Catalase pretreatment attenuates oleic acid-induced edema in isolated rabbit lung

1988 ◽  
Vol 65 (3) ◽  
pp. 1301-1306 ◽  
Author(s):  
S. A. Katz ◽  
M. Venkatachalam ◽  
R. K. Crouch ◽  
J. E. Heffner ◽  
P. V. Halushka ◽  
...  
Keyword(s):  
Free Radicals ◽  
Oleic Acid ◽  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Airway Pressure ◽  
Pulmonary Arterial Pressure ◽  
Vascular Dysfunction ◽  
Rabbit Lung ◽  
Lung Weight ◽  
Pulmonary Arterial

Because reactive O2 metabolites have been demonstrated to be potent mediators of vascular dysfunction and are synthesized by lung tissue, their involvement as mediators of oleic acid (OA)-induced pulmonary edema in the isolated Krebs-perfused rabbit lung was assessed. Injection of OA (0.1 ml) into the pulmonary artery after vehicle pretreatment induced marked increases in lung weight [50.4 +/- 13.9 vs. 4.2 +/- 2.0 (SE) g 45 min after OA or vehicle, respectively, P less than 0.05], an index of pulmonary edema, and airway pressure. OA also caused a significant though minimal increase in pulmonary arterial pressure. Pretreatment with catalase (1,000 U/ml), a scavenger of H2O2, significantly (P less than 0.05, Friedman's) attenuated the increases in lung weight (50.4 +/- 13.9 vs. 15.1 +/- 4.9 g), airway pressure, and pulmonary arterial pressure. In contrast to catalase, pretreatment with Cu-tryptophan (40 microM), a lipid-soluble scavenger of superoxide, provided no protective effect by itself, nor was there any potentiation of protection when combined with catalase. Further evidence implicating O2 metabolites in OA-induced edema was obtained by electron paramagnetic resonance (EPR) spectroscopy of perfusate samples to which the spin trap, sodium 3,5-dibromo-4-nitrosobenzenesulfonate (10 mM), was added. Analysis of these samples revealed the presence of free radicals after OA. Pretreatment with catalase (1,000 U/ml) and superoxide dismutase (250 U/ml) attenuated the EPR signal, indicating that proximal formation of O2 free radicals was in part responsible for the signal. These results suggest that reactive O2 metabolites are mediators of OA-induced pulmonary edema in the isolated perfused rabbit lung.

PAF increases vascular permeability without increasing pulmonary arterial pressure in the rat

2001 ◽  
Vol 90 (1) ◽  
pp. 261-268 ◽  
Author(s):  
Leonardo C. Clavijo ◽  
Mary B. Carter ◽  
Paul J. Matheson ◽  
Mark A. Wilson ◽  
William B. Wead ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Pulmonary Arterial Pressure ◽  
Ex Vivo ◽  
Platelet Activating Factor ◽  
Microvascular Permeability ◽  
Blue Dye ◽  
E Coli ◽  
Pulmonary Arterial

In vivo pulmonary arterial catheterization was used to determine the mechanism by which platelet-activating factor (PAF) produces pulmonary edema in rats. PAF induces pulmonary edema by increasing pulmonary microvascular permeability (PMP) without changing the pulmonary pressure gradient. Rats were cannulated for measurement of pulmonary arterial pressure (Ppa) and mean arterial pressure. PMP was determined by using either in vivo fluorescent videomicroscopy or the ex vivo Evans blue dye technique. WEB 2086 was administered intravenously (IV) to antagonize specific PAF effects. Three experiments were performed: 1) IV PAF, 2) topical PAF, and 3) Escherichia coli bacteremia. IV PAF induced systemic hypotension with a decrease in Ppa. PMP increased after IV PAF in a dose-related manner. Topical PAF increased PMP but decreased Ppa only at high doses. Both PMP (88 ± 5%) and Ppa (50 ± 3%) increased during E. coli bacteremia. PAF-receptor blockade prevents changes in Ppa and PMP after both topical PAF and E. coli bacteremia. PAF, which has been shown to mediate pulmonary edema in prior studies, appears to act in the lung by primarily increasing microvascular permeability. The presence of PAF might be prerequisite for pulmonary vascular constriction during gram-negative bacteremia.

