Edema affects intra-alveolar fluid pressures and interdependence in dog lungs

1981 ◽  
Vol 51 (4) ◽  
pp. 911-921 ◽  
Author(s):  
J. C. Parker ◽  
R. C. Allison ◽  
A. E. Taylor
Keyword(s):  
Time Course ◽  
Recovery Period ◽  
Positive Pressure ◽  
Base Line ◽  
Alveolar Wall ◽  
Lung Water ◽  
Lung Inflation ◽  
Volume Segment ◽  
The Mean ◽  
Line Pressure

The pressures in occluded, fluid-filled segments of lung were measured in closed-chest supine dogs ventilated with positive pressure at a constant tidal volume. Segment fluid pressures decreased in response to lung inflation and were used with esophageal and airway pressures to calculate an index of bronchiolar-parenchymal interdependence. Animals were subjected to three sequential 5% body wt infusions of Tyrode's solution followed by a 20- to 30 min-recovery period after each infusion. The interdependence index decreased significantly following each infusion, with infusions as small as 1% body wt producing a detectable decrease. The mean pressures in the Tyrode's solution-filled segments generally increased in response to the infusions, but the time course of the response was variable. The base-line pressure in Tyrode's solution-filled segments was -4.8 +/- 2.4 cmH2O. This increased to -1.1 +/- 2.7 cmH2O after a total of 15% body wt had been infused. At the same time, extravascular lung water increased by approximately 17%. Thus negative collapse pressures in the occluded segments were opposed by mechanical stresses transmitted through alveolar wall attachments. This counterbalancing stress was consistently reduced by both increased tissue hydration and increased pulmonary vascular pressure.

Time course of the bronchoconstriction induced by inhaled histamine and methacholine

1983 ◽  
Vol 54 (3) ◽  
pp. 821-826 ◽  
Author(s):  
A. Cartier ◽  
J. L. Malo ◽  
P. Begin ◽  
M. Sestier ◽  
R. R. Martin
Keyword(s):  
Flow Resistance ◽  
Time Course ◽  
Recovery Phase ◽  
Base Line ◽  
Prolonged Action ◽  
Initial Value ◽  
Pulmonary Flow ◽  
The Mean

Eleven asthmatic subjects inhaled doubling concentrations of histamine until a near sixfold increase in total pulmonary flow resistance had been reached. This last concentration (C6) of histamine and methacholine was administered on two subsequent separate visits. Specific lung conductance (sGL) dropped to 18.6 +/- 7.9 (SD) and 19.1 +/- 10.3% of initial value after histamine and methacholine, respectively (NS). Whereas the peak action occurred in a similar interval (1–4 min), the mean duration of the subsequent plateau, defined as values of sGL within 20% of the maximum fall was 16.8 +/- 9.8 min for histamine and 74.6 +/- 53.7 min for methacholine (P less than 0.01). The recovery phase from the end of the plateau to base line lasted 25.5 +/- 14.4 min for histamine and 56.7 +/- 38.3 min for methacholine (P less than 0.01). The duration of plateau and recovery phases were not linked with base-line sGL, maximum fall in sGL, or C6. We conclude that for the same induced bronchoconstriction methacholine has a more prolonged action than histamine.

Effect of interstitial edema on lung lymph flow in goats in the absence of filtration

1992 ◽  
Vol 72 (3) ◽  
pp. 1142-1148 ◽  
Author(s):  
K. Kambara ◽  
K. E. Longworth ◽  
V. B. Serikov ◽  
N. C. Staub
Keyword(s):  
Lymph Flow ◽  
Alveolar Wall ◽  
Half Time ◽  
Interstitial Edema ◽  
Lung Water ◽  
Pulmonary Arterial ◽  
The Mean ◽  
Lung Lymph ◽  
Normal Lungs ◽  
Lung Lymph Flow

