Elasticity of Small Pulmonary Veins in the Cat

1981 ◽  
Vol 103 (1) ◽  
pp. 38-42 ◽  
Author(s):  
R. T. Yen ◽  
L. Foppiano
Keyword(s):  
Venous Pressure ◽  
Pulmonary Veins ◽  
Air Pressure ◽  
Pleural Pressure ◽  
Lung Inflation ◽  
Alveolar Air ◽  
Compliance Coefficient

The distensibility of pulmonary veins of cats, in the diametric range of 100–1200 μm, was studied as a function of the venous pressure pv and pleural pressure pPL, while the alveolar air pressure was maintained at zero (atmospheric). The resulting percentage changes in diameter normalized with respect to the diameter at ΔP of 10 cm H2O (D10) are expressed as function of ΔP = pv − pPL. It was found that in most cases the diameter varies linearly with ΔP: D/D10=1+α(pv−pPL) where α is the compliance coefficient. The results show that smaller veins of the cat are more compliant than larger veins. For example, when pleural pressure is −10 cm H2O, the values of α for vessels in the ranges of diameters of 100–200 μm, 200–400 μm, 400–800 μm and 800–1200 μm are, respectively, 2.05, 1.44, 1.08 and 0.71 percent per cm H2O or Pa−1. The effects of lung inflation on the distensibility of pulmonary veins are also studied. Our results show that for vessel sizes in the range of 400–800 μm and 800–1200 μm the compliance constant α is not affected by inflation of the lungs (changes in pleural pressure to more negative values). For smaller veins in the size ranges 100–200 μm and 200–400 μm our results show an increase in compliance from 2.05 to 2.79 and from 1.44 to 2.01 percent per cm H2O or Pa−1, respectively, when pleural pressure is changed from −10 to −15 cm H2O. When the pleural pressure is more negative than −15 cm H2O, however, the compliance of the vessels in the foregoing two size ranges is observed to decrease.

Effect of lung inflation on pulmonary vascular resistance by arterial and venous occlusion

1982 ◽  
Vol 53 (5) ◽  
pp. 1110-1115 ◽  
Author(s):  
T. S. Hakim ◽  
R. P. Michel ◽  
H. K. Chang
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Venous Occlusion ◽  
Lung Inflation ◽  
Pressure Drops ◽  
Constant Flow Rate ◽  
Initial Decrease ◽  
Occlusion Technique ◽  
First Time

To explain the changes in pulmonary vascular resistance (PVR) with positive- and negative-pressure inflation (PPI and NPI, respectively), we studied their effects in isolated canine left lower lobes perfused at constant flow rate. The venous pressure was kept constant relative to atmospheric pressure during lung inflation. The total arteriovenous pressure drop (delta Pt) was partitioned with the arterial and venous occlusion technique into pressure drops across arterial and venous segments (large indistensible extra-alveolar vessels) and a middle segment (small distensible extra-alveolar and alveolar vessels). PPI caused a curvilinear increase in delta Pt due to a large Starling resistance effect in the alveolar vessels associated with a small volume-dependent increase in the resistance of alveolar and extra-alveolar vessels. NPI caused an initial decrease in delta Pt due to reduction in the resistance of extra-alveolar vessels followed by an increase in delta Pt due to a volume-dependent increase in the resistance of all vessels. In conclusion, we provided for the first time evidence that lung inflation results in a volume-dependent increase in the resistance of both alveolar and extra-alveolar vessels. The data suggest that while the volume-related changes in PVR are identical with PPI and NPI, there are pressure-related changes that can be different between the two modes of inflation.

scholarly journals Estimation of change in pleural pressure in assisted and unassisted spontaneous breathing pediatric patients using fluctuation of central venous pressure: A preliminary study

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0247360
Author(s):  
Nao Okuda ◽  
Miyako Kyogoku ◽  
Yu Inata ◽  
Kanako Isaka ◽  
Kazue Moon ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Spontaneous Breathing ◽  
Pediatric Patients ◽  
Venous Pressure ◽  
Balloon Catheter ◽  
Pleural Pressure ◽  
Respiratory Effort ◽  
Central Venous ◽  
Mechanically Ventilated ◽  
Esophageal Balloon

