A non-linear theory of the distribution of pulmonary ventilation.
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Biomedical subjects
Publications and source records attributed to M F Sudlow.
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1. The volume rate of forearm blood flow was measured with a mercury-in-rubber strain gauge, or with a water-filled plethysmograph, from 1 sec after termination of a 2-3 min period of venous congestion.2. When congesting pressure had been less than 18 mm Hg, average post-congestion flow (five subjects) was constant during approx. 10 sec and not significantly different from resting flow.3. When congesting pressure had been 30 mm Hg, average post-congestion flow (eight subjects) was 26% higher than resting, during 3-4 sec after release of congestion, but rose to 273% of resting during 4-6 sec after release of congestion.4. In other studies forearm vascular resistance had been found normal or increased during such venous congestion, and theoretical studies here indicated that passive mechanical factors could not account for the delayed occurrence of high post-congestion flow.5. It appears, therefore, that the forearm vascular bed dilates actively shortly after release of substantial venous congestion. It would seem more likely that a myogenic mechanism, rather than a metabolic one, is responsible.
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1. The pressure at the surface of a segment of forearm enclosed in a plethysmograph was abruptly reduced from atmospheric to -20 to -120 mm Hg.2. Forearm circumference (equivalent to the volume of a small segment of forearm (V(f))) was measured with a strain gauge. Pressure was measured in the plethysmograph (P(p)), in veins exposed (P(ve)) and not exposed (P(vne)) to suction, in the brachial artery not exposed to suction (P(bane)) and in forearm tissue (P(t)).3. Reduction of P(p) caused increase of V(f). This was not due to gas evolution, since bubbles would not be liberated at the pressures employed. Nor was increase of V(f) due to venous backflow since P(ve) fell, but P(vne) did not, even with upper arm circulation occluded or when P(vne) was raised by venous occlusion prior to reduction of P(p).4. Reduction of P(p) temporarily arrested venous outflow since P(ve) < P(vne) < P(bane) for 30 sec. With reduction of P(p) 30 sec after occlusion of the upper-arm circulation, P(ve) < P(vne) for > 1 min, indicating that arterial inflow was then minimal.5. Increase of V(f), following reduction of P(p), was therefore due to inflow of arterial blood, of soft tissue or interstitial fluid. Interstitial fluid could flow from regions external to the plethysmograph, or enter as the result of filtration across capillaries. Occlusion of the upper arm circulation was not expected to interfere with motion of forearm soft tissue or the intratissue flow of interstitial fluid. It appears that capillary filtration is small compared with observed blood flow. Therefore subtraction of V(foccl) measured at intervals after reduction of P(p) (upper arm circulation occluded) from V(f) similarly obtained (but upper arm circulation free) appeared to give change of forearm volume due to inflow of arterial blood (DeltaV(b)). V(b), the volume inflow rate of arterial blood during suction, was then obtained.6. Resting forearm flow was 1.8 ml./min/100 ml. in seven normal subjects (average mean arterial blood pressure 86 mm Hg). With P(p) = -90 mm Hg, V(b) was 10.2 ml./min/100 ml. Suction therefore reduced vascular resistance, measured as (P(bane)-P(ve)) /V(b).
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