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Biomedical subjects

T Varga

Publications and source records attributed to T Varga.

At least 37 records · Page 2Linked to original sources
PubMed1985

[Analysis of perinatal morbidity and mortality in cases of dysmaturity].

The authors have examined the case-histories of the intrauterine retarded neonates on the basis of their obstetrical material during a four years period. They did not find such pregnancy complications in more of the half of their cases, which should have drown the attention to the possibility of the intrauterine retardation. The perinatal mortality of the dysmature babies was significant higher than the global perinatal mortality of their ward. They emphasize the importance of the early diagnosis. They suggest to spread the screening examinations. We can prevent the intrauterine death with the help of the hospitalization of the screened pregnants and with the instrumental and endocrine monitorisation of the pregnancy.

Birth Weight↗
PubMed1980

Myocardial lesions in hemorrhagic hypotension.

The myocardial alterations were investigated in dogs after hemorrhagic hypotension. Development of metabolic acidosis with increased lactate concentration was observed in all cases. Focal hemorrhages and hypoxic changes developed in the subendocarial region. Typical so-called zonal lesions were demonstrable in the mural myocardium of both ventricles. The hypoxia, increased level of catecholamines, metabolic disturbances, and probably cardiotoxic products may play a role in the pathomechanism. The alterations which are potentially reversible are transformed into irreversible damage only in most severe cases. The necrosis is of hypercontraction type, and is associated with rapid calcification and mononuclear cell infiltration. The morphologic changes may explain the circulatory disturbances of cardiac origin and may represent the basis of development of the low cardiac output syndrome in hemorrhagic shock.

Animals↗
PubMed1980

[Blood group characteristics of Hapsburgs belonging to the line of Josef, Palatine of Hungary].

Results of the reported examination of blood-group characteristics and inheritance of historical personalities of Hungary evidence that blood-group determination or identification can be successfully carried out from bone or/and hair specimens having been buried and/or conserved for a long time. It should be mentioned, that determination of blood-group in such specimens and evaluation of results requires an exceptional carefulness since specific reactions may occur.

Austria↗
PubMed1979

Investigation of the short-time autolysis of rat hearts by means of SDS. Polyacrylamide gel electrophoresis and electron microscopy.

The short-time autolysis of hearts was regarded as a model of ischaemic heart failure. Therefore, isolated rat hearts were subjected to 30--120 min autolysis in a Locke solution at 37 degrees C. Electron microscopic examinations and myofibrillar preparations were made from the autolysed heart ventricles. The myofibrillar proteins were resolved by SDS-polyacrylamide gel electrophoresis. After 30 min autolysis the amount of a protein of 192,000 daltons greatly increased. At the same time on the electron micrographs the focal destruction of filament destruction on the A filament area and the mitochondrial structure altered too. After 60 min autolysis another protein of 36,400 daltons appeared. On the electron micrographs the focal desintegration of Z membranes and the focal destruction of I filaments can be observed. After 120 min autolysis further proteolytic products could not be detected by gel electrophoresis but on the electron micrographs the destruction of Z membranes and I filaments became more pronounced.

Animals↗
PubMed1979

[Myocardial damage in hemorrhagic hypotension].

Damage to the myocard caused by the loss of blood was studied in experiments on dogs. After long-lasting hypotonia focal lesions of the myocard of degenerative type have been found. Desorganization of the myofilaments and invagination of the disc could be seen in the area of the intercalar discs. Filaments in the other regions have not shown any alterations. In the mitochondria hypoxic lesions were revealed. One part of the alterations are not reversible. After 48 hours of survival focal necrosis with hyper contraction and calcification could be observed. It was surrounded by cellular infiltration containing mononuclear cells. Cellular necrosis revealed, may lie on the basis of the central lesion of the circulation appearing after long-lastng hypotonia.

Animals↗
PubMed1978

[Myocardial lesions in acute increase of the intracranial pressure (author's transl)].

Myocardial lesions occuring in diseases with acute increase of intracranial pressure were investigated. Morphologic alterations in heart muscle in spite of different lengh of surviving and various causes of the death were of similar type. In every case subendocardial haemorrhage could be observed on the septal surface and on the papillary muscle of the left ventricle. Focal intracellular edema, myocytolysis were revealed in 76%, focal necrosis of hypercontractic type developed in 52% of the cases. Cellular infiltration occurred around the alternations observed in 3 cases. It is concluded, that damage to the heart muscle is not caused directly by the increased intracranial pressure or catecholamine mobilisation, but seems to be the consequence of the acute myocardial hypoxia.

Adolescent↗
PubMed1976

Heart block: histological and clinical features.

The clinical types of A-V-block and the localization of the underlying lesion to the conduction pathway have been examined in 25 patients. On the evidence of the post mortem studies the lesions were of the following types: 1) Necrosis or fibrosis of ischaemic origin: 13 cases; 2) lesions of inflammatory character: 5 cases; 3) nonspecific lesions; 6 cases; 4) malignant infiltration: one case. Correlations between the site of lesion and the clinical type and pattern of block could be demonstrated in a large proportion of the cases. The characteristic features of the individual types of block and their localization are discussed and a review of the literature is given.

Acute Disease↗
PubMed1975

[Anoxic myocardial lesions in man, developed during extracorporeal circulation, studied by electron microscopy].

Anoxemic changes of the myocardium were examined at 20 patients operated on in extracorporal circulation. At a mild degree hypothermia (30 degrees C) morphological changes appear after a 20 minutes period of anoxaemia. Damage to the myocard of irreversible character could be revealed after an anoxaemic period of 43--55 minutes. An intermitting perfusion of the coronary arteries delayes the formation of the lesions, although in cases of ligation of the aorta for 90 minutes severe mitochondrial changes and deformation of cells were seen. The best method for protecting the myocard is an isotherm perfusion of the coronary arteries. Clinical and laboratory findings show that necrosis of the myocard has a focal character and may play a part in formation of postoperative lesions.

Cardiac Surgical Procedures↗
PubMed1975

[Morphological and toxicological studies of experimental diquat poisoning].

Lesions caused by a single subtoxic dosis of diquat were studied in rats. After the administration of diquat on the first day it was revealed in highest concentration in the lung, but in two weeks no traces of the drug could be demonstrated. On the first and third day activity of peroxidase in the liver and the number of peroxisomes as well significantly increases. On the first day after the administration of diquat in the lung damage to the surfactanct and increase of the capillary permeability was observed. Later degenerative changes of the pneumocytes I and II type, focal haemorrhagic edema and presence of alveolar macrophages can be revealed. In two and in four weeks a slight pulmonary fibrosis remains to show the damage to the lung. In kidney tubular lesions of toxic origin, in the phase of the regeneration increase of the number of lyosomes could be revealed. On the basis of this study and the data of other authors the possible mechanism of the intoxication with diquat is discussed.

Animals↗