We tested the effect of interstitial edema on lung lymph flow when no filtration occurred. In 16 anesthetized open-thorax ventilated supine goats, we set pulmonary arterial and left atrial pressures to nearly zero and measured lymph flow for 3 h from six lungs without edema and ten with edema. Lymph flow decreased exponentially in all experiments as soon as filtration ceased. In the normal lungs the mean half time of the lymph flow decrease was 12.7 +/- 4.8 (SD) min, which was significantly shorter (P less than 0.05) than the 29.1 +/- 14.8 min half time in the edematous lungs. When ventilation was stopped, lymph flow in the edematous lungs decreased as rapidly as in the normal lungs. The total quantity of lymph after filtration ceased was 2.7 +/- 0.8 ml in normal lungs and 9.5 +/- 6.3 ml in edematous lungs, even though extravascular lung water was doubled in the latter (8.4 +/- 2.4 vs. 3.3 +/- 0.4 g/g dry lung, P less than 0.01). Thus the maximum possible clearance of the interstitial edema liquid by the lymphatics was 6.3 +/- 4.8%. When we restarted pulmonary blood flow after 1–2 h in four additional goats, lymph flow recovered within 30 min to the baseline level. These findings support the hypothesis that lung lymph flow originates mainly from alveolar wall perimicrovascular interstitial liquid and that the contribution of the lung lymphatic system to the clearance of interstitial edema (bronchovascular cuffs, interlobular septa) is small.

Role of bronchopulmonary C-fiber afferents in the apneic response to cigarette smoke

1987 ◽  
Vol 63 (4) ◽  
pp. 1366-1373 ◽  
Author(s):  
L. Y. Lee ◽  
E. R. Beck ◽  
R. F. Morton ◽  
Y. R. Kou ◽  
D. T. Frazier
Keyword(s):  
Cigarette Smoke ◽  
Control Level ◽  
Vagal Afferents ◽  
Smoke Inhalation ◽  
Coolant Temperature ◽  
Positive Pressure ◽  
Base Line ◽  
Lung Inflation ◽  
C Fiber

The role of vagal bronchopulmonary C-fiber afferents in eliciting the immediate changes in breathing pattern after acute inhalation of cigarette smoke was assessed with a selective blockade of myelinated vagal afferents (innervating both stretch and irritant receptors) utilizing the method of differential cooling. In 15 of 17 chloralose-anesthetized dogs tested, spontaneous inhalation of cigarette smoke (19.7% avg conc, 500–700 ml vol) reproducibly caused the following immediate responses: apnea, bradycardia, and hypotension. These responses occurred within 1 to 2 breaths of smoke inhalation and were followed by a delayed hyperpnea. The apneic duration reached 326 +/- 33% (SE) (n = 15) of the mean base-line expiratory duration. Differential cold block of both vagi (coolant temperature 8.4 +/- 0.3 degrees C) abolished the reflex apnea induced by a positive-pressure (7–10 cmH2O) lung inflation but did not affect the apneic response to smoke inhalation (345 +/- 35%). The smoke-induced apnea was completely abolished by lowering the coolant temperature to -1.3 +/- 0.2 degrees C (n = 10) or by bilateral vagotomy (n = 5) and returned to the control level after both vagi were rewarmed. Based on these results, we suggest that the immediate apneic response to inhaled cigarette smoke is elicited by a stimulation of vagal C-fiber afferents in the lungs and airways.

Hypercapnia and right-duct lymph flow in pups and adult dogs

1977 ◽  
Vol 232 (3) ◽  
pp. H236-H240
Author(s):  
D. A. Stinson ◽  
P. M. Taylor ◽  
E. P. Rees ◽  
U. Boonyaprakob
Keyword(s):  
Pulmonary Artery ◽  
Recovery Period ◽  
Control Period ◽  
Blood Gases ◽  
Lymph Flow ◽  
Thoracic Duct Lymph ◽  
Positive Pressure ◽  
Lung Water ◽  
Pulmonary Hemodynamics ◽  
Duct Lymph

The effect of moderate hypercapnia on right-thoracic duct lymph flow, pulmonary hemodynamics, and lung water content was studied in seven 2- to 5-wk-old dogs and eleven adult dogs anesthetized with pentobarbital, paralyzed with succinylcholine, and maintained on intermittent positive-pressure ventilation. Following a 30-min control period in which arterial pH and blood gases were maintained within normal limits, the dogs were ventilated with 3-14% CO2 for 30 min; they were then returned to control conditions fro a 30-min recovery period. Hypercapnia was associated with a significant increase in lymph flow rate in both pups and adult dogs (P less than 0.05) and a significant increase in pulmonary artery and pulmonary artery wedge pressures in adult dogs (P less than 0.05). These data suggest that hypercapnia may increase the net flow of water out of the pulmonary vascular bed.

