scholarly journals Ventilation inhomogeneity in oleic acid-induced pulmonary edema

1997 ◽  
Vol 82 (4) ◽  
pp. 1040-1045 ◽  
Author(s):  
John Y. C. Tsang ◽  
Michael J. Emery ◽  
Michael P. Hlastala
Keyword(s):  
Oleic Acid ◽  
Pulmonary Edema ◽  
Phase Iii ◽  
Lung Water ◽  
Peripheral Airways ◽  
Ventilation Inhomogeneity ◽  
Distal Airway ◽  
Tissue Compliance ◽  
Permeability Pulmonary Edema ◽  
The Right

Tsang, John Y. C., Michael J. Emery, and Michael P. Hlastala. Ventilation inhomogeneity in oleic acid-induced pulmonary edema. J. Appl. Physiol.82(4): 1040–1045, 1997.—Oleic acid causes permeability pulmonary edema in the lung, resulting in impairment of gas-exchange and ventilation-perfusion heterogeneity and mismatch. Previous studies have shown that by using the multiple-breath helium washout (MBHW) technique, ventilation inhomogeneity (VI) can be quantitatively partitioned into two components, i.e., convective-dependent inhomogeneity (cdi) and diffusive-convective-dependent inhomogeneity (dcdi). Changes in VI, as represented by the normalized slope of the phase III alveolar plateau, were studied for 120 min in five anesthetized mongrel dogs that were ventilated under paralysis by a constant-flow linear motor ventilator. These animals received oleic acid (0.1 mg/kg) infusion into the right atrium at t = 0. MBHWs were done in duplicate for 18 breaths every 40 min afterward. Three other dogs that received only normal saline served as controls. The data show that, after oleic acid infusion, dcdi, which represents VI in peripheral airways, is responsible for the increasing total VI as lung water accumulates progressively over time. The cdi, which represents VI between larger conductive airways, remains relatively constant throughout. This observation can be explained by increases in the heterogeneity of tissue compliance in the periphery, distal airway closure, or by decreases in ventilation through collateral channels.

Rebreathing lung tissue volume of sheep with normal and edematous lungs

1986 ◽  
Vol 61 (3) ◽  
pp. 1132-1138 ◽  
Author(s):  
G. J. Huchon ◽  
A. Lipavsky ◽  
J. M. Hoeffel ◽  
J. F. Murray
Keyword(s):  
Oleic Acid ◽  
Pulmonary Edema ◽  
Blood Volume ◽  
Lung Tissue ◽  
Extravascular Lung Water ◽  
Lung Water ◽  
Lung Weight ◽  
Tissue Volume ◽  
Accuracy Of Measurements ◽  
Permeability Pulmonary Edema

To determine the accuracy of measurements of lung tissue volume (Vlt) by rebreathing acetylene in normal and edematous lungs, we compared gravimetric values of total lung weight (Ql) and extravascular lung water (Qwl) with Vlt in anesthetized control sheep (C) and sheep with hydrostatic pulmonary edema (HPE) or oleic acid-induced permeability pulmonary edema (PPE), five animals each. In eight additional sheep we determined that acetylene solubility in blood (0.117 +/- 0.010 ml X 100 ml-1 X Torr-1) differed significantly from that in lung-blood homogenates (0.095 +/- 0.009 ml X 100 ml-1 X Torr-1, P = 0.0017). The latter value was used in all calculations. In C, Vlt was 194% of Qwl and 98% of Ql; in HPE, Vlt was 144% of Qwl and 87% of Ql; and in PPE, Vlt was 112% of Qwl and 77% of Ql. We conclude that when the lungs are normal, Vlt reasonably measures Ql not Qwl. However in both HPE and PPE, Vlt progressively underestimates Ql and cannot differentiate between increased blood volume and increased Qwl.

