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Biomedical subjects

E Moerman

Publications and source records attributed to E Moerman.

At least 37 records · Page 2Linked to original sources
PubMed1984

Hemodynamic and humoral effects of prostaglandin inhibition in exercising humans.

This double-blind placebo-controlled study investigated whether indomethacin-induced (500 mg/3 days) prostaglandin synthesis inhibition (PG inhibition) affected systemic hemodynamics and several humoral factors in nine sodium-replete normal humans, during exercise. Independent of the level of physical activity, PG inhibition was accompanied by small but significant (P less than 0.001) increases in systolic (+4.3 mmHg) and diastolic (+1.8 mmHg) intra-arterial pressure: the changes in cardiac output (determined noninvasively), systemic vascular resistance, and exercise capacity did not reach a level of statistical significance. After PG inhibition, plasma 13,14-dihydro-15-keto/prostaglandin F2 alpha, plasma renin, and aldosterone were reduced (P less than 0.001) at rest sitting and exercise, but PG inhibition did not prevent the exercise-induced stimulation of the plasma renin-aldosterone system. The urinary sodium excretion, averaging 156 meq/24 h during placebo, decreased (P less than 0.001) by 28 meq/24 h during PG inhibition: urinary aldosterone and kallikrein and the plasma catecholamines remained unchanged. In resting and exercising sodium-replete subjects, prostaglandins seem to exert a depressor effect on the systemic circulation and to increase plasma renin activity, but they are probably not involved in the exercise-related stimulation of the plasma renin-aldosterone system.

Adult↗
PubMed1984

Cardiovascular, metabolic and hormonal changes during isoflurane N2O anaesthesia.

Isoflurane was used in 10 ASA I or II female patients, undergoing hysterectomy. It was given at a constant inspired concentration of 1.3% in a 50% N2O/50% O2 mixture, after induction of anaesthesia using etomidate (0.3 mg kg-1) and intubation following pancuronium (0.1 mg kg-1). No analgesic supplement was given. The patients were hyperventilated minimally (PaCO2 4.7-5.3 kPa). At standardized times (before induction, after induction, 5', 25', 50' and 75' min after surgical incision, awake and awake +60'), cardiovascular (blood pressure, cardiac output, stroke volume, heart rate), respiratory (blood gases), metabolic (oxygen consumption, blood glucose) and hormonal (noradrenaline, adrenaline, cortisol, prolactin) changes were measured. Blood pressure changes were very moderate (mean values were lower than before induction), but heart rate was increased significantly. Decreases in stroke volume and changes in cardiac output were not significant. Oxygen consumption was decreased below basal values during surgery. Blood glucose levels increased significantly in the course of surgery and remained raised postoperatively. Adrenaline and noradrenaline levels increased significantly. At each examination time, cortisol levels were decreased significantly. Prolactin levels had decreased significantly 75 mins after incision and remained low 60 mins after awakening.

Adult↗
PubMed1984

The rabbit as an experimental model for biopharmaceutical studies following rectal administration of theophylline.

In order to find a suitable animal model for biopharmaceutical studies after rectal application of theophylline, the pharmacokinetics of theophylline following the administration in rabbits of three different rectal preparations were examined and compared with those of the oral and i. v. route. No significant formulation related impact from the studied rectal dosage forms on the bioavailability of the drug was found. However, the unexpected rapid achievement of peak serum concentration after insertion of the suppository lacked any correlation with human experiments. It was concluded that the evaluation of rectal theophylline medication for man cannot directly be based on the data obtained from rabbits.

Administration, Oral↗
PubMed1983

Effects of prostaglandin synthesis inhibition on blood pressure and humoral factors in exercising, sodium-deplete normal man.

A double-blind placebo-controlled study was carried out in 10 sodium-deplete normal men to determine whether prostaglandin synthesis inhibition (PG-inhibition) by indomethacin (150 mg daily for three days plus an additional 50 mg on the morning of the active experiments) affected blood pressure and humoral factors at exercise. Urinary sodium excretion during placebo averaged 39 mEq/24 h. Independent of the level of physical activity, PG-inhibition increased (P less than 0.001) intraarterial systolic pressure by 12 mmHg and mean and diastolic pressure by 5 and 3 mmHg, respectively. Heart rate, body weight and exercise capacity were not significantly changed. Following PG-inhibition plasma 13,14-dihydro-15-keto-prostaglandin F alpha, plasma renin, angiotensin II and aldosterone were reduced (P less than 0.001) to a similar degree at rest and exercise. However, PG-inhibition did not abolish the exercise related stimulation of the plasma renin-angiotensin-aldosterone system. PG-inhibition had no significant effect on the plasma catecholamines nor on the urinary excretion of aldosterone and kallikrein. Twenty-four-h urinary sodium (-15 mEq; P less than 0.01) decreased. In sodium-deplete subjects prostaglandins seem to exert a depressor action on the systemic circulation, and to have a tonic influence on the renin system. Both these effects are similar at rest and exercise. Prostaglandins are probably not involved in the exercise-induced stimulation of the plasma renin-angiotensin-aldosterone system.

Adult↗
PubMed1983

Effects of beta 1-adrenoceptor agonism on plasma renin activity in normal men.

The contribution of beta 1-adrenoceptors to the regulation of plasma renin activity was investigated in nine healthy sodium-replete volunteers: seven subjects received a cumulative intravenous dose of 75 micrograms/kg prenalterol, a predominant beta 1-adrenoceptor agonist, and two subjects only vehiculum. In the seven actively treated subjects beta 1-adrenoceptor agonism increased (P less than 0.001) systolic intra-arterial pressure by an average of 16 +/- 4 mm Hg and heart rate by 19 +/- 3 beats min. These increases were significantly (P less than 0.04) different from the changes observed in the two control subjects (+ 3 +/- 4 mm Hg and -1 +/- 4 beats/min, respectively). Plasma renin activity, however, tended to decrease in both the actively (-38%) and saline (-28%) treated subjects. Predominant beta 1-adrenoceptor agonism, powerful enough to increase systolic pressure and heart rate does not increase plasma renin activity in supine sodium-replete normal man.

