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Biomedical subjects

R Fried

Publications and source records attributed to R Fried.

At least 73 records · Page 4Linked to original sources
PubMed1983

Polycythemia and the acute hypoxic response in awake rats following chronic hypoxia.

The acute hypoxic pressor response was studied in 22 chronically catheterized awake rats, 13 in whom the pulmonary arterial circulation had been remodeled by 10 days of exposure to hypobaric hypoxia. Five of these had their hematocrit lowered to normocytic levels after the chronic hypoxic exposure. Nine were controls. After 24 h in room air the pulmonary arterial pressure (Ppa) and pulmonary vascular resistance (Rp) of hypoxic-polycythemic rats was at least twice the control value; in the hypoxic-normocytic rats Ppa and Rp were less than that of hypoxic-polycythemic animals and greater than that of controls. Cardiac index, heart rate, and O2 saturation were similar in all groups. In 10% O2 a rise in Ppa and Rp occurred in all groups; in absolute terms the rise was greater in hypoxic rats than in controls and greater in polycythemic than in normocytic animals. In the intact animal the acute hypoxic pressor response can still be elicited in a pulmonary vascular bed structurally altered by chronic hypoxia. When calculated as a percent increase over base line, its intensity was greater than in room air controls and for Ppa was independent of hematocrit.

Acute Disease↗
PubMed1983

Response of bronchial smooth muscle to mast cell degranulation in situ.

We studied the response of bronchial smooth muscle to mast cell degranulation with Ascaris suum antigen (AA) and compound 48/80 (48/80) in 26 mongrel dogs in situ. Bronchial smooth muscle response was measured isometrically in situ from a segment of the right middle lobe bronchus; tracheal response was monitored isometrically as a control. After intra-arterial (ia) injection of AA into the bronchial circulation, bronchial contraction preceded tracheal contraction by 19.2 +/- 4.6 s (P less than 0.002). Bronchial contraction to AA (21.7 +/- 3.4 g) was substantially greater than to 48/80 (10.5 +/- 1.8 g, P less than 0.05) corresponding to differences in maximal systemic histamine concentrations (146 +/- 24.1 vs. 1000 +/- 236 ng/ml, P less than 0.01). In 5 dogs, the effect of leukotriene D4 (LTD4) and FPL 55712 was studied. Injection of 10(-8) mol ia LTD4 caused no bronchial contraction. In four dogs, 10(-7) mol FPL 55712 caused no bronchial relaxation after initial precontraction during immune degranulation with AA; intravenous chlorpheniramine (5 mg/kg) caused 69.7 +/- 9.4% relaxation. We demonstrate a model that permits selective immune degranulation of a single major resistance bronchus in situ. We conclude that AA-induced degranulation in dogs caused bronchial contraction predominantly by secretion of preformed mediator.

Animals↗
PubMed1982

Congenital pulmonary arteriovenous fistula producing pulmonary arterial steal syndrome.

This report describes a congenital pulmonary arterial steal syndrome manifested as cyanosis and acidosis in a newborn. A fistulous connection between the right pulmonary artery and a large, anomalous right common pulmonary vein stole blood from the pulmonary arteries. The anomaly was suspected because of a pericardiac shadow on frontal and lateral chest films, substantiated by M-mode echocardiogram, confirmed at cardiac catheterization with angiocardiography, and analyzed at postmortem examination.

Arteriovenous Malformations↗
PubMed1982

Regional distribution of superoxide dismutase in rat brain during postnatal development.

Superoxide dismutase in nervous system protects readily oxidizable compounds such as catecholamines against toxic effects of oxygen. We investigated superoxide dismutase activity during development in 5 brain regions selected for a wide range of catecholamine concentration and turnover: cerebellum, neocortex, striatum, hypothalamus and medulla-pons. The cytosolic and the particulate enzyme were measured from birth to 6 months of age. In cerebellum the cytosolic enzyme shows considerable activity on the first postnatal days; the particulate enzyme is less active, both reach a maximum at 3 months. In cortex and striatum both activities were low during the postnatal days and reach a plateau at 3 months. In hypothalamus both activities are higher during the postnatal days and reach a maximum at 3 months. In medulla-pons the values are 2 times higher than in all other regions; the cytosolic enzyme reaches a maximum at 2 months whereas the particulate enzyme reaches a plateau at 3 months. Thus our results show an increase of superoxide dismutase activity during development in all brain regions; the highest activities were found in regions with high catecholamine content.