Bronchoconstriction elicited by isocapnic hyperpnea in guinea pigs

1988 ◽  
Vol 65 (2) ◽  
pp. 934-939 ◽  
Author(s):  
D. W. Ray ◽  
C. Hernandez ◽  
N. Munoz ◽  
A. R. Leff ◽  
J. Solway
Keyword(s):  
Tidal Volume ◽  
Guinea Pigs ◽  
Room Temperature ◽  
Time Course ◽  
Minute Ventilation ◽  
Recovery Period ◽  
Dynamic Compliance ◽  
Base Line ◽  
Stimulus Response ◽  
Airway Response

We demonstrated spontaneous self-limited bronchoconstriction after eucapnic dry gas hyperpnea in 22 anesthetized, mechanically ventilated guinea pigs pretreated with propranolol (1 mg/kg iv). Eucapnic hyperpnea "challenges" of room temperature dry or humidified gas (5% CO2-95% O2) were performed by mechanically ventilating animals (150 breaths/min, 3-6 ml tidal volume) for 5 min. During a "recovery" period after hyperpnea, animals were returned to standard ventilation conditions (6 ml/kg, 60 breaths/min, 50% O2 in air, fully saturated at room temperature). After dry gas hyperpnea (5 ml, 150 breaths/min), respiratory system resistance (Rrs) increased in the recovery period by 7.7-fold and dynamic compliance (Cdyn) decreased by 79.7%; changes were maximal at approximately 3 min posthyperpnea and spontaneously returned to base line in 10-40 min. This response was markedly attenuated by humidification of inspired air. Four consecutive identical dry air challenges resulted in similar posthyperpnea responses in four animals. Increasing the minute ventilation during hyperpnea (by varying tidal volume from 3 to 6 ml) caused increased bronchoconstriction in a dose-dependent fashion in six animals. Neither vagotomy nor atropine altered the airway response to dry gas hyperpnea. We conclude that dry gas hyperpnea in anesthetized guinea pigs results in a bronchoconstrictor response that shares five similar features with hyperpnea-induced bronchoconstriction in human asthma: 1) time course of onset and spontaneous resolution, 2) diminution with humidification of inspired gas, 3) reproducibility on consecutive identical challenges, 4) stimulus-response relationship with minute ventilation during hyperpnea, and 5) independence of parasympathetic neurotransmission.

scholarly journals Time course of radiographic hip joint changes in patients with early axial spondyloarthritis

2021 ◽  
Vol 15 (1) ◽  
pp. 46-50
Author(s):  
E. M. Agafonova ◽  
D. G. Rumyantseva ◽  
A. V. Smirnov ◽  
Sh. Erdes
Keyword(s):  
Hip Joint ◽  
Time Course ◽  
Axial Spondyloarthritis ◽  
Disease Onset ◽  
Underlying Disease ◽  
Joint Involvement ◽  
Base Line ◽  
Radiological Progression ◽  
The Mean

