The left lung from a dog was removed, ventilated with negative pressure, and perfused with venous blood. Pulmonary arterial, venous, and alveolar pressures could be varied over a large range. The distribution of blood flow in the lung was measured with Xe133. Under these conditions, there was no blood flow above the level at which alveolar equaled arterial pressure (measured at the arterial cannula). Below this level there was a linear increase in blood flow down the lung when the venous pressure was kept low. Raising the venous pressure made the distribution of flow more uniform below the level at which venous and alveolar pressures were equal although flow still increased down this zone. The flow distribution could be completely accounted for by the mechanical effects of the pressure inside and outside the blood vessels which each behaved like a Starling resistance. It was possible to simulate the flow distributions found in man in various physiological and diseased states. pulmonary; hydrostatic effect; Starling resistance Submitted on November 15, 1963
Simultaneous measurement of eight foreign gases in blood by gas chromatography. J . appl. Physiol. 36, 600-605. (1978) Ventilation-perfusion inequality in asymptomatic asthma. ABSTRACT EndocrinologyUse of modified hydrometer to assess immunoglobulins content in mare colostrum LEBLANC. MICHELLE M. Proc. Am. Ass. equine Pract. 31, 157-162.
Bleeding into the lungs in thoroughbreds is extremely common; there is evidence that it occurs in essentially all horses in training. However, the mechanism is unknown. We tested the hypothesis that exercise-induced pulmonary hemorrhage (EIPH) is caused by stress failure of pulmonary capillaries. Three thoroughbreds with known EIPH were galloped on a treadmill, and after the horses were killed with intravenous barbiturate the lungs were removed, inflated, and fixed for electron microscopy. Ultrastructural studies showed evidence of stress failure of pulmonary capillaries, including disruptions of the capillary endothelial and alveolar epithelial layers, extensive collections of red blood cells in the alveolar wall interstitium, proteinaceous fluid and red blood cells in the alveolar spaces, interstitial edema, and fluid-filled protrusions of the endothelium into the capillary lumen. The appearances were consistent with the ultrastructural changes we have previously described in rabbit lungs at high capillary transmural pressures. Actual breaks in the endothelium and epithelium were rather difficult to find, and they were frequently associated with platelets and leukocytes that appeared to be plugging the breaks. The paucity of breaks was ascribed to their reversibility when the pressure was lowered and to the fact that 60-70 min elapsed between the gallop and the beginning of lung fixation. Capillary wall stress was calculated from pulmonary vascular pressures measured in a companion study (Jones et al. FASEB J. 6: A2020, 1992) and from measurements of the thickness of the blood-gas barrier and the radius of curvature of the capillaries. The value was as high as 8 x 10(5) dyn/cm2 (8 x 10(4) N/m2), which exceeds the breaking stress of most soft tissues. We conclude that stress failure of pulmonary capillaries is the mechanism of EIPH.
A B S T R A C T A new method has been developed for measuring virtually continuous distributions of ventilation-perfusion ratios (VA/Q) based on the steadystate elimination of six gases of different solubilities. The method is applied here to 12 normal subjects, aged 21-60. In nine, the distributions were compared breathing air and 100% oxygen, while in the remaining three, effects of changes in posture were examined. In four young semirecumbent subjects (ages 21-24) the distributions of blood flow and ventilation with respect to VA/Q were virtually log-normal with little dispersion (mean log standard deviations 0.43 and 0.35, respectively). The 95.5% range of both blood flow and ventilation was from VA/Q ratios of 0.3-2.1, and there was no intrapulmonary shunt (VA/Q of 0). On breathing oxygen, a shunt developed in three of these subjects, the mean value being 0.5% of the cardiac output. The five older subjects (ages 39-60) had broader distributions (mean log standard deviations, 0.76 and 0.44) containing areas with VA/Q ratios in the range 0.01-0.1 in three subjects. As for the young subjects, there was no shunt breathing air, but all five developed a shunt breathing oxygen (mean value 3.2%,) and in one the value was 10.7%. Postural changes were generally those expected from the known effects of gravity, with more ventilation to high VA/Q areas when the subjects were erect than supine. Measurements of the shunt while breathing oxygen, the Bohr CO2 dead space, and the alveolar-arterial oxygen difference were all consistent with the observed distributions. Since the method involves only a short infusion of dissolved inert gases, sampling of arterial blood and expired gas, and measurement of cardiac output and minute venti-
Inhaled radioactive CO2 is rapidly taken up by pulmonary blood. By external counting over the chest during breath holding, the clearance rate of radioactive CO2xs from the counting field can be recorded, and is proportional to the regional perfusion. In normal subjects, the clearance rate varied from about 20%/ sec. at the base of the lung to virtually nil at the apex, and the change was approximately linear with distance up the chest. The difference between upper and lower zones was reduced on moderate exercise and eliminated when the subject lay on his back. By relating the counting rate at the end of inspiration to the volume of lung in the counting field, the difference in ventilation between upper and lower zones was measured and found to be small. Variation in ventilation-perfusion ratio was thus determined. Alveolar-arterial O2 gradient expected from this ventilation-perfusion ratio inequality was calculated to be about 4 mm Hg. This suggests that the variation in blood flow between upper and lower parts of the lung in erect man accounts for the whole of the ventilation-perfusion ratio inequality in the normal lung. Submitted on November 23, 1959
No abstract
We previously showed that when pulmonary capillaries in anesthetized rabbits are exposed to a transmural pressure (Ptm) of approximately 40 mmHg, stress failure of the walls occurs with disruption of the capillary endothelium, alveolar epithelium, or sometimes all layers. The present study was designed to test whether stress failure occurred more frequently at high than at low lung volumes for the same Ptm. Lungs of anesthetized rabbits were inflated to a transpulmonary pressure of 20 cmH2O, perfused with autologous blood at 32.5 or 2.5 cmH2O Ptm, and fixed by intravascular perfusion. Samples were examined by both transmission and scanning electron microscopy. The results were compared with those of a previous study in which the lung was inflated to a transpulmonary pressure of 5 cmH2O. There was a large increase in the frequency of stress failure of the capillary walls at the higher lung volume. For example, at 32.5 cmH2O Ptm, the number of endothelial breaks per millimeter cell lining was 7.1 +/- 2.2 at the high lung volume compared with 0.7 +/- 0.4 at the low lung volume. The corresponding values for epithelium were 8.5 +/- 1.6 and 0.9 +/- 0.6. Both differences were significant (P less than 0.05). At 52.5 cmH2O Ptm, the results for endothelium were 20.7 +/- 7.6 (high volume) and 7.1 +/- 2.1 (low volume), and the corresponding results for epithelium were 32.8 +/- 11.9 and 11.4 +/- 3.7. At 32.5 cmH2O Ptm, the thickness of the blood-gas barrier was greater at the higher lung volume, consistent with the development of more interstitial edema. Ballooning of the epithelium caused by accumulation of edema fluid between the epithelial cell and its basement membrane was seen at 32.5 and 52.5 cmH2O Ptm. At high lung volume, the breaks tended to be narrower and fewer were oriented perpendicular to the axis of the pulmonary capillaries than at low lung volumes. Transmission and scanning electron microscopy measurements agreed well. Our findings provide a physiological mechanism for other studies showing increased capillary permeability at high states of lung inflation.
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