Background It is important to evaluate the size of respiratory effort to prevent patient self-inflicted lung injury and ventilator-induced diaphragmatic dysfunction. Esophageal pressure (Pes) measurement is the gold standard for estimating respiratory effort, but it is complicated by technical issues. We previously reported that a change in pleural pressure (ΔPpl) could be estimated without measuring Pes using change in CVP (ΔCVP) that has been adjusted with a simple correction among mechanically ventilated, paralyzed pediatric patients. This study aimed to determine whether our method can be used to estimate ΔPpl in assisted and unassisted spontaneous breathing patients during mechanical ventilation. Methods The study included hemodynamically stable children (aged <18 years) who were mechanically ventilated, had spontaneous breathing, and had a central venous catheter and esophageal balloon catheter in place. We measured the change in Pes (ΔPes), ΔCVP, and ΔPpl that was calculated using a corrected ΔCVP (cΔCVP-derived ΔPpl) under three pressure support levels (10, 5, and 0 cmH2O). The cΔCVP-derived ΔPpl value was calculated as follows: cΔCVP-derived ΔPpl = k × ΔCVP, where k was the ratio of the change in airway pressure (ΔPaw) to the ΔCVP during airway occlusion test. Results Of the 14 patients enrolled in the study, 6 were excluded because correct positioning of the esophageal balloon could not be confirmed, leaving eight patients for analysis (mean age, 4.8 months). Three variables that reflected ΔPpl (ΔPes, ΔCVP, and cΔCVP-derived ΔPpl) were measured and yielded the following results: -6.7 ± 4.8, − -2.6 ± 1.4, and − -7.3 ± 4.5 cmH2O, respectively. The repeated measures correlation between cΔCVP-derived ΔPpl and ΔPes showed that cΔCVP-derived ΔPpl had good correlation with ΔPes (r = 0.84, p< 0.0001). Conclusions ΔPpl can be estimated reasonably accurately by ΔCVP using our method in assisted and unassisted spontaneous breathing children during mechanical ventilation.

Pressure outside the extrapulmonary airway in dogs

1978 ◽  
Vol 45 (3) ◽  
pp. 437-441 ◽  
Author(s):  
S. G. Spiro ◽  
B. H. Culver ◽  
J. Butler
Keyword(s):  
Lung Volume ◽  
Standing Position ◽  
Pleural Pressure ◽  
Positive Pressure ◽  
Anterior Surface ◽  
Lung Inflation ◽  
Airway Narrowing ◽  
Thin Fluid ◽  
Airway Pressures ◽  
Anesthetized Dogs

We have measured the static and dynamic transmural pressures of extrapulmonary airways during positive pressure lung inflation in anesthetized dogs suspended in the standing position. Thin, fluid-filled catheters measured pressures within and on the anterior surface of the airways in the mediastinum and neck. The change from mediastinal to cervical static extra-airway pressures (Pea) was not abrupt but occurred through the thoracic outlet and the root of the neck. The static Pea in the mediastinum was more positive than pleural pressure when lung volume was increased with positive pressures. During forced deflation equal pressure points (EPP) were in labor bronchi from which airway narrowing extended towards the mouth. Under these conditions, the dynamic mediastinal Pea mouthward of the EPP remained close to pleural pressures even at high volumes. This suggested that forces of restitution generated in the surrounding tissues by the narrowing of the airways did have a small effect in reducing the pressure affecting their anterior surface.