Cyclooxygenase and lipoxygenase inhibition by BW-755C reduces acrolein smoke-induced acute lung injury

1994 ◽  
Vol 77 (2) ◽  
pp. 888-895 ◽  
Author(s):  
S. P. Janssens ◽  
S. W. Musto ◽  
W. G. Hutchison ◽  
C. Spence ◽  
M. Witten ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Pulmonary Arterial Pressure ◽  
Weight Ratio ◽  
Peak Inspiratory Pressure ◽  
Dry Weight ◽  
Lymph Flow ◽  
Pulmonary Arterial ◽  
Arterial Po2

Inhalation of smoke containing acrolein, the most common toxin in urban fires after carbon monoxide, causes vascular injury with non-cardiogenic pulmonary edema containing potentially edematogenic eicosanoids such as thromboxane (Tx) B2, leukotriene (LT) B4, and the sulfidopeptide LTs (LTC4, LTD4, and LTE4). To determine which eicosanoids are important in the acute lung injury, we pretreated sheep with BW-755C (a combined cyclooxygenase and lipoxygenase inhibitor), U-63557A (a specific Tx synthetase inhibitor), or indomethacin (a cyclooxygenase inhibitor) before a 10-min exposure to a synthetic smoke containing carbon particles (4 microns) with acrolein and compared the results with those from control sheep that received only carbon smoke. Acrolein smoke induced a fall in arterial PO2 and rises in peak inspiratory pressure, main pulmonary arterial pressure, pulmonary vascular resistance, lung lymph flow, and the blood-free wet-to-dry weight ratio. BW-755C delayed the rise in peak inspiratory pressure and prevented the fall in arterial PO2, the rise in lymph flow, and the rise in wet-to-dry weight ratio. Neither indomethacin nor U-63557A prevented the increase in lymph flow or wet-to-dry weight ratio, although they did blunt and delay the rise in airway pressure and did prevent the rises in pulmonary arterial pressure and pulmonary vascular resistance. Thus, cyclooxygenase products, probably Tx, are responsible for the pulmonary hypertension after acrolein smoke and to some extent for the increased airway resistance but not the pulmonary edema. Prevention of high-permeability pulmonary edema after smoke with BW-755C suggests that LTB4, may be etiologic, as previous work has eliminated LTC4, LTD4, and LTE4.

Hypoxic pulmonary vasoconstriction during steady and pulsatile flow in ferrets

1984 ◽  
Vol 57 (1) ◽  
pp. 205-212 ◽  
Author(s):  
T. J. Gregory ◽  
M. L. Ellsworth ◽  
J. C. Newell
Keyword(s):  
Arterial Pressure ◽  
Steady Flow ◽  
Pulsatile Flow ◽  
Airway Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Flow Curves ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Pulsatile Perfusion

We examined the effects of hypoxia and pulsatile flow on the pressure-flow relationships in the isolated perfused lungs of Fitch ferrets. When perfused by autologous blood from a pump providing a steady flow of 60 ml/min, the mean pulmonary arterial pressure rose from 14.6 to 31.3 Torr when alveolarPO2 was reduced from 122 to 46 Torr. This hypoxic pressor response was characterized by a 10.1-Torr increase in the pressure-axis intercept of the extrapolated pressure-flow curves and an increase in the slope of these curves from 130 to 240 Torr X l–1 X min. With pulsatile perfusion from a piston-typepump, mean pulmonary arterial pressure increased from 17.5 to 36.3 Torr at the same mean flow.Thishypoxic pressor response was also characterized by increases in the intercept pressure and slope of thepressure-flow curves. When airway pressure was raised during hypoxia, the intercept pressure increased further to 25 +/- 1 Torr with a further increase in vascular resistance to 360 Torr X l–1 X min. Thus, in contrast to the dog lung, in the ferret lung pulsatile perfusion does not result in lower perfusion pressures during hypoxia when compared with similar mean levels of steady flow. Since the effects of high airway pressure and hypoxia are additive, they appear to act at or near the same site in elevating perfusion pressure.

A canine model of neurogenic pulmonary edema

1985 ◽  
Vol 59 (3) ◽  
pp. 1019-1025 ◽  
Author(s):  
M. B. Maron
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Pulmonary Arterial Pressure ◽  
Canine Model ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Neurogenic Pulmonary Edema ◽  
Lung Water ◽  
Pulmonary Arterial ◽  
Alpha Chloralose

The purpose of this study was to evaluate the usefulness of the intracisternal administration of veratrine as a model of neurogenic pulmonary edema (NPE) in the alpha-chloralose-anesthetized dog. Veratrine (40–60 micrograms/kg) was injected into the cisterna magna of 17 animals, and systemic arterial, pulmonary arterial, and left ventricular end-diastolic (LVEDP) pressures were followed for 1 h. Eleven animals developed alveolar edema. In these animals, systemic arterial pressure increased to 273 +/- 9 (SE) Torr, pulmonary arterial pressure to 74.5 +/- 4.9 Torr, and LVEDP to 42.8 +/- 4.5 Torr, and large amounts of pink frothy fluid, with protein concentrations ranging from 48 to 93% of plasma, appeared in the airways. Postmortem extravascular lung water content (Qwl/dQl) averaged 7.30 +/- 0.46 g H2O/g dry lung wt. Six animals escaped developing this massive degree of edema after veratrine (Qwl/dQl = 4.45 +/- 0.24). These animals exhibited similar elevated systemic arterial pressures (268 +/- 15 Torr), but did not develop the degree of pulmonary hypertension (pulmonary arterial pressure = 52.5 +/- 6.7 Torr, LVEDP = 24.8 +/- 4.0 Torr) observed in the other group. These results suggest that both hemodynamic and permeability mechanisms may play a role in the development of this form of edema and that veratrine administration may provide a useful model of NPE.