Aging↗
PubMed1980

Effect of ethanol on superoxide dismutase activity in cultured neural cells.

Superoxide dismutase (EC 1.15.1.1) activity was investigated in several types of neural cells cultivated in the presence of 100 mM ethanol. Superoxide dismutase was inhibited by acute treatment with ethanol. Chronic treatment with ethanol specifically inhibited superoxide dismutase in glial cells. In all instances withdrawal of ethanol produced a quick return to control values. Inhibition of superoxide dismutase by ethanol may increase toxic oxygen radicals in nervous tissue.

Animals↗
PubMed1980

Implantation of disulfiram in rats.

The biochemical and pharmacological effects of disulfiram implantation were studied in rats. Sterile disulfiram pellets (1000 mg/kg) were implanted subcutaneously. Groups of 5 rats were killed after 3, 7, 14, 28 and 56 days. The release of disulfiram during the first week corresponded to a daily dose of 12--16 mg/kg and during the following period to 5--8 mg/kg. The activity of the low-Km aldehyde dehydrogenase in liver and brain, the carboxylesterase activity in liver and the dopamine-beta-hydroxylase activity in heart were significantly decreased by approximately 45, 35, 20 and 35% respectively at all periods tested. The rate of ethanol elimination, the activity of monoamine oxidase in the brain, and the content of cytochrome P-450 in the liver were unaffected. The level of norepinephrine in the brain was slightly decreased after 14 days. The acetaldehyde level in blood after ethanol injection (1.0 g/kg) was 55--60 microM in the disulfiram group and 25--30 microM in the control group. Ethanol administration caused a slightly decreased blood pressure and increased respiratory rate 14 days after implantation but not after 28 days.

Acetaldehyde↗
PubMed1979

Effects of superoxide radicals on transport (Na + K) adenosine triphosphatase and protection by superoxide dismutase.

Membrane (Na +K)ATPase isolated from rat brain was preincubated in a medium in which superoxide radicals were generated enzymatically. Exposure to superoxide radicals caused an irreversible inactivation, which could be prevented by further addition of superoxide dismutase. (Na + K)ATPase was also protected by addition of allopurinol, a xanthine oxidase inhibitor, during preincubation. The K-activated nitrophenylphosphatase associated with (Na + K)ATPase was also found to be inactivated by preincubation with superoxide radicals, which could be prevented by superoxide dismutase.

Allopurinol↗
PubMed1979

A comparative characterization of cytosolic superoxide dismutase/(SOD) from hog liver and erythrocytes.

1. Conditions of preparation and purification of superoxide dismutase from hog liver and erythrocytes were established. 2. The enzymes from both tissues were compared in respect to electrophoretic mobility, pI value, amino acid composition and spectrophotometric profiles and some differences were observed. 3. Conditions of enzyme dissociation were elaborated and molecular weights of subunits obtained from both kinds of SOD were found to be approx. 16,000. 4. Effect of heat and pH on the enzyme activity were tested. Both enzymes exhibited a relative thermostability.

Amino Acids↗
PubMed1979

Familial factors in bladder carcinoma.

Surprisingly, little is known about host factors in cases of bladder carcinoma. We investigated 2 families prone to transitional cell carcinoma of the bladder. A high degree of pathology verification of cancer of all anatomic sites and a meticulous recording of genealogy, associated diseases and environmental exposures, when known, have allowed a more cogent appraisal of cancer etiology. It is reasonable to assume that members of the subject families may be more susceptible to variable carcinogenic exposures, a concept that is in accord with a genetic-environmental interaction hypothesis for cancer etiology. In addition to increased surveillance of high risk patients for earlier detection of bladder cancer, cancer control measures also should take into consideration preventive programs directed toward the avoidance of known carcinogenic exposures, such as cigarette smoking in high risk relatives of cancer-affected probands. We propose that the etiology of familial bladder cancer may be complex, involving possible other associated malignant neoplasms and/or certain non-neoplastic disorders, in addition to specific carcinogenic exposures. There is a serious need for the detailed reporting of families prone to bladder cancer wherein all of these potentially important associated factors are considered, so that a fuller appraisal of etiology might be achieved.

Adult↗