Effect of urodilatin on platelet-activating factor-induced bronchoconstriction, vasoconstriction and edema formation in isolated rat lung

1996 ◽  
Vol 354 (5) ◽  
Author(s):  
Stefan Uhlig ◽  
RolandLewis Featherstone ◽  
Albrect Wendel ◽  
Otto-Henning Wilhelms
Keyword(s):  
Platelet Activating Factor ◽  
Rat Lung ◽  
Edema Formation ◽  
Isolated Rat Lung ◽  
Isolated Rat

Importance of vasoconstriction in lipid mediator-induced pulmonary edema

1989 ◽  
Vol 66 (6) ◽  
pp. 2667-2674 ◽  
Author(s):  
A. Sakai ◽  
S. W. Chang ◽  
N. F. Voelkel
Keyword(s):  
Pulmonary Edema ◽  
Weight Ratio ◽  
Dry Weight ◽  
Lipid Mediator ◽  
Lung Edema ◽  
Rat Lung ◽  
Edema Formation ◽  
Mediators Of Inflammation ◽  
Isolated Rat Lung ◽  
Isolated Rat

Lipid mediators of inflammation cause pulmonary edema, yet it is unclear to what degree hemodynamic alterations or increased vascular permeability contribute to lung edema formation. The isolated rat lung preparation was used to examine the effect of leukotriene C4 (LTC4) and platelet-activating factor (PAF) on pulmonary arterial pressure (Ppa), lung microvascular pressure (Pmv), lung wet-to-dry weight ratio, and the 125I-albumin escape index. We first defined the response of the isolated rat lung perfused with protein-free salt solution to hydrodynamic stress by raising the lung outflow pressure. Sustained elevation of the lung outflow pressure less than 5.5 cmH2O (4.01 mmHg) caused a negligible increase in Ppa and wet-to-dry lung weight ratio. Elevation of outflow pressures greater than 7.5 cmH2O (5.4 mmHg) increased the vascular albumin escape index more than the lung wet-to-dry weight ratio. Dibutyryl adenosine 3′,5′-cyclic monophosphate (db-cAMP) inhibited the increase in albumin escape index because of increased lung outflow pressure, suggesting perhaps a pressure-independent microvascular membrane effect of db-cAMP. Both LTC4 (2-micrograms bolus) and PAF (2–2,000 ng/ml perfusate) increased the albumin escape index in association with increases in Ppa and Pmv. Because the increased albumin escape index after LTC4 or PAF injection was largely accounted for by the increased vascular pressures and because db-cAMP and papaverine inhibited the rise in vascular pressures and in the albumin escape index, we conclude that vasoconstriction is an important contributor to LTC4- and PAF-induced edema formation in rat lungs.

Pulmonary preservation effect of nitroglycerine in isolated rat lung reperfusion model

2004 ◽  
Vol 36 (7) ◽  
pp. 1933-1935 ◽  
Author(s):  
S. Jheon ◽  
Y.M. Lee ◽  
S.W. Sung ◽  
J.H. Choh ◽  
K.Y. Kwon ◽  
...  
Keyword(s):  
Rat Lung ◽  
Isolated Rat Lung ◽  
Isolated Rat

High airway-to-blood transport of an opioid tetrapeptide in the isolated rat lung after aerosol delivery

Peptides ◽  
2002 ◽  
Vol 23 (3) ◽  
pp. 469-478 ◽  
Author(s):  
Ann Tronde ◽  
Eva Krondahl ◽  
Hans von Euler-Chelpin ◽  
Per Brunmark ◽  
Ursula Hultkvist Bengtsson ◽  
...  
Keyword(s):  
Rat Lung ◽  
Aerosol Delivery ◽  
Blood Transport ◽  
Isolated Rat Lung ◽  
Isolated Rat

scholarly journals Hypoxia recruits intrapulmonary arteriovenous pathways in intact rats but not isolated rat lungs

2012 ◽  
Vol 112 (11) ◽  
pp. 1915-1920 ◽  
Author(s):  
Melissa L. Bates ◽  
Brendan R. Fulmer ◽  
Emily T. Farrell ◽  
Alyssa Drezdon ◽  
David F. Pegelow ◽  
...  
Keyword(s):  
Intact Animal ◽  
Large Diameter ◽  
Rat Lung ◽  
Isolated Lung ◽  
Alveolar Hypoxia ◽  
Spontaneously Breathing ◽  
Isolated Rat Lung ◽  
Mixed Venous ◽  
Isolated Rat ◽  
Intact Rats

