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R Traystman

Publications and source records attributed to R Traystman.

2 recordsLinked to original sources

Collateral ventilation.

Ventilation may bypass obstructed airways through collateral channels, including interalveolar pores of Kohn, bronchiole-alveolar communications of Lambert, and interbronchiolar pathways of Martin. Resistance through these channels, like resistance through small airways, increases with decreasing lung volume and with hypocapnia. But whereas the distention of collateral channels and small airways by a variety of factors is similar, the efficiency of ventilation through collateral channels is less than the efficiency through airways. Gas inspired through collateral channels is contaminated with alveolar gas from surrounding lung so that the dead space for collateral ventilation is increased. When one part of the lung ventilates out of phase with the surrounding lung, pulmonary interdependence promotes more homogeneous ventilation. In the presence of airways obstruction, interdependence may be a primary factor governing the rate of collateral ventilation. In man, collateral ventilation is unimportant in normal lungs. However, with disease, it may be critical in producing or compensating for abnormalities. For example, the long time constant for collateral ventilation in the middle lobe may be responsible for atelectasis, which results in the middle lobe syndrome. On the other hand, the short time constant for collateral ventilation in emphysema may be essential for the distribution of ventilation beyond obstructed airways.

Airway Resistance

Vascular interdependence in postmortem human lungs.

Interdependence of arteries and the surrounding lung was estimated in excised, postmortem human lungs. At low vascular pressures, vessel diameter increased as the lung was inflated. At high vascular pressures, vessel diameter decreased as the lung was inflated. Compared to the effects of interdependence in excised dog lobes, those in human lungs at low transpulmonary pressures were small. The following conclusions were reached: (1) the diameter of intrapulmonary arteries is stabilized (more constant with changes in intravascular pressure) when the lung has a high transpulmonary pressure; (2) increases in pulmonary vascular resistance at high lung volumes may be related to extra-alveolar, as well as intra-alveolar, vessel compression; (3) interdependence in human lungs differs markedly from interdependence in dog lungs.

Adolescent