[Half-life of red blood cells in cyanotic heart lesions (determined by means of radioisotopes)].
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Biomedical subjects
Publications and source records attributed to B Halawa.
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Density of beta-adrenergic receptors in the lymphocytes, alpha 1- and alpha 2-adrenergic receptors in blood platelets, as well as blood serum norepinephrine levels have been assessed in 49 patients with congestive heart failure prior to, and 7 and 14 days of captopril and lisinopril administration. A decrease in beta-, alpha 1-, and alpha 2-adrenergic receptors density, an increase in blood serum norepinephrine, and normal epinephrine levels have been noted in these patients. A 7-day treatment with captopril, and a 14-day treatment with lisinopril have increased adrenergic receptors density, and decreased blood serum norepinephrine levels.
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Non-steroidal anti-inflammatory agents may moderately increase blood pressure thus affecting hypotensive agents effectiveness. This study aimed at evaluating arterial blood pressure, serum 6-keto-PGF1 and aldosterone as well as plasma renin activity in hypertensive patients treated with indomethacin or ibuprofen with captopril or indomethacin or ibuprofen with nifedipine. Captopril given at the same time as indomethacin or ibuprofen did not decrease both systolic and diastolic blood pressures. However, no interaction between nifedipine administered simultaneously with indomethacin or ibuprofen was noted. Serum 6-keto-PGF1 and aldosterone as well as plasma renin activity were decreased in both groups of treated patients. Mechanism of indomethacin and ibuprofen hypertensive action seems to se related with their ability to inhibit prostacyclin biosynthesis.
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Recent findings in animals indicate the influence of beta-endorphins on bronchial smooth muscle tone. The purpose of our study was to compare beta-endorphin concentrations in sera of asthmatics during the asymptomatic period and after histamine provocation. The study was performed in a group of 32 asthmatic patients and 12 healthy subjects. Beta-endorphin concentrations were evaluated by radioimmunoassay (J-125 beta-Endorphin Human) twice daily at 8 a.m. and 10 a.m., and also before and after histamine provocation. No significant differences were found in endorphin concentrations for both normal controls and asthmatics at 8 a.m. and 10 a.m. We demonstrated a statistically significant increase in endorphin concentrations in asthmatics as compared to the controls. We found a statistically significant decrease of beta-endorphin concentrations after histamine provocation in the asthmatic group.