THE PHYSIOLOGICAL MECHANISMS OF THE PULMONARY VENOUS HYPERTENSION

2018 ◽  
Vol 18 (2) ◽  
pp. 7-18
Author(s):  
V I Evlakhov ◽  
I Z Poyassov ◽  
V I Ovsyannikov
Keyword(s):  
Pulmonary Hypertension ◽  
Venous Pressure ◽  
Pulmonary Veins ◽  
Left Ventricular ◽  
Venous Hypertension ◽  
Physiological Mechanisms ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial ◽  
Mechanisms Of Development ◽  
Trigger Mechanisms

In the review regulatory mechanisms of functions of pulmonary venous vessels have been considered as well as the signifi cance of their impairment in the development of the pulmonary hypertension, caused by the left ventricular cardiac failure. One of the trigger mechanisms of the development of the pulmonary hypertension as a result of the elevation of the left atrial and pulmonary venous pressure is the reflectory constriction of the pulmonary arterioles (Kitayev’s reflex). Further, the development of endothelial dysfunction and pulmonary vessels remodeling with the phenomenon of “arterializations” of the pulmonary veins take place. The exact evaluation of the pulmonary vascular resistance value in the clinical practice is a difficult task. This parameter, being integrated, does not allow to evaluate the resistance values of pulmonary arterial and venous vessels in the conditions of pulmonary hypertension and to give exact characteristics of their changes, as a result. The mechanisms of development of the pulmonary venous hypertension could not be explicated using the simplified model of the pulmonary vasoconstriction, because the main features of the pulmonary circulation are the presence of arteriovenous and bronchopulmonary shunts, and pulsatile character of the blood flow. To understand the exact pathogenesis of this pathology the further fundamental investigation not only on the cell level, but also on organ and system levels are needed.

Regional differences in alveolar density in the human lung are related to lung height

2015 ◽  
Vol 118 (11) ◽  
pp. 1429-1434 ◽  
Author(s):  
John E. McDonough ◽  
Lars Knudsen ◽  
Alexander C. Wright ◽  
W. Mark Elliott ◽  
Matthias Ochs ◽  
...  
Keyword(s):  
Pressure Gradient ◽  
Regional Differences ◽  
Volume Fraction ◽  
Transpulmonary Pressure ◽  
Pleural Pressure ◽  
Lung Inflation ◽  
Residual Capacity ◽  
Alveolar Duct ◽  
The Difference

The gravity-dependent pleural pressure gradient within the thorax produces regional differences in lung inflation that have a profound effect on the distribution of ventilation within the lung. This study examines the hypothesis that gravitationally induced differences in stress within the thorax also influence alveolar density in terms of the number of alveoli contained per unit volume of lung. To test this hypothesis, we measured the number of alveoli within known volumes of lung located at regular intervals between the apex and base of four normal adult human lungs that were rapidly frozen at a constant transpulmonary pressure, and used microcomputed tomographic imaging to measure alveolar density (number alveoli/mm3) at regular intervals between the lung apex and base. These results show that at total lung capacity, alveolar density in the lung apex is 31.6 ± 3.4 alveoli/mm3, with 15 ± 6% of parenchymal tissue consisting of alveolar duct. The base of the lung had an alveolar density of 21.2 ± 1.6 alveoli/mm3 and alveolar duct volume fraction of 29 ± 6%. The difference in alveolar density can be negated by factoring in the effects of alveolar compression due to the pleural pressure gradient at the base of the lung in vivo and at functional residual capacity.

Development of portacaval shunts in portal-stenotic cats

1993 ◽  
Vol 71 (9) ◽  
pp. 671-674 ◽  
Author(s):  
Andres C. Inglés ◽  
Dallas J. Légaré ◽  
W. Wayne Lautt
Keyword(s):  
Portal Hypertension ◽  
Portal Vein ◽  
Experimental Model ◽  
Renal Vein ◽  
Left Renal Vein ◽  
Venous Pressure ◽  
Homogeneous Model ◽  
Pulmonary Veins ◽  
Inferior Mesenteric Vein ◽  
Mesenteric Vein

