Biomedical subjects
Publications and source records attributed to I Balogh.
It is a matter of common knowledge that under ischaemic or hypoxic conditions the oxygen demand of the myocardium could only be satisfied by enhancement of collateral blood flow. It is demonstrated that in a diabetic state an elevation of the myocardial blood flow could not develop due to lack of proper vasodilation in the coronary arterial bed.
The prolonged effect of nickel chloride and cadmium chloride on the rat fetal myocardium was studied experimentally administered to the pregnant mother through a gastric tube in doses of 12.5 mg/b. wt. It could be demonstrated that, due to nickel administration, changes simulating cardiomyopathy and severe mitochondrial lesions developed and the number of collagenous fibres and glycogen granules accumulated, while as a result of cadmium chloride administration, changes were apparent mainly in the endothelial cells, but with simultaneous mitochondrial impairments, too. Nickel and cadmium are contained by cigarette smoke. Based on experimental studies, authors propose new arguments on the damaging effect of smoking of pregnant women.
Rat hearts isolated according to Langendorff were perfused with Krebs-Henseleit medium containing 10(-7)-10(-4) mol/l CuCl2 solution. Using morphological studies combined with electron microscopic and cytochemical techniques, it was established that, by contrast to other tracer elements, severe lesions initially affect the capillary endothelium then the fibre system, being first characterized by edema of the capillary wall, accumulated pinocytotic vesicles and later by hyperconcentration necrosis. Using a concentration of 10(-4) mol/l, oxygen-paradox- or calcium-paradox-type impairments develop.
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In 18 alloxan-diabetic and 12 metabolically healthy dogs cardiac and skeletal muscles have been studied electronmicroscopically. Myopathy-like alterations, as widening of Z band material, alterations of mitochondria as well as of collagen fibers were observed in the diabetic myocardium. In skeletal muscle nemalin bodies were found. These latter alterations don't develop in insulin-treated diabetic state.
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In 7 men and 1 woman who died suddenly the functionally important areas of myocardium in the sino-auricular area and the subendocardial layers of left ventricle were obtained by necropsy no more than 3 h after death, and then prepared for study by electron microscopy. In three cases of five, in whom the cause of death was cardiovascular insufficiency, viral particles and bacteria were identified. In three other cases of sudden non-cardiac death they were not found. Viruses were found only in working cardiomyocytes, but near the sinus node. Bacteria were found in left ventricular subendocardium. Intercellular junctions between virus-damaged myocytes and intact cells were preserved. Based upon the functionally important sites where they were found, associated degeneration near them, and preservation of contacts among myocardial cells there, viruses and bacterial infections may play an important role in the patho-physiologic events leading to some cases of sudden death.
After 20% total body surface scalding inducing 3d degree burn in rats the following parameters were studied in ebb and flow phases, as well as in burn disease, 2 hours, 2 and 7 days postburn: atomic absorption spectrophotometric study of the serum and myocardial Ni levels; the effect of Ni ions (10(-8)-10(-4) M/l) in vitro on total coronary resistance in the isolated perfused rat heart; the effect of alpha and beta adrenergic blocking agents (phenoxibenzamine, oxprenolol) on Ni-induced coronary vasoconstriction; electron cytochemical study of the ultrastructural changes of the myocardium 7 days after scalding. It was found that: During the first 2-3 hours after scalding or bleeding there was a significant elevation of serum Ni level which levelled off by the end of the first week. Total coronary resistance (TCR) increasing effect of Ni ions was significantly augmented during the first 2-3 hours after burn and bleeding (ebb phase). In the scalded group it decreased to the control value by the 2-3d day (flow phase) and increased again a week later (burn disease). In the scalded groups in vivo pretreatment with oxprenolol (10(-4) g/kg) completely inhibited the Ni induced coronary spasm. PBZ treatment in vitro (10(-5) M/l) had similar effect in the three postburn periods tested. Ultrastructural changes and intracellular Ni-dimetilglyoxim complexes could be detected. Oxprenolol treatment continuously applied from the 4th day postburn (2 X 0.5 mg/kg) prevented the development of myocardial damage, while the electron dense complexes containing Ni were still detectable. In view of our previous data we assume that the endogenous Ni increase in the serum after burn may be cardiopathogenic. The phasic changes of the sensitivity of the coronary vessels to Ni ion and the similarity of the effects of alpha and beta adrenergic blocking agents may be explained by the alterations in the neuroendocrine system and metabolic disturbances.