Intrapulmonary arteriovenous anastomoses (IPAVS) directly connect the arterial and venous circulations in the lung, bypassing the capillary network. Here, we used solid, latex microspheres and isolated rat lung and intact, spontaneously breathing rat models to test the hypothesis that IPAVS are recruited by alveolar hypoxia. We found that hypoxia recruits IPAVS in the intact rat, but not the isolated lung. IPAVS are at least 70 μm in the rat and, interestingly, appear to be recruited when the mixed venous Po2 falls below 22 mmHg. These data provide evidence that large-diameter, direct arteriovenous connections exist in the lung and are recruitable by hypoxia in the intact animal.

Control of release of surfactant phospholipids in the isolated perfused rat lung

1981 ◽  
Vol 51 (1) ◽  
pp. 90-98 ◽  
Author(s):  
T. E. Nicholas ◽  
H. A. Barr
Keyword(s):  
Tidal Volume ◽  
Type Ii ◽  
Rat Lung ◽  
Cyclic Monophosphate ◽  
Type Ii Cell ◽  
Surfactant Phospholipids ◽  
Isolated Rat Lung ◽  
Isolated Rat

We used the isolated rat lung to investigate surfactant release. The lung was ventilated at 60.min-1 with 5% CO2–95% O2 and perfused at 10 ml.min-1 with Krebs-bicarbonate (4.5% albumin). After 20 min during which antagonist drugs were present, the lungs were either hyperventilated or agonist drugs were added. After another 15 min lungs were lavaged. Peak inspired pressures (PIP) in excess of 12 cmH2O produced progressively greater phospholipid (PL) yields. Whereas ventilating with PIP of 9 cmH2O and end-expired pressure(EEP) of 5 cmH2O produced 5.9 +/- 0.8 (mean +/-SD) (n = 17) mg PL. g dry lung-1, ventilating with PIP of 20 cmH2O and EEP of 0 cmH2O produced 10.1 +/- 1.3 (n = 26). PL release was unaffected by tetrodotoxin, propranolol, atropine, cyproheptadine, or indomethacin. PL was increased by salbutamol and dibutyryl adenosine 3',5'-cyclic monophosphate but not by pilocarpine or dibutyryl guanosine 3',5'-cyclic monophosphate. We conclude, that increasing tidal volume immediately releases surfactant, probably by distorting the type II cell and elevating cAMP. An intrapulmonary neural reflex is not involved in this response of the isolated rat lung, nor is histamine, 5-hydroxytryptamine, or a prostaglandin.

Adenosine transport by the lung

1988 ◽  
Vol 65 (1) ◽  
pp. 297-305 ◽  
Author(s):  
D. K. Das ◽  
H. Steinberg
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Circulation ◽  
Adenine Nucleotides ◽  
Adenosine Kinase ◽  
Rat Lung ◽  
Potent Vasodilator ◽  
Adenosine Transport ◽  
Rate Limiting ◽  
Isolated Rat Lung ◽  
Isolated Rat

Adenosine, a nucleoside and potent vasodilator, has been found to be taken up by the lung and converted by deamination into inosine and hypoxanthine. In a single circulation through an isolated rat lung, 69.3 +/- 3.3% of infused [14C]adenosine (10 microM) was removed from the circulation. Uptake of [14C]adenosine remained unchanged when deamination of adenosine was inhibited by 8-azaguanine or coformycin. In a single passage of adenosine through the pulmonary artery, very little of the deaminated products appeared in the pulmonary circulation, but when adenosine was recirculated through the pulmonary circulation inosine and hypoxanthine appeared in the venous effluent. These adenosine metabolites were also taken up by the lung. A major portion of the circulating adenosine was transported into the lung, where it was used to synthesize adenine nucleotides. Inhibition of adenosine kinase by iodotubercidin resulted in reduced formation of ATP and ADP. Uptake of adenosine by the lung was saturable on a concentration gradient and was a passive process because it was not affected by the absence of glucose or the presence of ouabain. Km and Vmax for adenosine transport were 0.227 mM and 4.6 mumol.min-1.g lung-1, respectively. Adenosine transport was inhibited by adenosine analogues, and the inhibitions were found to be competitive in nature. These results suggest that a specific and rate-limiting transport system exists in the lung for adenosine.