The goal of the present study was to investigate the formation of portacaval shunts in a new experimental model of chronic portal hypertension, portal vein stenosis in the cat. The procedure gradually occluded the portal vein by use of an Ameroid constrictor around the portal vein. After 4 weeks, the portal vein was completely occluded and portal venous pressure was elevated to 15.6 ± 0.3 mmHg (1 mmHg = 133.3 Pa) (n = 8). The hemodynamic changes did not affect the functional capacity of the liver. Latex injection was used to study the shunts. This revealed the spontaneous development of porta-systemic collaterals in all hypertensive cats, mainly between the gastrosplenic and right gastroepiploic veins and the left renal vein. Fine small branches also drained directly into the cava. The left renal vein was markedly dilated in all cats. Collateral circulation also developed between the inferior vena cava and the inferior mesenteric vein through both left internal testicular and iliolumbar veins. Some branches of the inferior mesenteric vein were connected directly to the cava. Esophageal varices in the mucosa or submucosa were not demonstrated. However, the presence of latex in the pulmonary veins and the visualization of periesophageal collaterals suggest the opening of porta-pulmonary shunts. A constant feature in all cats was the presence of a dilated azygos vein, which drained collaterals retroperitoneally and from the abdominal wall. In conclusion, an experimental model of prehepatic portal hypertension of gradual onset has been developed in cats. The formation of the porta-systemic shunts mimics other animal models and the human form of the disease. It is a homogeneous model and easily reproducible.Key words: portal hypertension, porta-systemic shunts, portal stenosis, Ameroid constrictor, cat.

Response of pulmonary veins to increased intracranial pressure and pulmonary air embolization

1980 ◽  
Vol 48 (6) ◽  
pp. 957-964 ◽  
Author(s):  
B. T. Peterson ◽  
S. E. Grauer ◽  
R. W. Hyde ◽  
C. Ortiz ◽  
H. Moosavi ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Edema ◽  
Left Atrial ◽  
Venous Pressure ◽  
Pulmonary Veins ◽  
Venous Hypertension ◽  
Increased Intracranial Pressure ◽  
Anesthetized Dogs ◽  
Brain Compression ◽  
End Tidal

Brain compression with subdural air causes pulmonary hypertension and noncardiogenic pulmonary edema (A. B. Malik, J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 42: 335-343, 1977). To see whether air emboli to the lungs rather than brain compression caused these findings, anesthetized dogs received intravenous air infusions, subdural air infusions, or brain compression from balloons inflated in the subdural space. Subdural air and intravenous air resulted in similar vascular responses. Pulmonary artery pressure (Ppa) increased 160% (P less than 0.01) and pulmonary venous pressure transiently rose 13 +/- 5 Torr (P less than 0.05) without an increase in left atrial pressure or cardiac output (Q). The end-tidal PCO2 fell 55% (P less than 0.01) and the postmortem weight of the lungs increased 55% (P less than 0.05). Brain compression with a subdural balloon instead of air only caused a 20% rise in Ppa and Q without pulmonary edema. Thus, pulmonary air emboli rather than brain compression accounts for the edema and pulmonary hypertension caused by subdural air. Catheters in pulmonary veins and the left atrium showed that air emboli cause transient pulmonary venous hypertension as well as a reproducible form of noncardiogenic pulmonary endema.

Renal responses to central vascular expansion are suppressed at night in conscious primates

1980 ◽  
Vol 239 (4) ◽  
pp. F343-F351 ◽  
Author(s):  
David A. Kass ◽  
Frank M. Sulzman ◽  
Charles A. Fuller ◽  
Martin C. Moore-Ede
Keyword(s):  
Sodium Excretion ◽  
Time Course ◽  
Venous Pressure ◽  
Urine Osmolality ◽  
Air Pressure ◽  
Saimiri Sciureus ◽  
Arterial Blood ◽  
Body Positive ◽  
Renal Responses ◽  
Diurnal Regulation

