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Biomedical subjects

T Reybrouck

Publications and source records attributed to T Reybrouck.

At least 55 records · Page 3Linked to original sources
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

Haemodynamic effects of captopril in hypertensive patients: comparison with saralasin.

1. Captopril (25 mg) reduced plasma angiotensin II (ANG II) by 53% (P less than 0.001) and mean brachial artery pressure (MBAP) by 18.7 mmHg (P less than 0.001) within 75 min in 26 hypertensive patients. After 2 months (on 150-600 mg/day) MBAP had decreased by 27.1 mmHg (n = 18) with no further change of plasma ANG II. delta MBAP was significantly related to control log plasm renin (PRA) and log ANG II in both conditions. 2. The acute depressor response to captopril was 11.2 mmHg greater (P less than 0.001) than delta MBAP during saralasin infusion (n = 12). 3. Heart rate slightly increased after acute administration of captopril (+3.3 beats/min; P less than 0.005), but cardiac output was not significantly affected; systemic vascular resistance decreased by 10% (P less than 0.01) with unchanged pulmonary vascular resistance. 4. During chronic administration, oxygen consumption, cardiac output and stroke volume increased by 15% (P less than 0.01), with unchanged heart rate; systemic vascular resistance had dropped by 30% (P less than 0.001). 5. Plasma ANG II and plasma aldosterone decreased, and PRA and ANG I increased acutely, with no further changes during chronic treatment.

Aldosterone↗
PubMed1978

Beta-blockers: once or three times a day?

In a double-blind, crossover trial 16 hypertensive patients were treated, in random order, with placebo, metoprolol 300 mg in a single daily dose, or metoprolol 300 mg/day in three doses. Both therapeutic regimens produced detectable plasma metoprolol concentrations and appreciable beta-blockade, estimated from exercise tachycardia, throughout the day. Fluctuations throughout the day in plasma drug concentrations and degree of beta-blockade were insignificant on the thrice-daily regimen, but they varied considerably on the single-dose regimen. Both therapeutic regimens also significantly lowered blood pressure throughout the day. Although the thrice-daily regimen again tended to produce a stronger and less fluctuating hypotensive action, the differences in hypotensive effect between the two regimens were not statistically significant. A single-dose of 300 mg of metoprolol can therefore be recommended if the only aim is to reduce blood pressure but not if a steady degree of beta-blockade is needed.

Adult↗
PubMed1978

Comparison of cardiac output determined by a carbon dioxide-rebreathing and direct Fick method at rest and during exercise.

1. To study the validity of a CO2-rebreathing method at rest and during graded exercise, cardiac output was measured simultaneously on 59 occasions in 16 subjects with normal pulmonary function with the CO2-rebreathing method and the direct Fick method for oxygen. The correlation coefficient between the results of both methods was significantly higher during exercise than at rest. 2. No systematic difference was shown between (a-v)CO2 content difference determined on whole blood and end-tidal gas, which justified the exclusion of a correction factor for blood to alveolar gas PCO2 gradients. 3. In the calculation of cardiac output by the direct Fick method for CO2 and by CO2 rebreathing, a standard CO2 dissociation curve was preferred to a synthetic CO2 dissociation curve, constructed by allowance for changes in haemoglobin concentration, pH and oxygen saturation. The latter curve tended to increase values for cardiac output and induced a large dispersion around the line of identity, when compared with simultaneous cardiac output estimates by the direct Fick method for oxygen.

Adult↗
PubMed1978

Effects of labetalol on systemic and pulmonary haemodynamics at rest and during exercise in hypertensive patients.

1. Labetalol was administered to 18 hypertensive patients for an average duration of 2.44 weeks, with an average final daily dose of 1.65 g. 2. Labetalol decreased resting heart rate by 16% and maximal exercise heart rate by 21%; the phenylephrine-induced rise of systolic brachial artery pressure was reduced by 36%. 3. During labetalol brachial artery pressure was lowered by 29/15 mmHg in the recumbent position, by 41/23 mmHg at rest sitting, and by 53/23 mmHg at maximal exercise; total peripheral resistance was not significantly affected at rest recumbent, but was reduced at sitting and at exercise; cardiac output decreased in all conditions. 4. Labetalol reduced mean pulmonary artery and capillary wedge pressures only in the sitting position. Pulmonary vascular resistance remained unchanged. 5. The drug produced significant decreases of plasma renin activity and of plasma aldosterone concentration.

Adult↗
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↗
PubMed1978

Effects of 1-sar-8-ala-angiotensin II on arterial pressure, renin and aldosterone in hypertension.

1-Sar-8-ala-angiotensin II did not change intra-arterial pressure in 25 sodium replete hypertensive patients, whilst the pressure changes were closely related to the plasma renin level during sodium depletion (r = -0.87; n = 32). The study indicates that arterial pressure is not dependent on angiotensin II in sodium replete patients and in sodium deplete subjects with low PRC, while it is angiotensin dependent during sodium depletion in the others. Plasma renin is unaffected in sodium replete subjects, but increases during saralasin in sodium deplete conditions. Saralasin stimulates aldosterone secretion only in sodium replete patients.