The diagnosis of coxitis remains one of the most difficult problems in the management of patients with axial spondyloarthritis (axSpA). In Russia, almost every two patients with axSpA were found to have hip joint (HJ) damage. However, until a certain time, there have been no methods to estimate the rate of progression of radiographic HJ changes in clinical practice. We have previously developed a formula for calculating the rate of coxitis progression, which simplifies the assessment of radiographic HJ changes and allows a physician to make a timely decision about changing therapy if rapidly progressing coxitis is detected.Objective: to estimate the rate of radiological progression of coxitis during a 24-month follow-up of patients with early axSpA.Patients and methods. Examinations were made in 38 patients (20 women and 18 men) who had been followed up for at least 2 years without radiographic and ultrasound signs of HJ joint involvement. The patients' mean age was 28.8±5.5 years; the disease duration was 22.7±15.7 months. HLA-B27 was positive in 35 (92%) patients. The summary stage of radiographic coxitis (ssRC) was used to assess HJ damage; the previously developed formula was applied to estimate the rate of radiological progression of coxitis (R-rpC).Results and discussion. The median cervical-capsular distance (CCD) was 5.2 mm at baseline and 4.9 mm at 2 years (p7 mm increase in the CCD. The mean ssRC was 0.34±0.75 scores at base line, 0.86±0.78 scores at 1 year; and this indicator increased up to 1.24±1.36 scores at 2 years (p=0.004). During 2 years of follow-up, there was no coxitis progression (the difference between ssRC2 and ssRC1 was 0) in 24 (63%) patients; ΔssRC increased by 1 score in 5 (13%); by 2 scores in 6 (16%), and by 4 scores in 3 (8%). On patient inclusion to the investigation, R-rpC averaged 0.5 (it was conventionally assumed that patients had no signs of HJ damage at the disease onset (ssRC=0). During therapy for the underlying disease, the mean R-rpC was 0.3 and 0.2 score/year within the first and second years, respectively. The mean R-rpC in the ΔssRC >0 group was as many as 0.85 score/year at one-year follow-up and 0.53 score/year at two-year follow-up.Conclusion. The developed procedure for estimating the progression of coxitis using ssRC is easy to use and can identify patients at high risk for coxitis progression.

Effect of lung inflation on diaphragmatic shortening

1988 ◽  
Vol 65 (6) ◽  
pp. 2383-2389 ◽  
Author(s):  
J. D. Road ◽  
A. M. Leevers
Keyword(s):  
Positive Pressure ◽  
Inspiratory Capacity ◽  
Mean Velocity ◽  
Maximum Increase ◽  
Transdiaphragmatic Pressure ◽  
Lung Inflation ◽  
Main Determinant ◽  
Residual Capacity ◽  
Anesthetized Dogs ◽  
The Mean

The effect of lung inflation on chest wall mechanics was studied in 11 vagotomized pentobarbital sodium-anesthetized dogs. Diaphragmatic shortening (percent change from initial length at functional residual capacity, %LFRC) and transdiaphragmatic pressure swings (delta Pdi) were compared with control values over a range of positive-pressure breathing that produced a maximum increase in lung volume to 40% of inspiratory capacity. There was no change in the electromyogram of the diaphragm or parasternal intercostals during positive-pressure breathing. delta Pdi and tidal volume (VT) fell to 52 +/- 3.3 and 42.5 +/- 5% (SE) of control. This was associated with a reduction in the initial resting length of 13 +/- 1.9 and 21 +/- 2.2%LFRC (SE) in the costal and crural diaphragms, respectively. Tidal diaphragmatic shortening, however, decreased to 66 +/- 7 and 57 +/- 7 and the mean velocity decreased to 78 +/- 10 and 63 +/- 8% (SE) of control for the costal and crural diaphragms, respectively. We conclude that the reduction in diaphragmatic shortening is the main determinant of the reduced delta Pdi and VT during lung inflation and relate this to what is currently known about diaphragmatic contractile properties.

Stimulation of plasma inactive renin by dexamethasone in the cat

1989 ◽  
Vol 257 (6) ◽  
pp. E879-E884
Author(s):  
N. Glorioso ◽  
C. Troffa ◽  
G. Tonolo ◽  
M. G. Melis ◽  
P. Manunta ◽  
...  
Keyword(s):  
Time Course ◽  
Consensus Sequence ◽  
Recovery Period ◽  
Base Line ◽  
Active Renin ◽  
Human Renin ◽  
Inactive Form ◽  
Inactive Renin ◽  
Selective Increase ◽  
Stimulation Of

An inactive form of renin in human plasma is the biosynthetic precursor, prorenin. The cat is a good animal model for studies of inactive renin. The gene for human renin contains sequences homologous to the glucocorticoid consensus sequence. The response of cat plasma (active and inactive renin) and of angiotensinogen to administration of dexamethasone (0.5 mg/kg im, daily) was studied in ketamine-sedated cats (20 mg/kg im). Inactive renin increased by twofold after 7 days of dexamethasone (P less than 0.01). After a 7-day recovery period, it returned to base line. Active renin did not change. Angiotensinogen fell by 35% (P less than 0.01). The time course of the selective increase of plasma inactive renin showed that inactive renin began to rise after 2 days, peaking after 5 days. Ketamine alone induced inactive renin to rise slightly but significantly (P less than 0.05), although the magnitude of the increment was much less than that observed in ketamine-sedated cats receiving dexamethasone (P less than 0.01). Active renin did not change, whereas angiotensinogen was reduced by 25% (P less than 0.01). Our findings support the hypothesis that glucocorticoids might have a selective role in the synthesis and/or secretion of the precursor of renin, at least in the cat.

