Biomedical subjects
Publications and source records attributed to B Halawa.
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Blood serum quinidine sulphate and propranolol levels have been measured in patients with cardiac arrhythmias treated simultaneously with mexiletine, flecainide, encainide and tocainide. It was found that mexiletine and encainide increase quinidine sulphate serum concentrations. Propranolol serum concentrations have been increased by mexiletine, encainide flecainide, and tocainide. Flecainide ant tocainide have not changed quinidine sulphate serum concentrations.
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Biological serum halt-life, relative volume of distribution and digoxin clearance following a single oral dose of digoxin with diltiazem or nifedipine were evaluated. Blood serum digoxin following its administration with diltiazem and nifedipine for 8 days were assayed. It was found that diltiazem and nifedipine did not affect tested pharmacokinetic parameters of digoxin and did not change digoxin serum levels during a 8-day administration in combination with diltiazem and nifedipine.
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Serum concentrations of the selected hormones were assayed in students who did not train long-distance races and in trained disabled individuals who passed the distance on a wheel chairs. Assays were carried out both prior to and after Marathon race. An exercise significantly increased serum concentrations of the following hormones in both groups: cortisol, ACTH, aldosteron, and plasma renin activity. An increase in total thyroxine, free thyroxine and decrease in LH were noted in disabled individuals. Increased concentrations of ACTH, free and total thyroxine, decreased concentrations of cortisol, LH, plasma renin activity, and aldosteron were found in disabled individuals who passed the distance of Marathon race on the wheel chairs comparing with those seen in the students.
It was shown that sodium ions outflow rate through the lymphocyte membranes is increased in hyperthyroid patients and decreased in patients with hypothyroidism. Sodium ions outflow rate normalizes following effective treatment of the disease. Changes in the sodium ions outflow rate do not effect their concentration in the lymphocytes.
Lymphocyte beta-adrenergic receptor density and plasma catecholamine concentrations were determined in 28 patients with acute myocardial infarction and compared with those in patients with angina pectoris and healthy persons. In patients with acute myocardial infarction beta-adrenergic receptor density was significantly lower (p less than 0.001) and plasma catecholamine levels significantly higher (p less than 0.001) as compared with corresponding values in patients with angina pectoris or healthy persons. beta-adrenergic receptor density in patients with angina pectoris were not significantly different from those in controls. A significant negative correlation between beta-adrenergic receptor density and plasma norepinephrine levels was observed in patients with acute myocardial infarction (r = -0.593; p less than 0.001; r = -0.615; p less than 0.001 respectively). It is suggested that decreased beta-adrenergic receptor density is a consequence of elevated plasma catecholamine levels in patients with acute myocardial infarction. It has been well documented that acute myocardial infarction is associated with enhanced activity of the sympathetic nervous system. Several studies have already been done showing that urinary excretion of catecholamines and plasma catecholamine concentrations are raised in the acute phase of myocardial infarction. Particularly high levels of plasma catecholamines appeared to be related to the severity of clinical course of myocardial infarction and were found in patients with cardiogenic shock, heart failure and arrhythmias. It is of interest that the peak elevation of plasma catecholamines correlated with the extent of myocardial damage as reflected by peak plasma CK activity and also correlated with acute and long-term mortality.(ABSTRACT TRUNCATED AT 250 WORDS)
Blood pressure, plasma renin activity, and serum aldosterone, adrenaline and noradrenaline were investigated in healthy individuals and patients with the primary moderate hypertension following a single oral dose of 10 mg nifedipine. It was found that the drug is hypotensive in both healthy individuals and hypertensive patients. It does not affect the effective plasma flow throughout the kidneys as well as serum aldosterone and adrenaline whereas serum noradrenaline and plasma renin activity are increased.
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In 27 patients with myasthenia thyroid function tests were done using radioassay methods. The levels of thyroxine (T4), triiodothyronine (T3), thyroxine-binding protein (BT4) and thyrotrophic hormone (TSH) were determined simultaneously in the serum. In 4 myasthenics the levels of T3 and T4 were determined after administration of exogenous TSH (Ambinon). The control group comprised 13 subjects without thyroid function disturbances. The investigations demonstrated a statistically significant decrease of T4 (at p less than 0.05) and T3 (at p less than 0.01) in myasthenia as compared with the control group. Administration of TSH raised the T3 level by 40% and that of T4 by 6%. The results obtained by the authors indicate presence of secondary hypothyroidism in myasthenia possibly due, to failure of the hypophyseo-hypothalamic system.
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