Factors controlling the metabolic response to glucose in isolated rat lung cells

Life Sciences ◽  
1977 ◽  
Vol 20 (9) ◽  
pp. 1599-1605 ◽  
Author(s):  
Julio Pérez-Díaz ◽  
Angeles Martín Requero ◽  
Matilde S. Ayuso-Parrilla ◽  
Roberto Parrilla
Keyword(s):  
Metabolic Response ◽  
Lung Cells ◽  
Rat Lung ◽  
Isolated Rat Lung ◽  
Isolated Rat

Effects of phorbol myristate acetate-stimulated human leukocytes on rat lung

1990 ◽  
Vol 68 (1) ◽  
pp. 235-240 ◽  
Author(s):  
M. L. Perry ◽  
S. G. Kayes ◽  
J. W. Barnard ◽  
A. E. Taylor
Keyword(s):  
Acute Lung Injury ◽  
Vascular Resistance ◽  
Phorbol Myristate Acetate ◽  
Endothelial Permeability ◽  
Human Albumin ◽  
Rat Lung ◽  
Myristate Acetate ◽  
Edema Formation ◽  
Capillary Filtration Coefficient ◽  
Isolated Rat

Human blood was separated into polymorphonuclear (PMN) and mononuclear (MN) leukocyte fractions, and 3 x 10(7) cells (PMN or MN) were added to isolated rat lungs perfused with 5% human albumin in buffer and stimulated with phorbol myristate acetate (PMA). Lungs perfused with either albumin alone, PMN, or MN but not stimulated with PMA showed no change in vascular resistance or endothelial permeability measured as the capillary filtration coefficient (Kf,c). Lungs that were stimulated with PMA with no cells showed no change in Kf,c (0.34 +/- 0.07 vs. 0.37 +/- 0.7), but vascular resistance increased in all segments of the circulation. Capillary pressure, the major force responsible for edema formation, nearly doubled in the absence of cells 40 min after PMA. Lungs perfused with either PMN or MN and stimulated with PMA were injured. Kf,c increased from 0.41 +/- 0.03 to 0.87 +/- 0.10 (PMN) and from 0.36 +/- 0.07 to 0.81 +/- 0.23 (MN) 90 min after PMA. In addition to the increased endothelial permeability, vascular resistances and pressures also increased in the cell-perfused PMA-stimulated lungs. These results demonstrate that cells other than granulocytes are capable of producing severe acute lung injury and cannot be ignored when the effects of PMA on neutrophil-depleted lungs are studied.

Measurements on the Elasticity of the Isolated Rat Lung

1951 ◽  
Vol 167 (3) ◽  
pp. 840-840 ◽  
Author(s):  
Richard W. Lawton ◽  
Doyle Joslin
Keyword(s):  
Lung Volume ◽  
Rat Lung ◽  
Total Lung Volume ◽  
Page Figure ◽  
Isolated Rat Lung ◽  
Isolated Rat

Page 117. Richard W. Lawton and Doyle Joslin, "Measurements on the Elasticity of the Isolated Rat Lung." Lines 11 to 7 from bottom of page, figure 7, and reference (12). Add the following statement: "At the end of a normal expiration the total lung volume is of the order of 5 cc. (12) or equivalent to the calculated V0 in this case. Tidal air should lie, therefore, between 0 and 1.0 to 1.5 cc. on the ordinate."

scholarly journals Therapeutic effect of surfactant inhalation during warm ischemia in an isolated rat lung perfusion model

2012 ◽  
Vol 25 (10) ◽  
pp. 1096-1105 ◽  
Author(s):  
Akihiro Ohsumi ◽  
Fengshi Chen ◽  
Daisuke Nakajima ◽  
Jin Sakamoto ◽  
Tetsu Yamada ◽  
...  
Keyword(s):  
Therapeutic Effect ◽  
Lung Perfusion ◽  
Warm Ischemia ◽  
Rat Lung ◽  
Perfusion Model ◽  
Isolated Rat Lung ◽  
Isolated Rat
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