Alveolar liquid pressure measured in the intact rabbit chest by micropuncture

Previous measurements in isolated lung showed that alveolar liquid pressure was near the pleural pressure at a lung volume near functional residual capacity (FRC). In this study we verified that alveolar liquid pressure in vivo was similar to that of the isolated lung. In anesthetized paralyzed rabbits (3#x2013;4 kg, n = 9) ventilated with 100% O2 in the left lateral position, we made a pleural window between the fifth and sixth ribs near midchest by removing tissue down to the parietal pleura. Window height was 6 cm above the base of the lung. During apnea, alveolar liquid and pleural pressures were measured by puncturing through the pleural window with micropipettes connected to a servo-nulling pressure-measuring system. Pressures were measured at airway pressures of 0 (FRC) and 10 cmH2O both in vivo and postmortem. In vivo, alveolar liquid and pleural pressures relative to ambient pressure averaged -2.3 +/- 1.4 (SD) and -1.8 +/- 0.9 cmH2O at FRC and increased to 3.3 +/- 1.8 and 1.8 +/- 1.6 cmH2O after inflation to an airway pressure of 10 cmH2O, respectively. Similar values were obtained postmortem. These results were similar to previous measurements in the isolated lung.

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Direct measurement of interstitial pulmonary pressure in in situ lung with intact pleural space

Journal of Applied Physiology ◽

10.1152/jappl.1990.69.6.2168 ◽

1990 ◽

Vol 69 (6) ◽

pp. 2168-2174 ◽

Cited By ~ 52

Author(s):

G. Miserocchi ◽

D. Negrini ◽

C. Gonano

Keyword(s):

Lateral Position ◽

Pleural Space ◽

Measuring System ◽

Parietal Pleura ◽

Interstitial Pressure ◽

Liquid Pressure ◽

Space Experiments ◽

Report Data ◽

Pleural Liquid Pressure

We developed an experimental approach to measure the pulmonary interstitial pressure with the micropuncture technique in in situ lungs with an intact pleural space. Experiments were done in anesthetized paralyzed rabbits that were oxygenated via an endotracheal tube with 50% humidified oxygen and kept in either the supine or the lateral position. A small area of an intercostal space was cleared of the intercostal muscles down to the endothoracic fascia. Subsequently a "pleural window" was opened by stripping the endothoracic fascia over a 0.2-cm2 surface and leaving the parietal pleura (approximately 10 microns thick). Direct micropuncture through the pleural window was performed with 2- to 3-microns-tip pipettes connected to a servo-null pressure-measuring system. We recorded pleural liquid pressure and, after inserting the pipette tip into the lung, we recorded interstitial pressure from subpleural lung tissue. Depth of recording for interstitial pressure averaged 263 +/- 122 (SD) microns. We report data gathered at 26, 53, and 84% lung height (relative to the most dependent portion of the lung). For the three heights, interstitial pressure was -9.8 +/- 3, -10.1 +/- 1.6, and -12.5 +/- 3.7 cmH2O, respectively, whereas the corresponding pleural liquid pressure was -3.4 +/- 0.5, -4.4 +/- 1, and -5.2 +/- 0.3 cmH2O, respectively.

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Alveolar liquid pressure in excised edematous dog lung with increased static recoil

Journal of Applied Physiology ◽

10.1152/jappl.1983.55.4.1277 ◽

1983 ◽

Vol 55 (4) ◽

pp. 1277-1283 ◽

Cited By ~ 9

Author(s):

K. C. Beck ◽

S. J. Lai-Fook

Keyword(s):

