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Biomedical subjects

E Frantík

Publications and source records attributed to E Frantík.

At least 37 records · Page 2Linked to original sources
PubMed1988

Carbon monoxide poisoning at a lowered myocardial adaptation capacity: animal ECG models.

Two animal models for testing foreign substances for the hypoxic type of cardiotoxicity proved to be valid and reproducible: i.e. decreased reserve capacity of the heart in rats recovered from the calciferol cardiopathy and increased heart work provoked by isoproterenol (5 mg/kg i.p.). In both cases obvious hypoxic ECG changes appeared at lower levels of exposure to carbon monoxide (500 ppm, 572 mg.m-3) and carboxyhemoglobin (18%), when compared with nonpretreated animals. The models have shown, that injured or overloaded heart displays a substantially increased sensitivity to CO poisoning.

Adaptation, Physiological↗
PubMed1987

Animal model of cardiotoxicity: carbon monoxide induced ECG hypoxia masked in light narcosis.

Inhalation exposure of restrained conscious rats to carbon monoxide (1000 ppm, 120 min.) led to a peak carboxyhaemoglobine concentration of 40-45%. At this concentrations spontaneous motor activity was not affected significantly but the physical capacity at endurance run was depressed by 70%. From the 30th min. of exposure a typical two-phasic change in heart rate with initial tachycardia and obvious but unstable hypoxic changes in ECG were observed. Quieting of animals (light anesthesia with phenobarbitone; 100 mg/kg ip) removed almost completely all pathological changes. The level and fluctuations of functional requirements to the circulation seem thus substantial for the development of the cardiotoxic effects.

Anesthesia↗
PubMed1987

Lower cardiovascular responsiveness in men with a positive family history of hypertension who remain normotensive in middle age.

Within the framework of a primary preventive study in 760 research workers aged 30-59, laboratory examinations of cardiovascular responsiveness to upright posture, cold and mental stress (Stroop word-colour interference test and ranking of three-digit numbers) were performed. Twenty men with essential hypertension (Stage I-II) not treated with antihypertensive drugs were selected from this population (Group 3) and matched with normotensive subjects with a negative (Group 1) and positive (Group 2) family history of hypertension, according to age, weight, neuroticism and Type A behaviour. Hypertensive men showed higher pressor responses to cold and mental stress tests than normotensive ones. Significantly lower anticipation and test responses were found in Group 2 as compared with Group 1 and 3, i.e. in those subjects who remained normotensive to higher age in spite of having a positive family history of hypertension. This fact suggests an important--intrinsic or modulating--role of cardiovascular responsiveness to physiological and psychological challenges in the manifestation of the genetic disposition for essential hypertension.

Adult↗
PubMed1985

Acrylonitrile inhalation in rats: II. Excretion of thioethers and thiocyanate in urine.

In male Wistar rats, the inhalation exposure to acrylonitrile (AN), 271 mg X m-3, 8 hours a day, 5 days a week, did not affect protein sulfhydryl concentration in liver and blood and decreased glutathione concentration in the liver, but not in the brain at the end of the fifth exposure. The urinary excretion of the main AN metabolites, thioethers (AN-mercapturic acids) and thiocyanate was proportional to the inhaled AN concentration (57, 125, 271 mg X m-3, respectively) in a single exposure for 12 hours, and their mutual ratio was greatly different from that after injection of AN. The results revealed that the urinary excretion of thioethers is a very sensitive and dose-related indicator of exposure to AN and extrapolation of the results indicates that the exposure to AN concentration below 10 mg X m-3 could thus be demonstrated.

Acetylcysteine↗
PubMed1984

Acrylonitrile inhalation in rats: I. Effect on intermediary metabolism.

In male Wistar rats the inhalation exposure to acrylonitrile (AN), 280 mg X m-3, 8 hours a day for five days significantly decreased the serum concentration of cholesterol and triglycerides, but the liver concentrations of phospholipids, and esterified fatty acids were unchanged. The liver microsomal protein and cytochrome P-450 content decreased significantly. On the other hand the levels of glucose, lactate and pyruvate in the blood and brain significantly increased up to 250% of controls. A microscopic examination of the lungs, liver, kidneys and adrenals did not show structural changes and the numbers and enzyme activities of alveolar macrophages were also unaffected. In single 12-hour inhalation exposures the elevation of blood glucose was proportional to the inhaled concentration of AN (average concentrations 57, 125, or 271 mg X m-3); the effect was significant at the lowest AN concentration and was intensified in the glucose tolerance test. The elevation of blood glucose proved to be the most sensitive and dose-related indicator of AN exposure of those observed.

Acrylonitrile↗