Biomedical subjects
M M Ibrahim
Publications and source records attributed to M M Ibrahim.
Limited value of the electrocardiogram in detecting hypertensive left ventricular hypertrophy.
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Studies on serum beta-glucuronidase activity and urinary tryptophan metabolites in human fascioliasis.
In the last few years, human fascioliasis has been reported more frequently from different parts of the world including Egypt. The present work aimed to study the ability of fascioliasis affected patients to metabolize tryptophan and to explore how this disease can affect the activity of the hydrolytic lysosomal enzyme beta-glucuronidase. Liver and kidney functions and complete blood pictures of the studied patients were considered. Eleven tryptophan metabolites together with 4-pyridoxic acid, the major metabolite of vitamin B6, were determined. Fascioliasis showed an abnormal pattern of tryptophan metabolism which resembled that described earlier by Kupke and Knapp and which indicated that those patients were suffering from vitamin B6 deficiency. This conclusion was proved by the decreased levels of 4-pyridoxic acid. Abnormally high levels of beta-glucuronidase were also encountered in the fascioliasis cases which points to the liver damage caused by the fluke.
Effect of the degree of effort on exercise echocardiography for the detection of restenosis after coronary artery angioplasty.
To determine whether the accuracy of exercise echocardiography is affected by the degree of effort during exercise, we examined 101 patients who had 6 months earlier undergone successful coronary artery angioplasty, with resting and immediate postexercise echocardiography and same-day coronary angiography. A positive exercise echocardiographic response was defined as the development of a new or worsening wall motion abnormality postexercise, compared with resting wall motion. Significant coronary disease (greater than 50% diameter stenosis) was present in 48 patients, 38 of whom had single-vessel disease and 10 of whom had two-vessel disease. Exercise echocardiography correctly identified 32 patients with significant disease (sensitivity 67%) and 44 patients without significant disease (specificity 83%). The effect of the degree of exercise effort on the sensitivity and specificity of the test was evaluated by three criteria; (1) the percentage of maximum predicted heart rate (MHR), (2) the duration of exercise (DUR), and (3) the double product (DP). To determine the influence of the degree of effort upon sensitivity and specificity, the effort criteria were compared between patients with true positive (TP) tests to those with false negative tests (FN), and in patients with true negative (TN) tests compared with those with false positive (FP) tests. No significant differences were detected in MHR, DUR, or DP between TP versus FN patients or between TN versus FP patients. These results indicate that for symptom-limited exercise echocardiography in postangioplasty patients, neither sensitivity nor specificity is significantly affected by the degree of effort during exercise.
Effect of gonadal steroid hormones on the metabolic rate of the cold-acclimated gonadectomized male and female Chalcides ocellatus (Forskal).
Male and female Chalcides ocellatus were gonadectomized and cold acclimated at 15 degrees for 1 week. Lizards were injected with testosterone and estradiol, and their oxygen consumption was determined at 15 degrees. Testosterone and estradiol caused a significant increase in the whole body rate of oxygen consumption in male and female lizards, respectively.
Effect of regression of left ventricular hypertrophy following sotalol therapy on diastolic function in hypertensive patients.
The effects of changes in left ventricular mass following beta-adrenergic blockade therapy (sotalol) on left ventricular filling indices were examined in 16 patients with essential hypertension aged 46 +/- 8.3 years (mean +/- s.d.). The peak atrial to peak early diastolic velocity (A:E) ratio and the peak filling rate (PFR = peak early diastolic velocity X mitral annulus area) were measured by the use of pulsed Doppler left ventricular inflow time-velocity plots following placebo and after 8-12 weeks of sotalol monotherapy (160 mg/day). Compared with normal controls of similar age, our patients had a larger left ventricular mass and impaired left ventricular filling indices. Following sotalol, mean arterial pressure (MAP) decreased by 14%, the heart rate by 15% and left ventricular mass by 11%, while diastolic filling improved (A:E 17% and PFR 21%). Six patients had a decrease in left ventricular mass of greater than 15% (group A); other patients (group B) showed a smaller reduction. In spite of comparable changes in MAP and heart rate in groups A and B, the patients in group A showed a smaller degree of improvement in the A:E ratio. It is concluded that sotalol can induce regression of left ventricular hypertrophy and improve left ventricular filling in hypertensive patients, and it seems that improvement in diastolic filling is related to a reduction in afterload rather than to a decrease in left ventricular mass.
Blood pressure responses to care procedures in ventilated preterm infants.
Responses of mean aortic blood pressure to sequences of routine care procedures in 22 ventilated, preterm infants were studied daily for the first 3 days of life. In the first 11 infants standard care procedures were used, whereas the next 11 infants were preoxygenated by a preceding 10% increase in inspired oxygen concentration; in these infants, chest physiotherapy was entirely omitted while the frequency of endotracheal suctioning was reduced. A total of 259 blood pressure responses were recorded. In general, responses were biphasic, consisting of an initial blood pressure drop followed by a greater blood pressure rise of longer duration. Baseline blood pressure, as well as the minimum and maximum blood pressure during the care procedures, increased with gestational age and with postnatal age. The blood pressure drop was most pronounced in the infants requiring the most intensive ventilatory support and was reduced by modifying the care procedures. The blood pressure rise was the least in the infants receiving pancuronium and phenobarbitone. Eight infants, 4 in each group, had intraventricular haemorrhage; in these infants, the care procedures induced more pronounced blood pressure drops in the first day of life when compared to the infants without haemorrhage.
