Pulmonary Artery Distensibility Research Articles

Measurement of pulmonary arterial distensibility in the dog.

Pulmonary arterial pressure and flow, and pulmonary capillary flow have been measured in 13 dogs, breathing air. These parameters were also measured during ventilation with 10% oxygen in nitrogen, and during an intravenous infusion of serotonin. Pulmonary arterial distensibility and compliance were calculated from the recorded pressure-flow data. While the animals breathed air, distensibility and compliance averaged 3·32%/cm H2O and 1·42 ml./cm H2O respectively. These values were greatly reduced during hypoxia and serotonin infusion – both of which conditions led to an increase in pulmonary arterial resistance. Under physiological conditions, the time constant (CR) of the pulmonary arterial system remained constant over a wide range of pulmonary arterial resistance.

Wave transmission in the pulmonary arterial system in disease in man.

Pulmonary capillary blood flow was measured by the nitrous oxide-body plethysmograph technique in 21 patients with valvular heart disease or pulmonary thromboembolism during routine diagnostic cardiac catheterization. The studies were performed with a high-frequency phonocardiogram recorded from the pulmonary area to indicate the pulmonary valve opening at the beginning of right ventricular ejection. The pulmonary artery to capillary flow conduction time was measured from the time of pulmonary valve opening to the foot of the pulmonary capillary flow pulse. The conduction time was greater than 160 msec when the pulmonary artery pressure was normal. The fall in the conduction time in disease indicated elevated pulmonary arterial pulse wave velocity and this correlated well with the level of pulmonary arterial pressure (correlation coefficient 0.92, P < 0.001). This suggests that there is a reduced pulmonary arterial distensibility in the chronic pulmonary hypertension of valvular heart disease and thromboembolic disorders.

Propagation of blood flow pulse in the normal human pulmonary arterial system. Analysis of the pulsatile capillary flow.

We studied a number of dynamic events associated with the pulsatile flow of blood in the pulmonary arterial system of six healthy men in the supine position. We used the nitrous oxide-body plethysmograph method to record the pulmonary capillary blood flow pulse and the phonocardiogram to determine the time of opening and closing of the pulmonary valve. The pattern of right ventricular ejection was modified by administration of atropine and isoproterenol and by exercise. The time of conduction of the flow pulse from the pulmonary valve to the lung capillaries averaged 120 msec. Acceleration of capillary blood during systole averaged 8.2 ml/sec/msec. The fraction of stroke volume which distended the pulmonary arterial system during systole averaged 67.2%. The peak flow rate averaged 186 ml/sec. Tachycardia resulted in a decrease in the fraction of the stroke volume stored in the arterial tree during systole. Isoproterenol and exercise resulted in an increase in average capillary blood acceleration. Conduction time is accounted for by pulmonary arterial distensibility, which also allows storage of the ejected blood during systole, which in turn helps to maintain continuity of blood flow in the capillaries. Despite these modifying effects of the pulmonary arterial system upon the flow wave, changes in the pattern of inflow pulse were detectable in the capillary flow pulse.

Effects of occlusion and further distension of unilateral pulmonary artery with an inflatable balloon upon systemic and pulmonary hemodynamics.

Effects of occlusion and further distension of unilateral pulmonary artery with an inflatable balloon upon systemic and pulmonary hemodynamics.

Effects of sympathetic nerve stimulation on the pulmonary arterial tree of the isolated lobe perfused in situ.

The hemodynamic response to sympathetic nerve stimulation (SNS) was studied in canine lung lobes isolated in situ and perfused with a pulsatile pump. For the same input pulse, both the rate of rise and the rate of fall of pulmonary arterial pressure increased during SNS; the peak systolic pressure was also higher during SNS, whereas diastolic pressure levels were either at, or below, control levels. The increase in pulse pressure produced little or no change in mean pulmonary artery pressure and resistance. During SNS, compliance per unit length in large arteries fell, pulse wave velocity increased, and elastic modulus increased. Phenoxybenzamine produced opposite changes. Norepinephrine injections increased resistance and produced smaller compliance changes than SNS. Flow loads imposed by short bursts of rapid pump rate at constant stroke volume caused increments of vascular volume which returned to control levels after return to the slower rate. Volume increments were smaller and restoration rates faster during SNS than during control. After phenoxybenzamine, volume increments were larger and restoration rates slower than control. The results indicate that the distensibility of the large pulmonary arteries and the precapillary bed is decreased during sympathetic stimulation, while calculated resistance is not changed.

Pressure-volume response of isolated living main pulmonary artery in dogs.

Isolation of the main pulmonary artery by obturation of the right and left branches under conditions which maintained vasal circulation to the wall was achieved by extracorporeal circulation. Pressure-volume response of the segment was measured directly using a reciprocating essentially sinusoidal volume input at rates of 90, 45, and 180 cycles/min. Using volumes which generated physiologic pressures, a steady-state response starting from rest occurred in 300—500 cycles. At steady state the pressure-volume response was linear and unchanged by these cycling rates. The relaxation pattern during the initial phase was consistent with a single mode of response and closely duplicated the stress-relaxation pattern of a single noncycled input of the same volume. In 34 experiments in 11 animals steady-state volume distensibility (DeltaV x 100/V0 DeltaP) was 2.51% cm H2O. Segment geometry was preserved by luminal casting. An ellipsoidal configuration was apparent in the distended state. pulmonary-artery distensibility; mechanical behavior of arteries; stress-relaxation; geometry of arteries; tethering; viscoelastic properties of arteries; dynamic elastic response; coefficient of distensibility Submitted on June 16, 1964

Effects of unilateral pulmonary artery or vein distension with a balloon on the pulmonary and femoral arterial pressures in anesthetized dogs.

(1) Unilateral pulmonary artery or vein was distended by a balloon in closed and open chest anesthetized dogs. A part of the experiments was per-formed under perfusion of unilateral lung in situ. Persistent elevation in the pulmonary arterial pressure is always observed during distension of unilateral pulmonary artery as well as a pulmonary vein. Transient fall in the femoral arterial pressure is often observed at the initial stage. Following it, persistent slight decrease during the distension and rebounded rise after release of the distension are sometimes observed.(2) The increase in the mean pulmonary arterial pressure correlated with degree of distension of the pulmonary vascular wall. The maximal change in the mean pulmonary arterial pressure is about 6mm. Hg or about 37% increase in arterial distension and about 3mm. Hg or about 22% increase in venous distension. The fall in the femoral arterial pressure correlates with changes in the intraluminal pressure of the inflated balloon. The maximal change of the transient hypotension is about 6% decrease in arterial distension and about 19% decrease in venous distension. The maximal change of the following persistent hypotension is about 3% decrease in arterial distension and about 12% decrease in venous distension. The cardiac output shows about 9% reduction.(3) The pulmonary hypertension is concluded to be due to pulmonary vasoconstriction elicited by stimulation of stretch receptors in the pulmonary artery and vein. Participation of the vagal and sympathetic pathways is not proved. The changes in the femoral arterial pressure are also concluded to be due to both decrease in vascular tone and decrease of the cardiac output.