A New Look at Pulmonary Edema

Physiology ◽  
1986 ◽  
Vol 1 (5) ◽  
pp. 150-153 ◽  
Author(s):  
GA Laine ◽  
SJ Allen ◽  
JP Williams ◽  
J Katz ◽  
JC Gabel ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Critically Ill Patients ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Colloid Osmotic Pressure ◽  
Fluid Accumulation ◽  
Fatal Complication ◽  
Therapeutic Measures ◽  
Pulmonary Arterial

Fluid accumulation within the lungs is a potentially fatal complication in critically ill patients. Sepsis and increased microvascular permeability are often implicated as the cause. This article shows that edema can be prevented by lowering systemic venous pressure (to permit pulmonary lymph to drain), by lowering pulmonary arterial pressure, and by maintaining plasma colloid osmotic pressure. It points out the importance of understanding the basic physiology behind pulmonary edema and therapeutic measures.

Protamine sulfate causes pulmonary hypertension and edema in isolated rat lungs

1987 ◽  
Vol 62 (4) ◽  
pp. 1363-1367 ◽  
Author(s):  
R. P. Fairman ◽  
C. N. Sessler ◽  
M. Bierman ◽  
F. L. Glauser
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Weight Ratio ◽  
Dry Weight ◽  
Protamine Sulfate ◽  
Pulmonary Vasculature ◽  
Lung Weight ◽  
Control Value ◽  
Pulmonary Arterial ◽  
Vascular Beds

The polycation protamine sulfate increases microvascular permeability in the kidney by reducing glomerular charge. We have exposed the pulmonary vasculature to protamine sulfate to determine whether electrical charges play a role in protein permeability in lung vascular beds. In anephric rats, protamine sulfate increased hematocrit approximately 25%. With protamine sulfate doses of 0.08 and 0.04 mg/g body wt, lung blood-free wet-to-dry weight ratios were increased (5.24 +/- 0.8 and 4.89 +/- 0.7) compared with control (3.85 +/- 0.3) (P less than 0.05). In isolated, ventilated, and perfused lungs 0.04 mg/g body wt protamine sulfate increased pulmonary arterial pressure from 5.2 +/- 1.4 to 16.3 +/- 3.9 mmHg (P less than 0.01). These lungs gained weight and lung wet-to-dry weight ratios were significantly increased (15.33 +/- 4.26 compared with 6.04 +/- 0.24 for control lungs). Poly-L-lysine, another polycation, also caused significant increases in pulmonary arterial pressure, lung weight, and lung wet-to-dry weight ratios. The addition of diphenhydramine to the perfusate 10 min before the addition of protamine sulfate did not prevent these changes. Heparin (90 U/mg protamine sulfate) reversed the abnormalities. Pulmonary arterial pressure (7.0 +/- 1.1 mmHg) was not significantly different from the control value, lung weight did not increase, and the lung wet-to-dry weight ratio was 6.24 +/- 0.23 (P greater than 0.05). We conclude that polycations have a significant effect on pulmonary vascular resistance and perhaps on permeability.

The endocannabinoid arachidonyl ethanolamide (anandamide) increases pulmonary arterial pressure via cyclooxygenase-2 products in isolated rabbit lungs

2005 ◽  
Vol 289 (6) ◽  
pp. H2491-H2496 ◽  
Author(s):  
Hans Wahn ◽  
Jürgen Wolf ◽  
Florian Kram ◽  
Stefan Frantz ◽  
Jens A. Wagner
Keyword(s):  
Arachidonic Acid ◽  
Arterial Pressure ◽  
Receptor Antagonist ◽  
Pulmonary Arterial Pressure ◽  
Lung Edema ◽  
Rabbit Lung ◽  
Acid Product ◽  
Cox Inhibitor ◽  
Pulmonary Arterial ◽  
Cox 2