Increased cardiac output increases shunt: role of pulmonary edema and perfusion

1985 ◽  
Vol 59 (4) ◽  
pp. 1313-1321 ◽  
Author(s):  
P. H. Breen ◽  
P. T. Schumacker ◽  
J. Sandoval ◽  
I. Mayers ◽  
L. Oppenheimer ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Oleic Acid ◽  
Pulmonary Edema ◽  
Lung Edema ◽  
Base Line ◽  
Lung Water ◽  
Arteriovenous Fistulas ◽  
Anesthetized Dogs ◽  
The Right

In low-pressure pulmonary edema increased cardiac output (QT) increases shunt (Qs/QT); we tested whether the mechanism is an increase in extravascular lung water in turn mediated by the accompanying increase in microvascular pressure. In six pentobarbital sodium-anesthetized dogs ventilated with O2 we administered oleic acid into the right atrium. From base line to 2 h post-oleic acid we measured concurrent significant increases in Qs/QT (6–29%, O2 technique) and extravascular thermal volume (ETV, 2.6–7.1 ml/g dry intravascular blood-free lung wt, thermal-green dye indicator technique) that were stable by 90 min. Then, bilateral femoral arteriovenous fistulas were opened and closed in 30-min periods to cause reversible increases in QT and associated Qs/QT. When fistulas were open the time-averaged QT increased from 5.1 to 6.9 min (P less than 0.05), the simultaneous Qs/QT rose from 30.7 to 38.4% (P less than 0.05), but ETV did not increase. We conclude that increasing lung edema does not account for our rise in Qs/QT when QT increased.

Histamine-induced pulmonary edema distal to pulmonary arterial occlusion

1985 ◽  
Vol 58 (4) ◽  
pp. 1092-1098 ◽  
Author(s):  
M. D. Walkenstein ◽  
B. T. Peterson ◽  
J. E. Gerber ◽  
R. W. Hyde
Keyword(s):  
Pulmonary Edema ◽  
Pulmonary Circulation ◽  
Arterial Occlusion ◽  
Arterial Blood Flow ◽  
Water Volume ◽  
Lung Water ◽  
Arterial Blood ◽  
Perfused Lung ◽  
Pulmonary Arterial ◽  
The Right

Histological studies provide evidence that the bronchial veins are a site of leakage in histamine-induced pulmonary edema, but the physiological importance of this finding is not known. To determine if a lung perfused by only the bronchial arteries could develop pulmonary edema, we infused histamine for 2 h in anesthetized sheep with no pulmonary arterial blood flow to the right lung. In control sheep the postmortem extravascular lung water volume (EVLW) in both the right (occluded) and left (perfused) lung was 3.7 +/- 0.4 ml X g dry lung wt-1. Following histamine infusion, EVLW increased to 4.4 +/- 0.7 ml X g dry lung wt-1 in the right (occluded) lung (P less than 0.01) and to 5.3 +/- 1.0 ml X g dry wt-1 in the left (perfused) lung (P less than 0.01). Biopsies from the right (occluded) lungs scored for the presence of edema showed a significantly higher score in the lungs that received histamine (P less than 0.02). Some leakage from the pulmonary circulation of the right lung, perfused via anastomoses from the bronchial circulation, cannot be excluded but should be modest considering the low pressures in the pulmonary circulation following occlusion of the right pulmonary artery. These data show that perfusion via the pulmonary arteries is not a requirement for the production of histamine-induced pulmonary edema.

Lung and chest wall impedances in the dog in normal range of breathing: effects of pulmonary edema

1992 ◽  
Vol 73 (3) ◽  
pp. 1040-1046 ◽  
Author(s):  
G. M. Barnas ◽  
D. Stamenovic ◽  
K. R. Lutchen
Keyword(s):  
Oleic Acid ◽  
Pulmonary Edema ◽  
Chest Wall ◽  
Mean Airway Pressure ◽  
Normal Range ◽  
Normal Ranges ◽  
Before And After ◽  
Measured Resistance ◽  
The Right ◽  
Severe Pulmonary Edema

