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Biomedical subjects

T Reybrouck

Publications and source records attributed to T Reybrouck.

71 records · Page 4Linked to original sources
PubMed1977

Plasma renin levels and systemic haemodynamics in essential hypertension.

1. Plasma renin concentration, intra-arterial pressure, cardiac output and total peripheral resistance have been studied in 50 patients with essential hypertension and normal renal function. 2. Total peripheral resistance and plasma renin were negatively correlated (r = -0-45), indicating that 'high-renin' essential hypertension is not necessarily associated with arteriolar vasoconstriction. 3. The inverse relation between mean arterial pressure and plasma renin (r = -0-46) suggests a role for the renal baroreceptor mechanism in the suppression of renin in 'low-renin' hypertension. 4. Cardiac output was positively related to plasma renin concentration (r = +0-42). 5. Multiple regression analysis indicates that the described relationships were independent of age.

Adult↗
PubMed1977

Effects of the angiotensin II antagonist 1-sar-8-ala-angiotensin II in hypertension in man.

The angiotensin II antagonist 1-sar-8-ala-angiotensin II (saralasin) was infused in forty-six patients with hypertension of various aetiology (essential, renal arterial or parenchymal disease, primary hyperaldosteronism), before and/or during sodium volume depletion obtained by chlorthalidone and low sodium diet. When saralasin was infused in twenty-five patients ingesting 130 mmol of sodium per day, including patients with proven renovascular hypertension, the changes in mean arterial pressure and ranged from +10 to -7 mmHg (mean: +0.20 mmHg) and were not related to the plasma renin concentration (PRC) (r = -0.11). During sodium volume depletion, saralasin induced changes in mean arterial pressure, ranging from +21 to -76 mmHg, which were closely related to log PRC (n = 32; r = -0.87). Combined sodium depletion and antagonism of angiotensin II 'normalized' mean arterial pressure (less than or equal to 100 mmHg) in twenty-one of the thirty-two patients, while pressure remained between 106 and 147 mmHg in eleven 'poor' responders, so that pressor mechanisms other than sodium volume and angiotensin must be responsible for the remaining elevation of pressure in these patients. The study indicates that arterial pressure is not dependent on the immediate pressor effects of angiotensin II in sodium replete patients, and in sodium deplete subjects whose PRC remains low, while it is at least partly angiotensin II dependent during sodium volume depletion in the others. The results cast doubts on the clinical usefulness of saralasin in the investigation of patients with hypertension, when studied in the conditions of the present study.

Adult↗
PubMed1977

Hemodynamic response to graded exercise after chronic beta-adrenergic blockade.

The effect of sustained beta-adrenergic blockade (BB) on the hemodynamic response to graded exercise has been studied in 31 patients with high blood pressure. Hemodynamic investigations were conducted during a control period and were repeated after 1 mo of BB. Similar readjustments were observed at rest and during submaximal and maximal exercise. No significant change occurred in maximal physical working capacity during beta blockade. This resulted from hemodynamic readjustments. Maximal exercise heart rate was reduced by 34%, and this was compensated for by a 31% enhancement in stroke index. Consequently cardiac index decreased by only 14%. In the Fick equation the decrease in cardiac index was further compensated by an increase of the total arteriovenous O2 difference of 8%, thereby maintaining O2 delivery to the tissues. At maximal exercise mean brachial artery pressure dropped 14.5%, while mean pulmonary artery pressure increased by 20%. It is concluded that the compensatory action of the stroke volume, resulting from the interaction of an increased preload and a decreased impedance, played a major role in the hemodynamic readjustments following chronic BB to maintain maximal working capacity.

Adult↗
PubMed1976

Comparative potency of atenolol and propranolol as beta-adrenergic blocking agents in man.

The comparative potency of two beta-blockers, propranolol and atenolol, in the inhibition of exercise tachycardia and isoproterenol-tachycardia has been studied in two groups of hypertensive patients, using oral doses which were increased weekly. A linear correlation was observed between the reduction in exercise tachycardia and the dose of each drug, up to a daily dose of propranolol 480 mg and atenolol 600 mg. Propranolol was slightly (0.7/1) more potent in decreasing maximal exercise tachycardia than atenolol when tested in low doses (below 100 mg); at higher doses (480 mg) no differences were found. However, atenolol was 10 times less potent than propranolol in blocking isoprenaline-induced tachycardia, which seems to be related to the cardioselectivity of atenolol.

Adult↗
PubMed1976

Mechanism of hypotensive effect during betaadrenergic blockade in hypertensive patients.