Fluid Pressure ◽

Transpulmonary Pressure ◽

Measuring System ◽

Radius Of Curvature ◽

Liquid Pressure ◽

Extravascular Fluid ◽

Air Liquid Interface ◽

Triton X ◽

Uniform Expansion ◽

Alveolar Liquid

Alveolar liquid pressure (Pliq) was measured by micropipettes in conjunction with a servo-nulling pressure measuring system in isolated air-inflated edematous dog lungs. Pliq was measured in lungs either washed with a detergent (0.01% Triton X-100) or subjected to refrigeration for 2-3 days followed by ventilation for 3 h. At 55% of total lung capacity (TLC, the volume at a transpulmonary pressure (Ptp) of 25 cmH2O before treatment), in both the Triton-washed and the ventilated lung, Ptp increased from 5 to 11 cmH2O, whereas Pliq, decreased from -3 to -11 cmH2O relative to alveolar air pressure. Similar increases in Ptp and decreases in Pliq were obtained at higher lung volumes. Alveolar surface tension (T) was estimated from the Laplace equation for a spherical air-liquid interface, assuming that the radius of curvature varies as (volume)n, for -1/3 less than n less than 1/3. For uniform expansion of alveoli (n = 1/3), estimated T was 6 and 18 dyn/cm at 55 and 85% TLC, respectively, before treatment and increased to 23 and 40 dyn/cm following either Triton washing or ventilation. If pericapillary interstitial fluid pressure (Pi) equaled Pliq in edematous lungs, increases in T might reduce Pi and increase extravascular fluid accumulation in lungs made stiff by either Triton washing or cooling and ventilation using large tidal volumes.

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Esophageal elastance in anesthetized humans

Journal of Applied Physiology ◽

10.1152/jappl.1983.54.5.1374 ◽

1983 ◽

Vol 54 (5) ◽

pp. 1374-1378 ◽

Cited By ~ 6

Author(s):

G. Hedenstierna ◽

P. O. Jarnberg ◽

L. Torsell ◽

I. Gottlieb

Keyword(s):

Lung Volume ◽

Supine Position ◽

Human Subjects ◽

Balloon Catheter ◽

Esophageal Pressure ◽

Lateral Position ◽

Left Lateral Position ◽

Volume Curve ◽

Residual Capacity ◽

A Minor

Esophageal elastance (Ees) was measured in 13 human subjects, awake and anesthetized by halothane, in the supine and left lateral postures. Static esophageal pressure was measured by an esophageal balloon catheter, respiratory volumes by pneumotachography, and functional residual capacity (FRC) by body plethysmography. In the supine awake subject, Ees averaged 3 cmH2O/ml at FRC and increased significantly with lung volume. Ees remained unaltered at FRC during anesthesia in the supine position, but lung volume dependence was no longer observed. In the left lateral position the awake subject displayed the same Ees at FRC as in the supine position and lung volume exerted only a small influence on Ees. The latter was reduced during anesthesia and tended to diminish with increasing lung volume. All variations in Ees caused by posture, anesthesia, and lung volume were small and affected the shape of the pressure-volume curve of the lung to only a minor degree.

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Effect of posture on static lung volumes and pulmonary mechanics in pneumonectomized rabbits

Journal of Applied Physiology ◽

10.1152/jappl.1993.74.1.415 ◽

1993 ◽

Vol 74 (1) ◽

pp. 415-422 ◽

Cited By ~ 2

Author(s):

L. E. Olson

Keyword(s):

Functional Residual Capacity ◽

Left Lung ◽

Lateral Position ◽

Phase Iii ◽

Pulmonary Mechanics ◽

Lung Volumes ◽

Left Lateral Position ◽

Single Breath ◽

Residual Capacity ◽

Induced Changes

Static lung volumes, lung (CL) and respiratory system compliance (Crs), and the slope of phase III of the single-breath O2 test (slope III) were measured in rabbits in the prone, supine, and right and left lateral positions. Control rabbits, rabbits that had the left lung removed (Px), and rabbits that had the left lung removed and replaced with wax (Px + W) were studied. Surgeries were performed > or = 7 wk before study. Lung volumes, Crs, and slope III were not different among groups. Total lung capacity, vital capacity, residual volume, Crs, and slope III were smallest in all rabbits in the prone position. Functional residual capacity and expiratory reserve volume were unaffected by posture in control rabbits but were larger in Px and Px + W rabbits in the left lateral position. CL was unaffected by posture but was smaller in Px and Px + W rabbits than in control rabbits. Pneumonectomy-induced changes in lung shape altered the effect of posture on functional residual capacity but not on regional lung function, as assessed by the single-breath O2 test.

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Pleural liquid pressure measured by micropipettes in rabbits

Journal of Applied Physiology ◽

10.1152/jappl.1984.56.6.1633 ◽

1984 ◽

Vol 56 (6) ◽

pp. 1633-1639 ◽

Cited By ~ 27

Author(s):

S. J. Lai-Fook ◽

K. C. Beck ◽

P. A. Southorn

Keyword(s):