Adult↗
PubMed1978

Aging and the cardiovascular system.

With advancing age blood pressure rises in most populations with the exception of some isolated tribes. In western countries 30 to 40% of the people above the age of 60 years have casual blood pressure levels greater than or equal to 160/95 mm Hg. Advancing age per se produces a number of physiological changes related to blood pressure, such as a decrease in cardiac output, an increase in peripheral vascular resistance and a decrease in plasma renin-angiotensin-aldosterone levels. The mechanism causing the elevation in pressure with age are unknown though increased rigidity of the great vessels contributes to the rise in systolic pressure. There is a decline in the sensitivity of the baroreceptor reflex, but the contribution of this to the elevation of pressure has not be elucidated. Elderly patients with uncomplicated essential hypertension have a low cardiac output and high peripheral vascular resistance. The rise in blood pressure is associated with an increased cardiovascular morbidity and mortality even in the elderly hypertensives. The available data on the efficacy of hypotensive treatment in the elderly is scanty. There are no data proving that hypotensive therapy prolongs life. Controlled studies on the prevention of organ damage especially cerebrovascular accidents are inconclusive, showing either a significant decrease or no effect. Isolated reports illustrate, however, that drastic blood pressure reduction can provoke serious side effects, thus decreasing the quality of life. Hypotensive treatment is indicated in elderly hypertensive patients with hypertensive retinopathy grade III or IV, congestive heart failure or cerebral haemorrhage, in elderly patients with a markedly elevated diastolic blood pressure (greater than or equal to 120 mm Hg) and a trial of hypotensive therapy should be offered in milder forms of hypertension when it is accompanied by certain specific symptoms such as angina, headache and dyspnoe. The management of elderly hypertensive patients is more difficult than in the young. General measures are often not well accepted. The dose adjustment of the hypotensive agent is more critical and volume depletion or orthostatic hypotension are more likely to occur.

Aged↗
PubMed1977

Haemodynamic response to graded exercise during chronic beta-adrenergic blockade with bunitrolol, an agent with intrinsic sympathomimetic activity.

The effect of chronic beta blockade on the haemodynamic response to graded exercise was studied in 18 hypertensive patients treated with bunitrolol, which has partial agonist activity. The patients first received a placebo for 5 to 12 days, then bunitrolol 30 mg daily for one week and subsequently the dose was doubled weekly as necessary up to 240 mg daily. At rest haemodynamic changes after beta blockade were only minor; heart rate decreased by 8% and no significant change was observed in stroke index, cardiac index, (a-v)O2 difference and VO2. The hypotensive effect was not significant and no significant change in mean pulmonary arterial and wedge pressure was observed. Maximal exercise capacity remained unchanged, because of haemodynamic responses. The maximal exercise heart rate was reduced by 25% during beta blockade, which was compensated by a 34% elevation in stroke index, whereas maximal cardiac index and (a-v)O2 difference remained unchanged. There was no consistent change in mean pulmonary artery pressure during maximal exercise, but the mean brachial artery pressure fell by 12%.

Adult↗
PubMed1977

Hypotensive effects of sodium volume depletion and 1-sar-8-ala-angiotensin II in relation to plasma renin in hypertensive patients.

The hypotensive effect of acute sodium volume depletion, produced by chlorthalidone and a low sodium diet, was inversely related to the plasma renin concentration (PRC) in 13 hypertensive patients of varying aetiology (r = 0.61; p less than 0.05); weight reduction induced by this therapy was not related to PRC (r = 0.12; p greater than 0.1). The angiotensin II antagonist 1-sar-8-ala-angiotensin II failed to reduce arterial pressure when the patients ingested 130 mEq sodium per day, but pressure fell when it was infused during sodium volume depletion, except when PRC remained low; the changes in pressure were related to the plasma renin level (r = 0.78; p less than o.005). The combined hypotensive response to acute sodium volume depletion and to angiotensin II blockade during sodium volume depletion was not related to PRC (r = 0.15; p greater than 0.1). The results demonstrate that acute sodium volume depletion caused similar weight loss in patients with high and low PRC values, and it would have had similar hypotensive effects but for angiotensin-induced vasoconstriction in the high renin patients. Since 1-sar-8-ala-angiotensin II also reduced arterial pressure in 6 patients during chronic diuretic therapy, angiotensin II must still induce vasoconstriction in these circumstances.

Adult↗
PubMed1977

Relationship between blood level of atenolol and pharmacologic effect.

Thirty-five hypertensive patients were treated with atenolol in weekly increasing doses (25, 50, 100, and 200 mg thrice daily). Factors determining the blood level of the drug were studied along with the relationship between blood level, the degree of cardiac beta blockade, and the antihypertensive effect of the drug. The blood level obtained varied with the daily dose, the time of blood sampling during the day, the body weight, and the creatinine clearance. The degree of beta blockade was assessed by measuring maximum-exercise tachycardia and was correlated with the blood level of atenolol. The reduction of the maximum exercise heart rate was independent of age. The hypotensive effect was not closely correlated with the blood level. Three days after the termination of long-term atenolol treatment, blood levels and beta blockage were still detectable.

Adult↗