The mechanism of the hypotensive effect during beta-adrenergic blockade in hypertension was studied in 38 patients with renal or essential hypertension using the new cardioselective beta blocker, Tenormin. During 5 weeks hospitalization the patients received first a placebo for 5 to 12 days, then a 75 mg. dose of Tenormin was given daily for 1 week, and thereafter the dose was doubled weekly as necessary up to 600 mg. daily. The blood pressure decreased from 180 +/- 26.2/118. "/- 13.6 mm. Hg on placebo to 151 +/-25.5/96 +/-13.8 mm. Hg during the final hospitalization period on Tenormin (600 mg. daily). Six patients developed fluid retention and as this occurred blood pressure control was lost. A subsequent follow-up on an outpatient basis of 15 of the patients showed that when the active drug was replaced by a placebo blood pressure rose again, confirming that the initial fall in blood pressure was a genuine effect. Multistage bicycle ergometer exercise tests were performed at weekly intervals to test the degree of beta blockade and indicated that this was nearly complete when a dose of 600 mg. per day was used. A significant correlation between the hypotensive effect and the degree of beta blockade, assessed by exercise tachycardia, was observed. A slight but statistically significant decrease (26 per cent) was observed in the plasma renin concentration, measured recumbent in the morning. This decrease was, however, not correlated with the hypotensive effect of the drug. Although the cardiac output decreased significantly (from 5.5 +/-1.7 to 4.3 +/- 1.1 L per minute, p less than 0.001), no correlation was found in individual patients between the cardiac output and the blood pressure decrease. On the other hand, for the total group of catheterized patients (n = 28) the calculated total peripheral resistance did not change significantly. Yet a significant correlation was found between the changes in total resistance and the hypotensive effect. This suggests that the reaction of the peripheral vessels rather than the cardiac output decrease determines whether the drug will produce a major decrease of blood pressure in patients with hypertension.

Adult↗
PubMed1976

Haemodynamic effects of Sar1-Ala8-angiotensin II in patients with renovascular hypertension.

Sar1-Ala8-angiotensin II was infused intravenously (10 mug/kg/min) in 14 patients with renovascular hypertension, including 11 with renal artery stenosis. Brachial artery pressure and heart rate remained unchanged in six patients who were on a daily sodium intake of 130 mEq. In 12 tests performed after sodium depletion, the decrease in mean arterial pressure ranged from 13 to 76 mm Hg and showed a significant correlation with the plasma renin concentration prevailing immediately before the infusion of the drug (r = 0.81; p less than 0.001). The hypotensive response was due to a drop in total peripheral resistance. Heart rate and cardiac output showed slight increases 10 min after the start of saralasin infusion.

Adult↗
PubMed1976

The relationship between beta-blockade, hyporeninaemic and hypotensive effect of two beta-blocking agents.

In two consecutive series of hypertensive patients the hypotensive effect, the hyporeninaemic effect and the blockade of cardiac beta-receptors was studied using weekly increasing doses of propranolol or atenolol. With both beta-blockers, cardiac blockade and hypotensive effect increased in a parallel fashion when the dosage was increased suggesting that the hypotensive effect is related to cardiac beta-blockade. On the other hand lack of parallelism between the hypotensive effect and the hyporeninaemic effect suggests that the hypotensive effect was not related to a major extent to the hyporeninaemic effect of the drugs in the dosage range studied here.

Adrenergic beta-Antagonists↗
PubMed1975

Limitations to maximum oxygen uptake in arms, leg, and combined arm-leg ergometry.

Our purpose was to study the effect of arm, leg, and combined arm-leg ergometry on the oxygen uptake (Vo2), cardiac output (Q), ventilation, and anaerobic threshold (AT) of three healthy men. At submaximum work intensities, Vo2 was not significantly different in the three tasks, but differences were observed for heart rate, ventilation, and Q. The AT was reached at progressively higher work rates in arm, leg and combined arm-leg ergometry, respectively. The Vo2 max in arm ergometry averaged 68 percent of the Vo2max in leg ergometry and 60 percent of Vo2 max in combined arm-leg ergometry. Two subjects with Vo2max's less than 45 ml/kg-min had a mean Vo2max in combined arm-leg ergometry 19 per cent higher than in leg ergometry. A third subject, with a Vo2max greater than 50 ml/kg-min, showed no change. Differences in Vo2max were primarily due to the differences in Q. Skeletal muscle blood flow appears to be a critical factor in the limitation of Vo2max in arm or leg ergometry.

Adult↗