning was supposed. This dimethylglioxime cytochemical technique is applicable in forensic medical practice, primarily because it is not disturbed by autolysis.

Animals↗
PubMed1983

Comparative electron-microscopic investigation of postmortem human heart muscle biopsy.

Based on Harvard criteria findings, comparative morphological investigation on postmortem heart muscle biopsy following coronary insufficiency after sudden cardiac death have been reported. The subendothelial layer of the left ventricular wall has revealed a severe interstitial edema, various types of actin-myosin filamental destruction, mitochondrial damage, and disseminated muscle fiber necrosis. One of the first alterations observed was the change in transmembrane calcium and intracellular calcium metabolism. A decrease in succinic dehydrogenase and cytochrome oxidase activity was discovered early.

Adolescent↗
PubMed1983

Endogenous nickel release as a possible cause of coronary vasoconstriction and myocardial injury in acute burn of rats.

The aim of the present study was to test the hypothesis that endogenous nickel release may play a role in myocardial depression in the acute phase of burn shock in rats. Serum nickel concentration (Se-Ni) measured by atomic absorption spectrophotometry, the sensitivity of isolated perfused hearts to exogenous nickel chloride (0.01 mumol/l), and ultrastructural myocardial alterations, as well as subcellular localization of endogenous Ni by the dimethylglyoxim method, were analyzed in the first week after standardized third-degree full thickness skin thermal burn covering 20-25% of the body surface. In the first 2 days after burn a significant fivefold increase of Se-Ni concentration was observed which leveled off by the end of the first postburn week. The coronary vascular resistance increasing effect of exogenous NiCl2 grew significantly in the first 3 h after burn, decreased to control in the 2nd postburn day, and increased again in the second half of the week after burn. Both ultrastructural damages and nickel containing reaction products could be observed in the myocardium 7 days after burn. The experimental results suggest that endogenous nickel release may play a role in coronary vasospasm and consequent myocardial depression in the acute phase of burn shock in the rat.

Acute Disease↗
PubMed1982

Effect of nickel on uterine contraction and ultrastructure in the rat.

The in vitro effects of nickel chloride (NiCl2) on uterine contractile activity and ultrastructure were studied in uterine strips isolated from 20-day-pregnant Wistar rats. Ni2+ had a dual action on uterine spontaneous contractions. In low concentrations (10(-7) M to 10(-5) M), NiCl2 increased basal tone significantly but had no effect on the amplitude or frequency of development of isometric force. High concentrations of NiCl2 (10(-4) M to 10(-3) M inhibited spontaneous contractile activity and decreased basal tone, which was antagonized by elevation of the extracellular concentration of Ca2+. Electron microscopic localization of Ni by the dimethyl glyoxime cytochemical technique showed that, after incubation of uterine strips in a physiologic medium that contained 10(-6) M NiCl2, electron-dense Ni-dimethyl glyoxime particles could be observed in the cytoplasm and in the mitochondria of uterine smooth muscle cells. Exposition of Ni caused mitochondrial structural damage and accumulation of glycogen. The experimental results indicate that, because of its oxytocic action, the increase in the serum level of Ni in the advanced stage of human labor (Rubányi and associates, 1982) may support separation of the placenta and/or may contribute to the prevention of atonic bleeding in the postpartum period.

Animals↗