Renal and hemodynamic responses to central vascular volume expansion induced by 4 h of continuous lower bodv positive air pressure (LBPP) were examined in conscious, chair-restrained squirrel monkeys in a light/dark (12:12) cycle. LBPP (30 mmHg) during both day (1200–1600) and night (0000–0400) induced similar 4 cmH2O stable increases in central venous pressure (P < 0.001), rises in heart rate of 25 beat/min (P < 0.001), and small transient elevations in mean arterial blood pressure. In contrast, while daytime LBPP induced a significant increase in urine flow (V) from 2.12 ± 0.31 to 3.5 ± 0.42 ml/h (P < 0.05), and sodium excretion (UNaV) from 71.1 ± 14 to 271.2 ± 37 μeq/h (P < 0.001), there was a marked nocturnal inhibition of the response to LBPP, with no significant increases in V or UNaV. Urine osmolality decreased by more than 50% at both times of pressure exposure; potassium excretion was not significantly affected by either exposure, and drinking was suppressed during daytime LBPP. Comparisons of the time course and diurnal regulation of the urinary responses suggest that several separate efferent control pathways are involved. volume regulation; sodium excretion; squirrel monkey (Saimiri sciureus); lower body positive air pressure; circadian rhythms; Henry-Gauer reflex Submitted on October 29, 1979 Accepted on April 10, 1980

Lung inflation can cause pulmonary edema in zone I of in situ dog lungs

1980 ◽  
Vol 49 (5) ◽  
pp. 815-819 ◽  
Author(s):  
R. K. Albert ◽  
S. Lakshminarayan ◽  
W. Kirk ◽  
J. Butler
Keyword(s):  
Weight Gain ◽  
Venous Pressure ◽  
Lower Lobe ◽  
Alveolar Pressure ◽  
Weight Changes ◽  
Lung Water ◽  
Lung Weight ◽  
Lung Inflation ◽  
Pulmonary Arterial

We investigated whether increases in lung water can occur due to lung inflation in zone I when alveolar vessels are collapsed. Static left lower lobe alveolar pressure, pulmonary arterial pressure, and pulmonary venous pressure were controlled in living, anesthetized, open-chested dogs. The lobe was inflated with 6% CO2 in air and suspended from a strain gauge, which allowed continual weight recording. The lung was held in zone I conditions. Arterial and venous pressures were equal at either 1 or 5 cmH2O, relative to the base of the 10- to 14-cm-high lobes. Weight changes were measured for 5 min after 5-cmH2O increments of alveolar pressure from 0 or 5 to 30 cmH2O. Lung weight gain due to edema occurred with inflation to alveolar pressures above 10 cmH2O. Greater lung distension resulted in greater rates of weight gain. Weight loss occurred on deflation. The fluid may have leaked from distended extra-alveolar vessels. This mechanism could explain the increased lung water seen with mechanical ventilation and/or positive end-expiratory pressure breathing.

Relationship of pulmonary arterial and venous pressure to diffusing capacity

1964 ◽  
Vol 19 (3) ◽  
pp. 381-386 ◽  
Author(s):  
W. H. Lawson ◽  
Helen N. Duke ◽  
Richard W. Hyde ◽  
Robert E. Forster
Keyword(s):  
Blood Flow ◽  
Pulmonary Edema ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Pulmonary Veins ◽  
Diffusing Capacity ◽  
Arterial Perfusion ◽  
Single Breath ◽  
Capillary Bed ◽  
Relationship Of

Single-breath carbon monoxide diffusing capacity (DlCO) was determined in ten isolated perfused cat lungs at 37 C during a) forward (arterial) perfusion through the pulmonary artery and b) reverse (venous) perfusion through the left atrium. Blood flow, inflow and outflow pressure, lung volume, and transpulmonary ventilating pressure were approximately equal in a and b, but in all ten lungs DlCO was greater in b than a. In five lungs during forward (arterial) perfusion blood flow was increased from a mean of 62–180 ml/min while left atrial outflow pressure was maintained about zero mm Hg. At the higher blood flow DlCO was not significantly changed although vascular resistance decreased a mean of 34% and arterial pressure increased a mean of 98%. We conclude that a) transmural pressure in the pulmonary veins is more important than that in the arteries in determining the size of the capillary bed as measured by DlCO, and b) the size of the capillary bed and total vascular resistance can vary independently. When pulmonary edema occurred in five lungs DlCO did not change significantly. pulmonary capillary bed size; pulmonary edema and lung diffusing capacity; pulmonary blood flow and lung diffusing capacity Submitted on February 11, 1963

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