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Biomedical subjects

L Billiet

Publications and source records attributed to L Billiet.

At least 19 recordsLinked to original sources
PubMed1981

Phentolamine therapy in severe chronic asthmatiform bronchitis.

Continuous phentolamine infusion for 3 days in 6 patients with severe chronic bronchial obstruction produced a marked improvement in subjective well-being and arterial blood gas values. Ventilatory function and pulmonary arterial pressure remained virtually unchanged but a chronic oral corticosteroid therapy could be substantially reduced during 4 weeks of oral treatment with phentolamine 100 mg three times daily.

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

Emphysema with minor airway obstruction and abnormal tests of small airway disease.

In 9 patients complaining primarily of exertional dyspnea, the diagnosis of early emphysema was made on the basis of a decrease of the elastic recoil of the lung and of the single breath diffusing capacity, in the presence of only minor airway obstruction as estimated from the routine pulmonary function tests. Closing volume, the alveolar plateau, dynamic compliance and maximal flow at 50% of the vital capacity were markedly abnormal; the maximal flow-static recoil pressure relationships suggest, however, that none of the patients suffered from small airway disease. We conclude that one should systematically consider early emphysema in the differential diagnosis of small airway disease.

Adult↗
PubMed1978

Phentolamine infusion in cor pulmonale due to chronic obstructive pulmonary disease.

Continuous phentolamine infusion, produced a marked decrease in pulmonary arterial pressure and pulmonary vascular resistance with an increase in cardiac output, in the majority of a group of 13 patients with chronic obstructive pulmonary disease and cor pulmonale. Changes in vital capacity, forced expiratory volume in one second, arterial blood gas values and peripheral blood pressure were not significant except in one patient. The changes in the pulmonary circulation are probably due to the alpha blocking effect of phentolamine, although a direct effect of the drug on vascular smooth muscle can not be excluded.

Adult↗
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

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

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↗