Effect of superior vena caval hypertension on alloxan-induced lung injury in dogs

1990 ◽  
Vol 68 (2) ◽  
pp. 478-483 ◽  
Author(s):  
F. Ando ◽  
M. Arakawa ◽  
K. Kambara ◽  
H. Miyazaki ◽  
T. Segawa ◽  
...  
Keyword(s):  
Time Course ◽  
Low Dose ◽  
Superior Vena ◽  
Gravimetric Method ◽  
Base Line ◽  
Lung Water ◽  
Superior Vena Caval ◽  
Anesthetized Dogs ◽  
Water Accumulation ◽  
Permeability State

To investigate how fast and to what extent superior vena caval hypertension (SVCH) increases lung water in acute increased-permeability state, we studied the time course of lung water accumulation for 3 h in anesthetized dogs under different treatments: 1) controls without intervention (5 dogs), 2) SVCH alone (5 dogs), 3) mild lung microvascular injury induced by low-dose alloxan (75 mg/kg) alone (5 dogs), and 4) SVCH coupled with low-dose alloxan (5 dogs). Neither low-dose alloxan alone nor SVCH alone [superior vena caval pressure (Psvc) = 11.0 +/- 3.1 (SD) mmHg] increased lung water significantly. The SVCH coupled with low-dose alloxan (Psvc = 11.3 +/- 2.7 mmHg) doubled extravascular lung thermal volume measured by the thermal-dye dilution technique within 1 h (5.3 +/- 0.9 ml/kg at base line and 10.9 +/- 4.7 ml/kg at 1 h), then remained unchanged (12.5 +/- 5.7 ml/kg at 3 h). This increase in lung water was confirmed by gravimetric method (5.69 +/- 1.71 g/g blood-free dry wt). We conclude that SVCH is one of the factors that may promote lung water accumulation in increased-permeability state.

Effect of raised thoracic pressure and volume on 99mTc-DTPA clearance in humans

1986 ◽  
Vol 60 (5) ◽  
pp. 1493-1497 ◽  
Author(s):  
K. B. Nolop ◽  
D. L. Maxwell ◽  
D. Royston ◽  
J. M. Hughes
Keyword(s):  
Continuous Positive Airway Pressure ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
High Volume ◽  
Solute Flux ◽  
Positive Pressure ◽  
Base Line ◽  
Half Time ◽  
The Mean ◽  
Low Volume

Although positive airway pressure is often used to treat acute pulmonary edema, the effects on epithelial solute flux are not well known. We measured independently the effect of 1) positive pressure and 2) voluntary hyperinflation on the clearance of inhaled technetium-99m-labeled diethylenetriaminepentaacetic acid (99mTc-DTPA) in six nonsmokers and six smokers. Lung volumes were monitored by inductance plethysmography. Each subject was studied in four situations: 1) low end-expiratory volume (LO-), 2) low volume plus 9 cmH2O continuous positive airway pressure (LO+), 3) high end-expiratory volume (HI-), and 4) high volume plus continuous positive airway pressure (HI+). The clearance half time of 99mTc-DTPA for the nonsmokers decreased from 64.8 +/- 7.0 min (mean +/- SE) at LO- to 23.2 +/- 5.3 min at HI- (P less than 0.05). Positive pressure had no synergistic effect. The mean clearance half time for the smokers was faster than nonsmokers at base line but unaffected by similar changes in thoracic volume and pressure. We conclude that, in nonsmokers, positive airway pressure increases 99mTc-DTPA clearance primarily through an increase in lung volume and that smokers are immune to these effects.

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