Several cannabinoids elicit systemic vasodilation, mainly via CB1 cannabinoid and vanilloid receptors. However, effects in the pulmonary circulation are unknown. Using the isolated, ventilated, buffer-perfused rabbit lung, we have shown that the endocannabinoids arachidonyl ethanolamide (anandamide) and 2-arachidonyl glycerol (2-AG) dose-dependently increase pulmonary arterial pressure (+19.9 ± 3.4 mmHg, 5 μM, and +39.5 ± 10.8 mmHg, 0.4 μM, respectively). 2-AG induced lung edema. The CB1 receptor antagonist AM-251 (0.1 and 5 μM) and the VR1 vanilloid receptor antagonist capsazepine (10 μM) failed to reduce anandamide's effects. The metabolically stable anandamide and 2-AG analogs R-methanandamide and noladin ether, Δ9-tetrahydrocannabinol, and the synthetic cannabinoid HU-210, which is no arachidonic acid product, were without effect. The unspecific cyclooxygenase (COX) inhibitor aspirin (100 μM, P < 0.001) and the specific COX-2 inhibitor nimesulide (10 μM, P < 0.01) completely prevented pulmonary hypertension after 5 μM anandamide. COX-2 RNA was detected in rabbit lungs. The synthetic thromboxane receptor antagonist SQ 29,548 was without effect, but the specific EP1 prostanoid receptor antagonist SC-19220 (100 μM) inhibited the pressure increase after anandamide ( P < 0.05). PCR analysis detected fatty acid amidohydrolase (FAAH), an enzyme that degrades endocannabinoids, in rabbit lung tissue. Furthermore, the specific FAAH inhibitor methyl arachidonyl fluorophosphonate (0.1 μM) blocked pressure effects of anandamide ( P < 0.01). Finally, anandamide (99 ± 55 pmol/g) and 2-AG (19.6 ± 8.4 nmol/g) were found in native lungs. We conclude that anandamide increases pulmonary arterial pressure via COX-2 metabolites following enzymatic degradation by FAAH into arachidonic acid products.

Pulmonary hypertension after postlavage lung injury in rabbits: possible role of polymorphonuclear leukocytes

1991 ◽  
Vol 71 (5) ◽  
pp. 1990-1995 ◽  
Author(s):  
R. Burger ◽  
A. C. Bryan
Keyword(s):  
Pulmonary Hypertension ◽  
Gas Exchange ◽  
Lung Injury ◽  
Arterial Pressure ◽  
Airway Pressure ◽  
Pulmonary Arterial Pressure ◽  
Lung Lavage ◽  
High Frequency Ventilation ◽  
Mean Airway Pressure ◽  
Pulmonary Arterial

Previous studies showed that repeated lung lavage leads to a severe lung injury with very poor gas exchange, a substantial protein leak into the alveoli with hyaline membrane formation, pulmonary hypertension, and migration of granulocytes (PMN) into the alveolar spaces. Depletion of PMN leads to a better gas exchange and a markedly decreased protein leak with only scanty hyaline membranes. In this study we show that there is sustained pulmonary hypertension after the lung lavage, but in PMN-depleted rabbits there is no postlavage increase in pulmonary arterial pressure. Changing the shunt fraction by manipulating mean airway pressure still leads to a hypoxic vasoconstriction with increase of pulmonary arterial pressure. Thus, after lung lavage, pulmonary reactivity to hypoxia is still preserved. Comparisons between high-frequency ventilation and conventional mechanical ventilation at the same mean airway pressures showed that equal mean airway pressure in these two very different modes of ventilation do not translate into the same mean functional lung volumes.

Effect of end-expiratory airway pressure on accumulation of extravascular lung water

1975 ◽  
Vol 38 (5) ◽  
pp. 907-912 ◽  
Author(s):  
R. H. Demling ◽  
N. C. Staub ◽  
L. H. Edmunds
Keyword(s):  
Hydrostatic Pressure ◽  
Arterial Pressure ◽  
Osmotic Pressure ◽  
Extravascular Lung Water ◽  
Airway Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Occlusion ◽  
Colloid Osmotic Pressure ◽  
Lung Water ◽  
Pulmonary Arterial

The effect of end-expiratory airway pressure on the accumulation of extravascular lung water during lobar venous occlusion for 2 h was studied in closed-chest artifically ventilated dogs. Dogs were divided into two groups by end-expiratory airway pressures of 0 or 10 cmH2O. High-pressure lobar pulmonary edema was produced by lobar venous occlusion, which elevated microvascular hydrostatic pressure. After occlusion of the lobar pulmonary vein, lobar venous pressure (and microvascular hydrostatic pressure) rapidly became identical to pulmonary arterial pressure. We measured extravascular lung water (post mortem) and pulmonary arterial pressure and calculated plasma colloid osmotic pressure to determine the relationship between the accumulation of lung water and the difference between pulmonary microvascular pressure and plasma colloid osmotic pressure (net intravascular filtration pressure). At comparable net intravascular filtration pressures, dogs ventilated at the higher end-expiratory airway pressure accumulated more extravascular lung water. This study indicates that increasing end-expiratory airway pressure from zero to 10 cmH2O increases the accumulation of extravascular lung water when microvascular hydrostatic pressure is raised.

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