Increased Pulmonary Vascular Resistance in the Dependent Zone of the Isolated Dog Lung Caused by Perivascular Edema

Little information is available on the pressurevolume relationship of the human pulmonary circulation. Observations have been almost exclusively confined to limited groups of cardiac patients (1-6) in whom coexistence of extravascular alterations, such as interstitial perivascular edema (7, 8), may hinder the interpretation of the results. On the other hand, extrapolation to man of animal studies on the pressure-volume characteristics of the whole pulmonary vascular bed or part of it is not always warranted because of species variation and wide experimental differences. Finally, the combined evaluation of pulmonary vascular resistance and transmural pressure may provide information on the distensibility of resistive vessels but does not allow deductions on the distensibility of the pulmonary circulation as a whole, since the distribution of volume does not parallel that of resistance.Previous reports have shown that the infusion of a plasma expander raised the pulmonary arterial and wedge pressures to the same extent (9); if the change in pressure was assumed to be practically uniform throughout the bed, such an infusion seemed to provide an opportunity to assess the compliance of the pulmonary vascular bed by determining the ratio of the change in volume to the change in pressure.The values of the distensibility of the pulmonary circulation obtained with dextran infusion during the first studies were thought to be exceedingly low. We then decided to test some drug that could enhance the distensibility of the pulmonary vascular bed. Atropine sulfate, which was

Section: Pulmonary Vascular Distensibilitymentioning

confidence: 99%

Pulmonary vascular distensibility and lung compliance as modified by dextran infusion and subsequent atropine injection in normal subjects.

Giuntini¹,

Maseri²,

Bianchi³

1966

“…For perfusion, Muir et al (23) found that gross alveolar edema was required for a reduction in local blood flow. Except at extremely low flows and arterial-venous differences (24), the distribution of blood flow in the isolated lung preparation is relatively insensitive to edema (22) (25). In the one preparation (lung 7) with severe edema, lower zone blood volume and flow was reduced relative to that in the middle and upper zones.…”

Section: Introductionmentioning

confidence: 96%

Distribution of extravascular fluid volumes in isolated perfused lungs measured with H215O.

Jones¹,

Jones²,

Rhodes³

et al. 1976

A B S T R A C T The distributions per unit volume of extravascular water (EVLW), blood volume, and blood flow were measured in isolated perfused vertical dog lungs. A steady-state tracer technique was employed using oxygen-15, carbon-11, and nitrogen-13 isotopes and external scintillation counting of the 511-KeV annihilation radiation common to all three radionuclides. EVLW, and blood volume and flow increased from apex to base in all preparations, but the gradient of increasing flow exceeded that for blood and EVLW volumes. The regional distributions of EVLW and blood volume were almost identical. With increasing edema, lower-zone EVLW increased slightly relative to that in the upper zone. There was no change in the distribution of blood volume or flow until gross edema (100% wt gain) occurred when lower zone values were reduced. In four lungs the distribution of EVLW was compared with wetto-dry ratios from lung biopsies taken immediately afterwards. Whereas the isotopically measured EVLW increased from apex to base, the wet-to-dry weight ratios remained essentially uniform. We concluded that isotopic methods measure only an "exchangeable" water pool whose volume is dependent on regional blood flow and capillary recruitment. Second, the isolated perfused lung can accommodate up to 60% wt gain without much change in the regional distribution of EVLW, volume, or flow. To date, measurements of extravascular lung water (EVLW) 1 in vivo have been limited to determinations for the lungs as a whole (3, 4), although some regional determinations have been made post mortem from lung biopsies (5). Measurements of total EVLW have used the double-indicator dilution technic (6). By using appropriate y-emitting tracers, detectable by external counting, regional measurements of EVLW could be made in vivo. However, tracer dilution technics are subject to extrapolation errors, and are perfusion-dependent; consequently the EVLW pool tends to be underestimated (7,8). An additional difficulty in using the indicator dilution techniques for a lung region is the need to determine the absolute blood flow through that zone.This paper presents a steady-state technique for obtaining the distribution of EVLW in the intact, isolated, perfused lung. The method rests on subtracting the steady-state distribution of blood volume, by using 11CO-labeled red cells, from that for water by using H2150 (9). The advantage of an equilibrium technique is that more time is available for the tracer to mix with the total exchangeable water pool; data analysis is simpler and less subjective than transit-time determination by extrapolation. Furthermore, by using an additional isotope, nitrogen-13, the distribution of regional blood flow can be obtained by arterial injection of "N2 in solution, and regional alveolar gas volume by rebreathing the lung with "N2 gas. Thus, with these isotopic procedures it is possible to compare the distribution of EVLW directly with that of regional blood flow, blood volume, and alveolar 'Abbreviations used in this paper: EVLW,...

“…Since the bulk flow of water in tissues does follow Starling's law, filtration coefficients have been found to be useful for comparing the permeability characteristics of different tissues (2). Filtration coefficients for the dog lung can be calculated from the data of groups I and II by substitution in Starling's law, assuming that the interstitial fluid pressure (Pif) approaches and exceeds zero as interstitial edema accumulates (23,25). The filtration coefficient, k, is expressed per square centimeter of capillary surface area; the alveolar surface area of the dog, approximately 50 m2 (33), is taken as an estimate of the pulmonary capillary surface area for the dogs of groups I and II, having an average body weight of 14 kg and an average dry lung weight of 23 g. For a (Pif -lrif) of zero, the filtration coefficient calculated from the mean data of group I is 0.12 x 10-8, and from the mean data of group II, 0.26 X 10-ml per second per cm2 per mm Hg AP.…”

Section: Introductionmentioning

confidence: 99%

The Application of Starling's Law of Capillary Exchange to the Lungs*

Levine¹,

Mellins²,

Senior³

et al. 1967

124

Summary. The forces governing the movement of water across the pulmonary capillaries were studied in 39 intact, spontaneously breathing dogs. A situation favoring the net movement of water out of the pulmonary capillaries was created by means of partial pulmonary venous obstruction (left atrial balloon catheter) followed by rapid saline hemodilution. A predetermined difference between pulmonary capillary and plasma colloid osmotic pressures was maintained for periods of 1 to 2 hours. Left atrial (PLA) and plasma colloid osmotic pressures (7rp1) were measured directly. The water content of the lungs was measured serially by an indicator-dilution technique, and at autopsy by drying the lungs. The rate of accumulation of lung water was measured in four groups of animals: in three of the groups, the capillary hydrostatic and colloid osmotic pressures were varied; in the fourth group, the right lymphatic duct was obstructed in addition.The average rate of water accumulation in the lungs varied in a nonlinear way with the level of the capillary hydrostatic-plasma colloid osmotic pressure difference and was unaffected by the level of the capillary hydrostatic pressure. At low levels of PLA -7rpl, water accumulated in the lung at an average rate of 0.09 g per g dry lung per hour per mm Hg pressure difference.At higher levels of PLA -7rpl the average rate of accumulation was 0.22 g per g per hour per mm Hg AP; in most of the experiments in this group water accumulated in the lungs slowly during the first 30 minutes of the test period and more rapidly as the period was extended. Obstruction of right lymphatic duct outflow did not alter the rate of water accumulation. Based on the control data of the present experiments, the pericapillary pressure in normal lungs is estimated to be of the order of -9 mm Hg in the normal dog lung. The filtration coefficient for the pulmonary capillaries is estimated to be of the order of one-tenth to one-twentieth of that for canine muscle capillaries. The data of the present study indicate that edema formation in lung tissue cannot be defined solely in terms of intravascular forces, but may be governed to a significant degree by changes in pericapillary forces in the pulmonary interstitium.