We evaluated the effect of pulmonary edema on the frequency (f) and tidal volume (VT) dependences of respiratory system mechanical properties in the normal ranges of breathing. We measured resistance and elastance of the lungs (RL and EL) and chest wall of four anesthetized-paralyzed dogs during sinusoidal volume oscillations at the trachea (50–300 ml, 0.2–2 Hz), delivered at a constant mean airway pressure. Measurements were made before and after severe pulmonary edema was produced by injection of 0.06 ml/kg oleic acid into the right atrium. Chest wall properties were not changed by the injection. Before oleic acid, EL increased slightly with increasing f in each dog but was independent of VT. RL decreased slightly and was independent of VT from 0.2 to 0.4 Hz, but above 0.4 Hz it tended to increase with increasing flow, presumably due to the airway contribution. After oleic acid injection, EL and RL increased greatly. Large negative dependences of EL on VT and of RL on f were also evident, so that EL and RL after oleic acid changed two- and fivefold, respectively, within the ranges of f and VT studied. We conclude that severe pulmonary edema changes lung properties so as to make behavior VT dependent (i.e., nonlinear) and very frequency dependent in the normal range of breathing.

Analysis of rebreathing measurements of pulmonary tissue volume in pulmonary edema

1980 ◽  
Vol 48 (1) ◽  
pp. 66-71 ◽  
Author(s):  
M. Friedman ◽  
S. H. Kaufman ◽  
S. A. Wilkins
Keyword(s):  
Oleic Acid ◽  
Pulmonary Edema ◽  
Lung Water ◽  
Pulmonary Tissue ◽  
Tissue Volume ◽  
Acid Injection ◽  
Pulmonary Tissue Volume ◽  
Rebreathing Method

A rebreathing method (usood volume (VTPC) was evaluated in 13 dogs. In seven, pulmonary edema was induced by oleic acid injection. Six dogs served as controls. Values of VTPC calculated by three algorithms were compared to postmortem lung water. The first algorithm uses the C18O intercept to determine time 0 and all data to construct the alveolar disappearance curves. The second uses the beginning of inspiration as time 0. The last uses data only during the last third of expiration. The best correlation (r = 0.90) between VTPC and total lung water was obtained utilizing the first algorithm. In the control animals, mean VTPC was 188 ml, and in the edema dogs was 278 ml. Mean VTPC for all dogs was 96 +/- 14% of total lung water using the first algorithm. Another algorithm (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 44: 782-795, 1978) was evaluated inthe edema dog group. This method gave values of VTPC 53% higher than those obtained by the first algorithm.

Regional measurements of pulmonary edema by using magnetic resonance imaging

1998 ◽  
Vol 84 (6) ◽  
pp. 2143-2153 ◽  
Author(s):  
S. D. Caruthers ◽  
C. B. Paschal ◽  
N. A. Pou ◽  
R. J. Roselli ◽  
T. R. Harris
Keyword(s):  
Magnetic Resonance Imaging ◽  
Oleic Acid ◽  
Magnetic Resonance ◽  
Pulmonary Edema ◽  
Surface Area ◽  
Extravascular Lung Water ◽  
Three Dimensional ◽  
Indicator Dilution ◽  
Resonance Imaging ◽  
Lung Water

A three-dimensional magnetic resonance imaging (MRI) method to measure pulmonary edema and lung microvascular barrier permeability was developed and compared with conventional methods in nine mongrel dogs. MRIs were obtained covering the entire lungs. Injury was induced by injection of oleic acid (0.021–0.048 ml/kg) into a jugular catheter. Imaging followed for 0.75–2 h. Extravascular lung water and permeability-related parameters were measured from multiple-indicator dilution curves. Edema was measured as magnetic resonance signal-to-noise ratio (SNR). Postinjury wet-to-dry lung weight ratio was 5.30 ± 0.38 ( n = 9). Extravascular lung water increased from 2.03 ± 1.11 to 3.00 ± 1.45 ml/g ( n = 9, P < 0.01). Indicator dilution studies yielded parameters characterizing capillary exchange of urea and butanediol: the product of the square root of equivalent diffusivity of escape from the capillary and capillary surface area ( D 1/2 S) and the capillary permeability-surface area product ( PS). The ratio of D 1/2 Sfor urea to D 1/2 Sfor butanediol increased from 0.583 ± 0.027 to 0.852 ± 0.154 ( n = 9, P < 0.05). Whole lung SNR at baseline, before injury, correlated with D 1/2 Sand PS ratios (both P < 0.02). By using rate of SNR change, the mismatch of transcapillary filtration flow and lymph clearance was estimated to be 0.2–1.8 ml/min. The filtration coefficient was estimated from these values. Results indicate that pulmonary edema formation during oleic acid injury can be imaged regionally and quantified globally, and the results suggest possible regional quantification by using three-dimensional MRI.