Contractile performance following regression of left ventricular hypertrophy in hypertensive patients.
The left ventricular end systolic stress-end systolic dimension (ESS-ESD) relation was used to assess the effect of regression in left ventricular hypertrophy on myocardial contractility in 14 hypertensive patients (mean age 47 years) treated with guanfacine (a sympatholytic central alpha-adrenergic agonist) for 10 weeks. Echocardiography (M-mode under two-dimensional guidance) was used to determine left ventricular dimensions, posterior wall thickness (PWT) and septal thickness (ST) before and during the last week of therapy. Left ventricular mass (LVM) expressed as cross-sectional area (CSA) and meridianal wall stress at end systole were derived. Echocardiography was carried out at rest and during i.v. infusion of sodium nitroprusside to alter left ventricular afterload. A minimum of four systolic arterial pressure-ESD points were available for analysis and the value for the slope ESS-ESD was calculated for each patient. Guanfacine produced a significant decrease (P < 0.005) in arterial pressure, wall thickness and CSA. The linear ESS-ESD slope was similar in patients with and without left ventricular hypertrophy and did not change in the whole group or in four patients who had a decrease in CSA of > 10%. It is concluded that guanfacine can induce regression of left ventricular hypertrophy in hypertensive patients and that a decrease in LVM does not influence the intrinsic contractile performance of the left ventricular.
Traditional medical practices in some Somali communities.
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Maternal-fetal relationships in the parathyroidectomized rat. Intestinal calcium transport, serum calcium, immunoreactive parathyroid hormone and calcitonin.
We studied the role of the parathyroids in the adaptation of intestinal Ca transport that occurs during pregnancy, and whether maternal hypoparathyroidism causes fetal hyperparathyroidism. Serum Ca of pregnant parathyroidectomized (PTX) rats was significantly greater than nonpregnant, PTX animals. Intestinal active Ca transport was increased 2.1- and 2.2-fold by pregnancy in intact and PTX rats, respectively. Serum levels of immunoreactive parathyroid hormone (PTH) were nondetectable in PTX-pregnant rats. Fetuses from PTX rats appeared grossly normal. The serum PTH was not different in fetuses from PTX compared to fetuses from intact mothers and serum Ca, Mg, and P were normal. Thus, alleviation of maternal hypocalcemia during pregnancy in PTX rats may be due to an adaptive increase in intestinal Ca transport, which does not require the parathyroids. Fetuses from PTX mothers were euparathyroid and were protected from Ca deficiency during pregnancy.
Maintenance of normocalcemia by continuous infusion of the synthetic bovine parathyroid hormone (1-34) in parathyroidectomized rats.
This work was conducted to estimate the replacement dose of the synthetic bovine parathyroid hormone [PTH(1-34)] that is required for maintenance of serum calcium (Ca) in parathyroidectomized (PTX) rats. Male rats were PTX and used in this study only if serum Ca was reduced to at least 7 mg/dl. We found that a solution of 2% cysteine, 150 mM NaCl, and 1 mM HCL was superior to 20 mM acetic acid for maintenance of biological activity of PTH (1-34) in situ during the period of hormone infusion studied. The PTH dose-calcemic response relationship was investigated using PTH in doses of 0.6, 1, and 3 U/h. The infusion of 1 U PTH per hour raised Ca to the normal level, whereas rats infused with 0.6 U/h were hypocalcemic and 3 U/h resulted in marked hypercalcemia. To extend this observation we carried out an infusion of 1 U PTH per hour for 14 days. We found that this infusion rate of bovine PTH (1-34) provided a relatively stable level of serum calcium with modest fluctuation from normocalcemic to somewhat hypercalcemic levels for the entire 14-day period of PTH infusion. Serum calcitonin was also elevated during the infusion period and then returned to the initial level when PTH treatment was stopped. After the minipumps containing PTH were removed, the serum Ca dropped rapidly to 5 mg/dl, which was significantly lower than the control (vehicle-infused) or initial values of serum Ca (7 mg/dl). Infusion of PTH at 3 U/h for 4 days did not produce this rebound hypocalcemia after the pumps were removed. Serum Ca in those experiments returned to the initial level after hormone treatment was discontinued.
Some physiological changes during anesthesia for laparoscopy.
Twenty women studied for diagnostic or therapeutic laparoscopy with intraperitoneal insufflation of carbon dioxide. There were circulatory changes, dysrrhythmias, elevated central venous pressure and arterial blood pressure, hypercarbia, decrease in pH and increased peak air way pressure. With abdominal decompression all changes returned to within normal values.
Respiratory functions in late pregnancy.
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Factors influencing cardiac hypertrophy in hypertensive patients.
