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Biomedical subjects

L Cabanes

Publications and source records attributed to L Cabanes.

25 records · Page 2Linked to original sources
PubMed1990

Inflation of antishock trousers increases bronchial response to methacholine in healthy subjects.

We studied changes in lung volumes and in bronchial response to methacholine chloride (MC) challenge when antishock trousers (AST) were inflated at venous occlusion pressure in healthy subjects in the standing posture, a maneuver known to shift blood toward lung vessels. On inflation of bladders isolated to lower limbs, lung volumes did not change but bronchial response to MC increased, as evidenced by a greater fall in the forced expiratory volume in 1 s (FEV1) at the highest dose of MC used compared with control without AST inflation (delta FEV1 = 0.94 +/- 0.40 vs. 0.66 +/- 0.46 liter, P less than 0.001). Full inflation of AST, i.e., lower limb and abdominal bladder inflated, significantly reduced vital capacity (P less than 0.001), functional residual capacity (P less than 0.01), and FEV1 (P less than 0.01) and enhanced the bronchial response to MC challenge compared with partial AST inflation (delta FEV1 = 1.28 +/- 0.47 liter, P less than 0.05). Because there was no significant reduction of lung volumes on partial AST inflation, the enhanced bronchial response to MC cannot be explained solely by changes in base-line lung volumes. An alternative explanation might be a congestion and/or edema of the airway wall on AST inflation. Therefore, to investigate further the mechanism of the increased bronchial response to MC, we pretreated the subjects with the inhaled alpha 1-adrenergic agonist methoxamine, which has both direct bronchoconstrictor and bronchial vasoconstrictor effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Adrenergic betareceptors and cardiac insufficiency].

Noradrenergic sympathetic tone is always increased in chronic left ventricular failure of which it is one of the main compensatory mechanisms. Beta-1-adrenergic stimulation increases the heart rate and left ventricular contractility. However, the efficacy of this "compensatory" mechanism is limited on the one hand by the energetic cost of inotropic stimulation and, on the other hand, by the phenomenon of desensitisation and down-regulation of myocardial beta-1-receptors during intense and prolonged noradrenergic stimulation as observed in chronic cardiac failure. These physiopathological concepts raise the question of the indications of drugs affecting betareceptors in cardiac failure. Positive inotropic beta-mimetics can only be used during short periods of acute decompensation: low dose betablocker therapy protects the betareceptors from the phenomenon of desensitisation and seem to exert a beneficial action in this way in some cases of cardiac failure; these preliminary results require confirmation by large scale controlled therapeutic trials. Finally, a new pharmacological class of drugs, the beta-1 adrenergic partial agonists, seems to be useful in the management of moderate degrees of cardiac failure due to ischemic heart disease.

Adrenergic beta-Agonists↗
PubMed1990

[Mechanisms of exertion dyspnea in cardiac insufficiency].

Effort dyspnea in cardiac failure corresponds to a subjective perception of difficulty in breathing which is itself secondary to a disproportion between the central bulbar respiratory regulation and the level of pulmonary ventilation attained. In cardiac failure, this situation is the result of dysfunction of both the respiratory apparatus and the skeletal striated muscle during exercise. During exercise a rise in left ventricular end diastolic pressure causes: a reduction in pulmonary compliance. The bronchial and alveolar capillaries drain into the pulmonary veins. The congestion of these capillaries and the resulting oedema makes the lung "stiffer"; an increase in the resistances of the small airways due to direct compression by congested bronchial vessels. The physiological dead space increases: the respiratory muscles ventilate pulmonary zones which are not perfused to no benefit. The reduction of pulmonary compliance, the increased resistances of the airways and of the physiological dead space all contribute to increase the work of the respiratory muscles. In addition to these mechanical phenomena, there is greater stimulation of the respiratory centre in the brain stem by the metabolic abnormalities of the skeletal striated muscles. During effort, they rapidly function under anaerobic conditions and the resulting hyperproduction of lactate and carbon dioxide stimulates the respiratory centres.

Anaerobic Threshold↗
PubMed1990

[Vasomotility of the bronchial circulation in cardiac failure].

The bronchial circulation is a physiological left-to-left shunt; the venous return of the bronchial arteries vascularising the intra-pulmonary bronchi drains directly into the left heart chambers. In cardiac failure, increased left ventricular filling pressures affects the bronchial circulation and causes stasis and congestion. Congestion of the arterial and venous bronchial microcirculation leads to thickening of the bronchial mucosa and submucosa, resulting in a tendency to obstruct small and medium-sized airways. The bronchial circulation can be explored indirectly in cardiac failure by the spirometric response to adrenergic agonists and antagonists administered by inhalation: bronchial vasomotor phenomena explain the symptomatology of cardiac asthma and also seem to play a role in the genesis of the dyspnoea of effort in patients with cardiac failure.

Bronchi↗
PubMed1988

Systemic alkalosis as a provocative test for coronary artery spasm in patients with infrequent resting chest pain.

Systemic alkalosis was used to detect coronary spasm in 237 patients with infrequent, resting, angina-compatible chest pain. The provocative test was performed without previous coronary arteriography but only in patients with negative submaximal exercise test results. Rapid infusion of alkaline solution followed by maximal hyperventilation raised arterial pH above the 7.65 value necessary for diagnostic significance in 196 (83%) patients. In 24 (12%) of these patients the provocative test induced significant ischemic ST segment changes. In all patients with a positive response, coronary artery disease, which was predominantly vasospastic (19 patients) or atheromatous with a vasospastic contribution (five patients), was demonstrated by coronary arteriography followed, if necessary, by ergot derivative injection. Chest pain and ECG changes were always reversed within 5 minutes by intravenous nitroglycerin. Coronary arteriography was not performed in all patients with a negative response; therefore, the sensitivity of the procedure could not be assessed. However, 36 patients with a negative response to hyperventilation underwent coronary arteriography; 33 (92%) had normal arteriograms and a negative response to ergot derivatives. Hyperventilation appears to be a safe and specific diagnostic procedure in a subset of patients in whom the probability of coronary artery disease may not be judged sufficient to warrant coronary arteriography as a primary diagnostic approach.

Adult↗