A positron emission tomographic comparison of diffuse and lobar oleic acid lung injury

1988 ◽  
Vol 64 (6) ◽  
pp. 2357-2365 ◽  
Author(s):  
D. P. Schuster ◽  
J. W. Haller ◽  
M. Velazquez
Keyword(s):  
Oleic Acid ◽  
Lung Injury ◽  
Dorsal Region ◽  
Lung Water ◽  
Positron Emission ◽  
Transcapillary Escape Rate ◽  
Severity Of Injury ◽  
Water Accumulation ◽  
The Right ◽  
Lung Lobes

We tested whether severity of injury measured from the pulmonary transcapillary escape rate for transferrin (PTCER), lung water accumulation, and changes in regional pulmonary blood flow (PBF) would be similar after oleic acid (OA) injection into either all lung lobes or directly into the pulmonary artery feeding the left caudal lobe (LCL) only. Measurements were made with positron emission tomography. After 0.015 ml/kg OA was injected into the LCL (Lobar, n = 5), lung water increased in the left dorsal region from 37 +/- 5 to 50 +/- 8 ml/100 ml lung (P less than 0.05), PTCER was 533 +/- 59 10(-4)/min, and regional PBF decreased 62%. No significant change occurred in the uninjured right dorsal lung where PTCER was 85 +/- 32. In the left ventral region PTCER was 357 +/- 60, PBF decreased only 31%, and the increase in lung water was less (25 +/- 3 to 30 +/- 6). In contrast after 0.08 ml/kg OA was injected via the right atrium (Diffuse, n = 6), PTCER (283 +/- 94) was lower in the left dorsal region of this group than in the corresponding region of the Lobar group (P less than 0.05). The increase in lung water, however, was the same, but no change occurred in PBF distribution. These results indicate important differences between the two methods of causing lung injury with OA. After injury lung water accumulates primarily in dependent portions of lung and is not always accompanied by a decrease in regional PBF. These decreases, when they occur, may instead indicate severe vascular injury.

Edema from cyclooxygenase products of endogenous arachidonic acid in isolated lung

1989 ◽  
Vol 67 (2) ◽  
pp. 846-855 ◽  
Author(s):  
M. R. Littner ◽  
F. D. Lott
Keyword(s):  
Arachidonic Acid ◽  
Pulmonary Edema ◽  
Enzyme Inhibitor ◽  
Calcium Ionophore ◽  
Dry Weight ◽  
Lung Water ◽  
Isolated Lung ◽  
Pulmonary Arterial ◽  
Area Product ◽  
Permeability Pulmonary Edema

We infused A23187, a calcium ionophore, into the pulmonary circulation of dextran-salt-perfused isolated rabbit lungs to release endogenous arachidonic acid. This led to elevations in pulmonary arterial pressure and to pulmonary edema as measured by extravascular wet-to-dry weight ratios. The increase in pressure and edema was prevented by indomethacin, a cyclooxygenase enzyme inhibitor, and by 1-benzylimidazole, a selective inhibitor of thromboxane (Tx) A2 synthesis. Transvascular flux of 125I-albumin from vascular to extravascular spaces of the lung was not elevated by A23187 but was elevated by infusion of oleic acid, an agent known to produce permeability pulmonary edema. We confirmed that A23187 leads to elevations in cyclooxygenase products and that indomethacin and 1-benzylimidazole inhibit synthesis of all cyclooxygenase products and TxA2, respectively, by measuring perfusate levels of prostaglandin (PG) I2 as 6-ketoprostaglandin F1 alpha, PGE2, and PGF2 alpha and TxA2 as TxB2. We conclude that release of endogenous pulmonary arachidonic acid can lead to pulmonary edema from conversion of such arachidonic acid to cyclooxygenase products, most notably TxA2. This edema was most likely from a net hydrostatic accumulation of extravascular lung water with an unchanged permeability of the vascular space, since an index of permeability-surface area product (i.e., transvascular albumin flux) was not increased.