Adrenergic beta-Agonists↗
PubMed1983

Influence of the stress of venepuncture on basal levels of plasma renin activity in infants and children.

The influence of venepuncture on plasma renin activity (PRA), cortisol, and serum noradrenaline and adrenaline concentration in infants and children was evaluated by comparing values obtained immediately on insertion of an indwelling intravenous line (venepuncture value) and 5 and 60 minutes later. PRA values 5 min after venepuncture in the total group of infants and children were significantly higher (P less than 0.001) than venepuncture values. There was no significant difference between PRA values at 60 min compared to venepuncture or 5 min values. A well performed venepuncture does not systematically affect the PRA values obtained. A significant difference between values for noradrenaline, adrenaline and cortisol at the various points of time could not be demonstrated. The number of lower values for noradrenaline and adrenaline at 60 min, however, prevailed. The stress of a well performed venepuncture is not an explanation for the greater scatter of basal PRA levels in infants and young children.

Age Factors↗
PubMed1980

Alpha- and beta-adrenoceptor blockade does not affect ventilation during exercise in man.

Alpha- and beta-adrenoceptor blockade does not affect ventilation during exercise in man. Med. Sci. Sports Exercise, Vol. 12, No. 5, pp. 375-379, 1980. Combined alpha- and beta-adrenoceptor blockade was used to study the role of the exercise induced stimulation of the adrenergic system on exercise hyperpnea. Twelve subjects performed an uninterrupted graded exercise test until exhaustion, before and during treatment with the alpha- and beta-adrenoceptor blocker labetalol. In the control study, plasma noradrenaline rose on the average 4.3 times during maximal exercise and plasma adrenaline 2.7 times, with similar data during labetalol. Labetalol did not affect oxygen uptake, carbon dioxide output, respiratory exchange ratio, pulmonary ventilation, nor the ventilatory equivalents for O2 and for CO2 at rest recumbent, at rest sitting, and during submaximal and maximal exercise, nor did it affect the anaerobic threshold. These findings do not substantiate a role for the adrenergic system in exercise hyperpnea in the conditions of the present study.

Adrenergic alpha-Antagonists↗
PubMed1979

Plasma theophylline level and effect on lung function after oral and rectal administration of aminophylline.

Twelve patients with partly reversible, chronic airway obstruction, according to a double blind randomized cross-over design, received on three consecutive days oral aminophylline 500 mg, a 500 mg aminophylline suppository and a placebo. The effects on ventilatory function were studied and the plasma concentration of theophylline was measured. After rectal administration, the plasma concentration of theophylline rose to 5 to 10 microgram/ml, and after oral ingestion the plasma level in most patients exceeded 10 microgram/ml. Administration of the aminophylline suppository resulted in moderate improvement in ventilatory function, and although the improvement was less pronounced than after oral administration, the use of a suppository in the treatment of patients with chronic obstructive lung disease should not be rejected.

Administration, Oral↗
PubMed1978

Effects of angiotensin antagonism at rest and during exercise in sodium-deplete man.

Mean intra-arterial pressure (P-), heart rate (HR), cardiac index (CI), total peripheral resistance index (TPRI), and plasma renin activity (PRA), norepinephrine (PNE), and epinephrine (PE) were estimated in five normal male subjects placed on a low-sodium diet for the previous 7 days. Subjects were studied during rest in recumbency and during intravenous infusion of either glucose or saralasin in a) recumbent position, b) sitting position on the bicycle ergometer, and c) during submaximal graded exercise. At rest recumbent saralasin induced pressure changes that were closely related to logPRA. During exercise the increase in P- was significantly lower during saralasin as compared to glucose from 110 W on, related to a greater reduction in TPRI. The increase of PRA during exercise was about three times greater with saralasin as compared to glucose, but the rises in PNE and PE were similar in both series of tests. Angiotensin II may thus have a role in the maintenance of P- in the supine sodium-deplete normal subjects, and stimulation of the renin angiotensin system during physical exercise contributes to a minor extent to the increase in P- in these conditions.

Angiotensin II↗
PubMed1975

Heat-labile enzymes in skin fibroblasts from subjects with progeria.

To characterize further the genetic basis of progeria, thermolability studies were performed on three genetically distinct enzymes in crude extracts of cultured skin fibroblasts derived from two subjects with that syndrome. At early passage the progeric fibroblasts, as compared to controls, contained a significantly higher percentage of heat-labile glucose-6-phosphate dehydrogenase (12.83 plus or minus 1.72 vs 1.11 plus or minus 0.44 [mean plus or minus S.E.M.], p smaller than 0.001), 6-phosphogluconate dehydrogenase (9.71 plus or minus 0.68 vs. 0.67 plus or minus 0.22, p smaller than 0.001), and hypoxanthine-guanine phosphoribosyltransferase (31.41 plus or minus 1.89 vs 7.67 plus or minus 1.71, p smaller than 0.001), and the differences were maintained throughout the in vitro life-span. These data, in conjunction with previous reports of defective HL-A antigens, indicate a widespread defect in genetic expression. The most likely cause appears to be an aberration in protein synthesis or degradation, or both, although multiple somatic mutations cannot be ruled out. Increased thermolability of enzymes in cultured cells may provide a screening test for persons predisposed to progeria and other disorders of premature aging.

Adult↗