1. Seventeen male patients with essential hypertension were studied after 4 weeks of placebo and after 8 weeks of beta-adrenoceptor-blockade therapy with atenolol (100 mg/kg). 2. The influence of the following factors on left ventricular wall thickness and left ventricular mass index as determined by echocardiography was examined: patient's age, duration of hypertension, arterial pressure, blood pressure variability, supine heart rate, maximal exercise heart rate, left ventricular wall stress and 24 h urinary catecholamines. 3. Left ventricular mass index was related to systolic blood pressure (r = 0.54, P less than 0.05) and to extent of increase in heart rate with maximal exercise (r = 0.62, P less than 0.05). No significant correlation was present between mass index and other variables. 4. After atenolol therapy, left ventricular mass index decreased by 14 g/m2 (12%). Changes in mass were related to its initial value (r = 0.69, P less than 0.01) and to % change in wall stress (r = 0.64, P less than 0.05). Patients who had a decrease in mass index of 10% or greater had an initially lower diastolic pressure (P less than 0.001). Other factors did not appear to influence significantly the regression of hypertensive left ventricular hypertrophy.
Clinical evaluation of atenolol in hypertensive patients.
Atenolol, a cardioselective beta-adrenergic blocking agent, was given as the sole hypotensive drug for 8-12 weeks to 20 patients with hypertension of varying degrees of severity. Initial systolic blood pressure ranged from 162-238 mm Hg (mean +/- SEM 196 +/- 5.5 mm Hg) and diastolic blood pressure ranged from 105-143 mm Hg (118 +/- 2.5 mm Hg). Three patients had accelerated hypertension, six had cardiomegaly with recent exertional dyspnea and three were diabetics. Atenolol, 100-300 mg once daily, controlled both the supine and standing blood pressure and markedly attenuated the initial hypertensive response to severe exercise. In 17 patients (85%), atenolol therapy reduced blood pressure more than 20/10 mm Hg; however, adequate blood pressure control was not achieved in severe hypertension. A significant hypotensive action developed within 2 weeks of treatment, and control of hypertension was maintained for 2 weeks after sudden interruption of therapy. No patient had postural or postexercise hypotension. The drug appeared to exert its maximum hypotensive effect at the 100-mg dosage. The magnitude of the hypotensive response was related to the initial systolic blood pressure (r = 0.77, p less than 0.01) and the degree of inhibition of exercise tachycardia (r = 0.66, p less than 0.01). The atenolol plasma level and its hypotensive action were not related. Except for impairment of glucose tolerance in diabetic patients, atenolol had minimal side effects.
Effect of atenolol on left ventricular function in hypertensive patients.
1. Atenolol (100 mg/day) was given to 12 hypertensive patients for 8 weeks, and its effects on mean arterial pressure, cardiac index and ejection phase indices of myocardial performance were examined by echocardiography. 2. Echocardiographic studies were made before treatment after 4 weeks on placebo and repeated after 4 and 8 weeks of atenolol therapy. Mean arterial pressure fell by 14 and 21% after 4 and 8 weeks respectively. Cardiac index fell by 22 and 20%, and stoke index fell by 11 and 7%. Calculated peripheral resistance did not change significantly. 3. Ejection phase indices, namely fractional shortening, ejection fraction and normalized mean rate of circumferential fibre shortening, did not change. End-diastolic volume index did not change and there was no relationship between changes in heart rate and end-diastolic volume index. 4. The study shows that atenolol in the resting state has no effect on certain echocardiographic indices of left ventricular function when given orally to hypertensive patients with normal left ventricular size and function. The reduction in cardiac and stroke indices were presumably secondary to a decrease in cardiac venous filling.
Effect of atenolol on left ventricular function in hypertensive patients.
No information is available about the effects of oral atenolol, a cardioselective beta-adrenergic blocking agent with no intrinsic sympathomimetic activity, on left ventricular function. Atenolol, 100 mg/day, was given to 12 hypertensive patients for 8 weeks, and its effects on mean arterial pressure (MAP), cardiac index (CI) and ejection indexes of myocardial performance were examined by echocardiography. Echocardiographic studies were performed before treatment, after 4 weeks of placebo, and repeated after 4 and 8 weeks of atenolol therapy. MAP fell by 14% and 21% after 4 and 8 weeks, respectively. CI fell by 22% and 20% and stroke index (SI) fell by 11% and 7%. Calculated peripheral resistance did not change significantly. Fractional shortening, ejection fraction and normalized mean rate of circumferential fiber shortening did not change. The normalized mean posterior wall velocity decreased after 4 weeks but returned to pretreatment levels after 8 weeks. The septal velocity increased after 8 weeks. End-diastolic volume index (EDVI) did not change, and there was no relationship between changes in heart rate and EDVI. The study shows that atenolol in the resting state has no effect on certain echocardiographic indexes of left ventricular (LV) function when given orally to hypertensive patients with normal LV size and function. The reduction in CI and SI were presumably secondary to a decrease in cardiac venous filling.
Effects of prostaglandin F2 alpha on blood constituents and certain hormones in Najdi sheep.
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