Dorsal Surface ◽

Absolute Magnitude ◽

Vertical Gradient ◽

Repeated Measurements ◽

Parietal Pleura ◽

Liquid Pressure ◽

Lung Lobe ◽

Residual Capacity ◽

Lung Base ◽

Pleural Liquid Pressure

Pleural liquid pressure (Ppl) was measured by the micropipette servo-nulling method. In anesthetized, paralyzed, and mechanically ventilated rabbits, windows were made by dissecting away the intercostal muscle layers, exposing the parietal pleura over the right caudal lung lobe. Repeated measurements of Ppl were made at the windows by puncturing the parietal pleura with micropipettes during apnea at functional residual capacity. In five supine rabbits, Ppl relative to atmospheric pressure averaged -3.32 +/- 1.22 (SD) cmH2O at a distance of 5.64 +/- 0.34 (SD) cm above the lung base and -1.64 +/- 0.79 cmH2O at a distance of 2.35 +/- 0.64 cm above the lung base; the vertical Ppl gradient was 0.51 cmH2O/cm height. Ppl interpolated to midlung height was equal in absolute magnitude to mean lung static recoil (Pst) of 2.00 cmH2O. In prone rabbits, Ppl measured near the dorsal surface, 3.9 cm above the lung base, averaged -1.32 +/- 0.46 cmH2O on the costal surface, not statistically different in magnitude from mean Pst of 1.59 +/- 0.09. In contrast, Ppl measured at the same vertical height off the edge of the caudal lung in the costo-diaphragmatic recess was -4.64 +/- 0.65 cmH2O. We concluded from these data that Ppl was equal to pleural surface pressure over the costal surface and that the vertical gradient in Ppl was not hydrostatic, except in large fluid spaces off the sharp edges of the lung.

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Vasopressin-induced pulmonary vasodilation in rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.257.2.h415 ◽

1989 ◽

Vol 257 (2) ◽

pp. H415-H422 ◽

Cited By ~ 5

Author(s):

B. R. Walker ◽

J. Haynes ◽

H. L. Wang ◽

N. F. Voelkel

Keyword(s):

Hypoxic Pulmonary Vasoconstriction ◽

Systemic Resistance ◽

Constant Infusion ◽

Bolus Administration ◽

Pulmonary Hemodynamics ◽

Pulmonary Vasodilation ◽

Isolated Lung ◽

Series Of Experiments

Experiments were performed to determine the pulmonary vascular responses to exogenous or endogenous arginine vasopressin (AVP) in rats. Both in vitro and in vivo approaches were used to examine the direct pulmonary vasoactive properties of AVP and how those properties affect pulmonary hemodynamics in the intact animal. In conscious, unrestrained rats, constant infusion of AVP (4.0 mU.kg-1.min-1 iv) resulted in a fall in mean pulmonary artery pressure (PAP), although systemic pressure was increased. Coincident with the fall in PAP were similar reductions in cardiac output and heart rate. Similarly, bolus administration of AVP reduced PAP, and this effect was augmented during hypoxia. Another series of experiments examined the effect of endogenous AVP released by arterial hypoxemia on pulmonary hemodynamics in conscious rats. Administration of a specific V1-vasopressinergic antagonist had no effect on the PAP response to hypoxia; however, systemic resistance tended to fall following V1-antagonism. To determine the vasoactive properties of AVP independent of these changes in blood flow, a series of experiments were performed on isolated, perfused rat lungs. Injection of 25, 200, or 2,000 mU of AVP into the circulation of the isolated lung was without effect under normoxic conditions. In contrast, 25 mU AVP elicited reproducible pulmonary vasodilation when injected during ongoing hypoxic pulmonary vasoconstriction. This vasodilatory response was unaffected by meclofenamate or by the platelet-activating factor receptor antagonist SRI 63-441, but was blocked by a specific V1-vasopressinergic antagonist. We conclude that although AVP exerts profound systemic vasoconstriction, the pulmonary circulation appears relatively unaffected by exogenous or endogenous AVP in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effect of dynamic position changes on adenoma detection rate during colonoscope withdrawal: systematic review and meta-analysis

Endoscopy International Open ◽

10.1055/a-1265-6634 ◽

2020 ◽

Vol 08 (12) ◽

pp. E1842-E1849

Author(s):

Venkat Nutalapati ◽

Madhav Desai ◽

Vivek Sandeep Thoguluva-Chandrasekar ◽

Mojtaba Olyaee ◽

Amit Rastogi

Keyword(s):

