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Biomedical subjects

C Lenfant

Publications and source records attributed to C Lenfant.

At least 127 records · Page 7Linked to original sources
PubMed1983

A new method for measurement of respiratory resistance.

A new method for measuring the resistance of the total respiratory system is presented. The method uses a device comprising a solenoid valve, a multiperforated plate, and a pneumotachograph. The multiperforated plate serves as a constant resistor (Rk) that is used to partially occlude the airway opening, thus rapidly and briefly reducing airflow during natural expiration. If it is assumed that the driving pressure remains constant during the very short period the airway is partially occluded, the respiratory flow immediately preceding the addition of Rk (V) and the flow reduction during partial occlusion (delta V) allow calculation of the resistance of the total respiratory system. The resistance of 14 normal subjects and 18 patients with chronic obstructive pulmonary disease (COPD) was measured with this new method as well as with the body plethysmographic method: 90% of the interrupter values fell within +/- 0.6 cmH2O . l-1.s of the plethysmographic values, and all fell within +/- 0.8 cmH2O . l-1.s.

Airway Resistance↗
PubMed1980

Prostaglandin F-2 alpha functions as a local hormone on human airways.

Vasoactive hormones may be classified either as 'local' or as 'circulating', depending on whether they are or are not removed by the pulmonary circulation. Prostaglandin F-2 alpha is partially removed by the human pulmonary circulation. We examined the hypothesis that, with respect to the human lung, PGF-2 alpha functions as a local mediator. Prostaglandin F-2 alpha was given to normal and asthmatic subjects via both intravenous and aerosolized routes, and we measured specific airway conductance, spirometry, functional residual capacity, and closing volume. Aerosolized PGF-2 alpha induced significant changes of all measured parameters in both normals and asthmatics, while intravenous PGF-2 alpha-induced changes were limited to the FVC in both normals and asthmatics. The data suggest that intravenous PGF-2 alpha induced constriction of peripheral lung units. The greater sensitivity of the peripheral lung units of asthmatics versus normals to PGF-2 alpha, suggest that the increased sensitivity of airway smooth muscle of asthmatics versus normals to PGF-2 alpha is not restricted to the conducting airways, but extends to the smooth muscle of the peripheral lung units. The data is consistent with the hypothesis that, with respect to the lung, PGF-2 alpha functions as a local hormone, but, furthermore, suggest that, possibly of greater importance than the definition of a hormone as 'local' or 'circulating', is the definition of the intrinsic properties of the muscles on which the hormone is exerting its effects.

Adolescent↗
PubMed1978

Effect of acute and established anemia on O2 transport at rest, submaximal and maximal work.

Effects of acute and maintained isovolemic anemia on oxygen transport was studied during rest and exercise in normal males. Following 34% reduction in hemoglobin concentration (Hb), supine and standing Q rose acutely by 56% and 20%, respectively, but returned nearly to the control value by 10-14 days, producing a decrease in PVO2. Redistribution of blood flow appeared to compensate significantly for the decrease in systemic oxygen transport. 2,3-Diphosphoglycerate rose by 18%, in vivo PO2 at half-saturation of hemoglobin (P50) rose by approximately 2 mm over 7-9 days and probably afforded some compensation. The relationship between VO2 and external work intensity was independent of Hb. During exercise, Q/VO2 and VE/VO2 were increased in acute anemia, but PVO2, for a given VO2, decreased below control levels. After 10-14 days the relative increase in VE with exercise persisted; the increase in Q was less pronounced; and PVO2 was further decreased. With both acute and extablished anemia maximal exercise capacity and maximal VO2 (VO2 max) decreased in proportion to the Hb reduction.

Acute Disease↗
PubMed1977

The influence of atropine and cromolyn on human bronchial hyperreactivity to aerosolized prostaglandin F2 alpha.

The mechanism of prostaglandin F2 alpha(PGF2alpha)-induced airway constriction was explored by determining the influence of atropine and cromolyn on the bronchoconstrictive properties of PGF2alpha. Increasing doses of aerosolized PGF2alpha were given (150, 300, 600, 1200 microgram) and the response of subjects was determined by measurements of spirometry, specific airway conductance (SGaw), and closing volumes. In normal subjects, PGF2alpha induced small but significant decreases of SGaw and spirometric parameters (FVC, FEV1), whereas there was no effect on the closing volumes. In contrast, in asthmatics, PGF2 alpha induced large decreases of SGaw and spirometric parameters. Asthmatics experienced severe and prolonged shortness of breath and wheezing, whereas normal controls experienced neither. Neither atropine nor atropine plus cromolyn was capable of preventing or substantially reversing the PGF2alpha-induced symptoms and airway constriction. The data suggest that reflex bronchoconstriction via irritant receptors is not a major mechanism of PGF2alpha-induced airway constriction. Although a minor vagally mediated reflex component may participate in the PGF2alpha-induced bronchoconstriction, it is masked by an overwhelming non-reflex mechanism that is probably a direct constricting effect of airways smooth muscle that is exquisitely sensitive to PGF2alpha.

Adolescent↗