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Biomedical subjects

S Mallov

Publications and source records attributed to S Mallov.

8 recordsLinked to original sources
PubMed1977

Quantitative determination of stress-induced myocardial damage in rats.

The degree of myocardial damage produced in rats by exposing them to unsignalled, irregular foot-shock stress was determined in three ways: by measuring (1) enzymes (LDH, GOT and GPT) released into the circulation, (2) the rate of release of one of these enzymes (LDH) from isolated perfused hearts into the perfusate, and (3) the cardiac uptake, in vivo, of the radioactively labeled bone-seeking agents, technetium-99m-stannous pyrophosphate or technetium-99m-methylene diphosphonate. The latter two methods permitted quantitative determination of the degree of myocardial damage produced. Determination of cardiac technetium-99m uptake was found to be simple, quantitative, highly sensitive and truly indicative of cardiac damage, and therefore most suitable for studies of the effects of stress on cardiac injury.

Animals↗
PubMed1977

Drug interactions.

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Analgesics, Opioid↗
PubMed1977

Myocardial uptake of Tc-99m skeletal agents in the rat after experimental induction of microscopic foci of injury.

The cardiac uptake of Tc-99m tagged skeletal agents was studied after myocardial injury produced by subcutaneous catecholamine injection and random foot-shock stress. Rats stressed for 2 hr developed microfocal myocardial injury, without gross change, whereas those stressed for 12 hr sustained more confluent and sometimes grossly visible damage. Tc-99m MDP and Tc-99m PPi concentrations in these hearts were significantly above control (undamaged) heart levels, producing positive gamma-camera images. Subcutaneous epinephrine injections resulted in grossly visible lesions, with tracer concentrations higher than those previously reported in vasoocclusive infarcts. We postulate that the stress-induced scattered microfocal lesions may accumulate radiopharmaceutical on a per-gram basis in the same way as the larger catecholamine-induced lesions, since tracer delivery to the injured areas in each case is probably less impeded than in frankly vasoocclusive models. Such microfoci, then, could provide an explanation for some of the "false positive" myocardial scans observed clinically.

Animals↗
PubMed1977

Protective effect of ethanol against epinephrine-induced myocardial necrosis in rats.

Myocardial necrosis was produced in rats by the subcutaneous injection of a single dose of epinephrine (3 mg base/kg). The severity of the cardiac injury produced was assessed by visual inspection, determination of the release of LDH, CPK, GOT, and HBDH from isolated perfused hearts, and measurement of cardiac uptake of technetium-99m-methylene diphosphonate in vivo. Ethanol, given in doses of 0.5 to 6.0 gm/kg 15 minutes or two hours prior to epinephrine administration protected the hearts against the epinephrine-produced injury, the degree of protection increasing with dose. Investigations of possible mechanisms of action of ethanol indicated that the protective action of the latter does not appear to be due to a lowering of plasma free fatty acid levels, a reduction of cardiac contractility, a non-specific caloric effect, an interference with epinephrine-induced platelet aggregation, or ethanol-induced analgesia.

Animals↗
PubMedDate not supplied

Inhibition of epinephrine-induced myocardial necrosis in rats by administration of single doses of ethanol.

The oral administration of single doses (0.5-6.0 g/kg) of ethanol to rats, shortly before injecting them with a large dose (3.0 mg base/kg) of epinephrine subcutaneously, significantly reduced the severity of the myocardial damage produced by the epinephrine. The larger the dose of ethanol, the greater was the protective effect. The results were the same, regardless of the method used to determine the degree of cardiac injury. Experiments employing various agents to determine the mechanisms of ethanol action have tentatively suggested that a platelet de-aggregating or an osmotic effect of alcohol may be involved.

Animals↗