Systematic Review ◽

Detection Rate ◽

Meta Analysis ◽

Lateral Position ◽

Adenoma Detection Rate ◽

Position Change ◽

Withdrawal Time ◽

Left Lateral Position ◽

Adenoma Detection ◽

Withdrawal Phase

Abstract Background and study aims The adenoma detection rate (ADR) is an important quality metric of colonoscopy. Higher ADR correlates with lower incidence of interval colorectal cancer. ADR is variable between endoscopists and depends upon the withdrawal technique amongst other factors. Dynamic position change (lateral rotation of patients with a view to keep the portion of the colon being inspected at a higher level) helps with luminal distension during the withdrawal phase. However, impact of this on ADR is not known in a pooled sample. We performed a systematic review and meta-analysis to study the impact of dynamic position changes during withdrawal phase of colonoscopy on ADR Methods A comprehensive search of MEDLINE, EMBASE, Google Scholar, and the Cochrane Database was conducted from each database’s inception to search for studies comparing dynamic position changes during colonoscope withdrawal with static left lateral position (control). The primary outcome of interest was ADR. Other studied outcomes were polyp detection rate (PDR) and withdrawal time. Outcomes were reported as pooled odds ratio (OR) with 95 % confidence intervals (CI) with statistical significance (P < 0.05). RevMan 5.3 software was used for statistical analysis. Results Six studies were included in our analysis with 2860 patients. Of these, dynamic position change was implemented in 1177 patients while 1183 patients served as the controls. ADR was significantly higher in the dynamic position change group with pooled OR 1.36 (95 % CI, 1.15–1.61; P < 0.01). There was low heterogeneity in inclusion studies (I2 = 0 %). PDR was numerically higher in position change group (53.4 % vs 49.6 %) but not statistically significant (P = 0.16). Mean withdrawal time did not significantly change with dynamic position change (12.43 min vs 11.46 min, P = 0.27). Conclusion Position change during the withdrawal phase of colonoscopy can increase the ADR compared to static left lateral position. This is an easy and practical technique that can be implemented to improve ADR.

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Comparison of the hemodynamic effects of nitric oxide and endothelium-dependent vasodilators in intact lungs

Journal of Applied Physiology ◽

10.1152/jappl.1990.68.2.735 ◽

1990 ◽

Vol 68 (2) ◽

pp. 735-747 ◽

Cited By ~ 51

Author(s):

S. L. Archer ◽

K. Rist ◽

D. P. Nelson ◽

E. G. DeMaster ◽

N. Cowan ◽

...

Keyword(s):

Nitric Oxide ◽

Methylene Blue ◽

Pulmonary Hypertension ◽

Feedback Inhibition ◽

Pressor Response ◽

Pulmonary Vasculature ◽

Hemodynamic Effects ◽

Isolated Lung

The effects of endothelium-dependent vasodilation on pulmonary vascular hemodynamics were evaluated in a variety of in vivo and in vitro models to determine 1) the comparability of the hemodynamic effects of acetylcholine (ACh), bradykinin (BK), nitric oxide (NO), and 8-bromo-guanosine 3′,5′-cyclic monophosphate (cGMP), 2) whether methylene blue is a useful inhibitor of endothelium-dependent relaxing factor (EDRF) activity in vivo, and 3) the effect of monocrotaline-induced pulmonary hypertension on the responsiveness of the pulmonary vasculature to ACh. In isolated rat lungs, which were preconstricted with hypoxia, ACh, BK, NO, and 8-bromo-cGMP caused pulmonary vasodilation, which was not inhibited by maximum tolerable doses of methylene blue. Methylene blue did not inhibit EDRF activity in any model, despite causing increased pulmonary vascular tone and responsiveness to various constrictor agents. There were significant differences in the hemodynamic characteristics of ACh, BK, and NO. In the isolated lung, BK and NO caused transient decreases of hypoxic vasoconstriction, whereas ACh caused more prolonged vasodilation. Pretreatment of these lungs with NO did not significantly inhibit ACh-induced vasodilation but caused BK to produce vasoconstriction. Tachyphylaxis, which was agonist specific, developed with repeated administration of ACh or BK but not NO. Tachyphylaxis probably resulted from inhibition of the endothelium-dependent vasodilation pathway proximal to NO synthesis, because it could be overcome by exogenous NO. Pretreatment with 8-bromo-cGMP decreased hypoxic pulmonary vasoconstriction and, even when the hypoxic pressor response had largely recovered, subsequent doses of ACh and NO failed to cause vasodilation, although BK produced vasoconstriction. These findings are compatible with the existence of feedback inhibition of the endothelium-dependent relaxation by elevation of cGMP levels. Responsiveness to ACh was retained in lungs with severe monocrotaline-induced pulmonary hypertension. Many of these findings would not have been predicted based on in vitro studies and illustrate the importance for expanding studies of EDRF to in vivo and ex vivo models.

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