The relationship between the degree of pulmonary inflation and the pulmonary vascular resistance was studied in an open-chested dog preparation. It was possible to control the state of inflation and the blood flow to the lung under study. Vascular resistance could then be observed under controlled conditions. In most cases the resistance at complete collapse was very slightly higher than at moderate levels of inflation. In a few instances collapse was associated with a more marked elevation of resistance. Higher levels of inflation resulted in elevation of vascular resistance. At high levels of pulmonary blood flow and pulmonary arterial pressure, the flow resistance curve is lower than at low levels of blood flow. The resistance values obtained during deflation of the lung were consistently different at equal transpulmonary pressures from those obtained during inflation. The possible reasons for this hysteresis are discussed. Evidence is presented that the increased resistance at high levels of lung inflation is due to the effect of transpulmonary pressure on the vessels surrounding the alveoli. Submitted on January 11, 1960
A method has been developed by which flow to each lung, as well as pulmonary artery and left atrial pressures can be measured and varied at will. Vascular resistances were determined over a wide range of these variables. Both pressures have a marked effect on vascular resistances; the higher either pressure, the lower the resistances. This effect is most marked at low levels of pressure and flow. The absolute levels of the pressures, by affecting vascular distension, are major determinants of pulmonary vascular resistance.T HE existence of vasomotor activity in the pulmonary vascular bed is well established, though the degree and significance of such activity have been much debated. Recent interest has focused on the influence of hypoxia and drugs on pulmonary vascular reactions, and on changes of pulmonary vascular resistance associated with mitral stenosis and certain types of congenital heart disease. Confusion exists in this subject because of insufficient knowledge of the mechanical factors which influence resistance. Changes of vasomotor tone can be inferred only if the background of mechanical factors is sufficiently known. Since the pulmonary vascular bed is a highly distensible system, one would expect that changes of luminal pressure might have a large effect on resistance through changes of caliber of the system. Some information on this effect has been provided by the work of
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