Assessment of temporal changes in pulmonary edema with NMR imaging

1989 ◽  
Vol 66 (3) ◽  
pp. 1197-1208 ◽  
Author(s):  
D. M. Phillips ◽  
P. S. Allen ◽  
S. F. Man
Keyword(s):  
Relaxation Time ◽  
Oleic Acid ◽  
Pulmonary Edema ◽  
Signal Intensity ◽  
Transverse Relaxation Time ◽  
Lung Edema ◽  
Lung Water ◽  
Transverse Relaxation ◽  
Acid Infusion ◽  
Potential Applicability

Nuclear magnetic resonance imaging (NMRI) parameters [longitudinal relaxation time (T1), transverse relaxation time (T2), and signal intensity] acquired at a magnetic field of 2.35 T were validated with a study of nine different phantom gel solutions. This technique was then applied to study 13 anesthetized supine cats, among which 10 had lung edema induced by oleic acid (0.075 ml/kg); the result was compared with postmortem analyses of lung water. Three animals (series A) were imaged until the edema was first visualized in NMRI, usually 15–20 min after oleic acid infusion. Another seven animals (series B) were imaged over 4–5 h. As lung water increased, so did the signal intensity. When edema first appeared, T1, T2, and the volume of the edematous region within the slice in the upper lobes showed no gravity-dependent differences; this was confirmed by postmortem measurements (series A) of lung water. With time, gravity-dependent regions displayed greater volumes of edematous regions and greater T1 values (P less than 0.01), suggesting a continued accumulation of lung water. In comparison, nondependent regions displayed constant volumes of edematous region and lesser T1 values (P less than 0.01), suggesting an increased protein concentration but no change in lung water. This study suggests the potential applicability of NMRI parameters in the assessment of pulmonary edema.

Effect of eicosanoid inhibition on the development of pulmonary edema after acute lung injury

1996 ◽  
Vol 80 (3) ◽  
pp. 915-923 ◽  
Author(s):  
D. P. Schuster ◽  
A. H. Stephenson ◽  
S. Holmberg ◽  
P. Sandiford
Keyword(s):  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Experimental Models ◽  
Nuclear Medicine Imaging ◽  
Lung Water ◽  
Edema Formation ◽  
Cyclooxygenase Inhibition ◽  
Positron Emission

In experimental models of acute lung injury, cyclooxygenase inhibition improves oxygenation, presumably by causing a redistribution of blood flow away from edematous lung regions. This effect on perfusion pattern could also reduce alveolar edema formation. On the other hand, pulmonary pressures usually increase after cyclooxygenase inhibition, an effect that could exacerbate edema accumulation. Therefore we tested the following hypothesis: the total accumulation of pulmonary edema in dogs during a 24- to 28-h period of observation after acute lung injury caused by oleic acid will be less in a group of animals treated with meclofenamate (n = 6) or with the thromboxane-receptor blocker ONO-3708 (n = 5) than in a group of animals treated with oleic acid alone (placebo, n = 6). Lung water concentrations (LWC), the regional pattern of pulmonary perfusion, and protein permeability were measured with the nuclear medicine imaging technique of positron emission tomography. After 24-28 h, LWC was significantly less (P < 0.05) in the ONO-3708 group than in the meclofenamate group (a similar trend was seen compared with the placebo group, P = 0.12). After 24-28 h, pulmonary arterial pressures were highest in the meclofenamate group. Regardless of group, the only significant correlation with the change in LWC was with the integral of pulmonary pressures over the 24- to 28-h period. The data suggest that thromboxane inhibition will reduce edema accumulation in acute lung injury but that this effect depends on reducing as much as possible the simultaneous development of pulmonary hypertension from other causes.

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