Pulmonary circulation demonstration using an isolated rat lung model.

We have developed a pulmonary circulation laboratory exercise that effectively illustrates basic concepts typically taught in a graduate physiology curriculum. The demonstration uses an isolated, perfused rat lung model to delineate the mechanisms by which pulmonary vascular resistance can be altered either passively or in an active manner by contraction or relaxation of vascular smooth muscle. The exercise further offers an opportunity to closely observe an experimental preparation commonly used to study the pulmonary circulation and allows students the opportunity to interpret the resulting physiological data. Student evaluations indicate that the demonstration was received with enthusiasm and provides an effective teaching tool for reinforcing concepts in pulmonary vascular physiology.

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Adenosine transport by the lung

Journal of Applied Physiology ◽

10.1152/jappl.1988.65.1.297 ◽

1988 ◽

Vol 65 (1) ◽

pp. 297-305 ◽

Cited By ~ 2

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.

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Release of neuroendocrine products in the pulmonary circulation during intermittent hypoxia in isolated rat lung

Respiratory Physiology & Neurobiology ◽

10.1016/j.resp.2008.02.014 ◽

2008 ◽

Vol 162 (1) ◽

pp. 1-7 ◽

Cited By ~ 2

Author(s):

Sveinung Sørhaug ◽

Sigurd Steinshamn ◽

Bjørn Munkvold ◽

Helge L. Waldum

Keyword(s):

Pulmonary Circulation ◽

Intermittent Hypoxia ◽

Rat Lung ◽

Isolated Rat Lung ◽

Isolated Rat

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Injurious ventilatory strategies increase cytokines and c-fos m-RNA expression in an isolated rat lung model.

Journal of Clinical Investigation ◽

10.1172/jci119259 ◽

1997 ◽

Vol 99 (5) ◽

pp. 944-952 ◽

Cited By ~ 899

Author(s):

L Tremblay ◽

F Valenza ◽

S P Ribeiro ◽

J Li ◽

A S Slutsky

Keyword(s):

Lung Model ◽

Rna Expression ◽

Rat Lung ◽

Isolated Rat Lung ◽

Isolated Rat

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Reduction of oedema formation after preconditioning with dopamine in an isolated rat lung model is mediated by adrenergic receptors

Annals of Transplantation ◽

10.12659/aot.882001 ◽

2011 ◽

Vol 16 (3) ◽

pp. 97-107 ◽

Cited By ~ 3

Author(s):

Christine Hanusch ◽

Charlotte Hauser ◽

Antje Geisler ◽

Kai Nowak ◽

Andreas Dacho ◽

...

Keyword(s):

Adrenergic Receptors ◽

Lung Model ◽

Rat Lung ◽

Oedema Formation ◽

Isolated Rat Lung ◽

Isolated Rat

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Muscarinic agonists and antagonists cause vasodilation in isolated rat lung

Journal of Applied Physiology ◽

10.1152/jappl.1995.78.4.1404 ◽

1995 ◽

Vol 78 (4) ◽

pp. 1404-1411 ◽

Cited By ~ 10

Author(s):

P. S. Wilson ◽

P. L. Khimenko ◽

J. W. Barnard ◽

T. M. Moore ◽

A. E. Taylor

Keyword(s):

Airway Pressure ◽

Lung Model ◽

Peak Airway Pressure ◽

Receptor Subtypes ◽

Rat Lung ◽

Muscarinic Agonists ◽

Selective Antagonist ◽

M1 Receptors ◽

Isolated Rat Lung ◽

Isolated Rat

The present study investigated the ability of atropine and different muscarinic receptor subtypes to affect acetylcholine (ACh)-induced bronchoconstriction and vasodilation in the isolated rat lung model. ACh (10(-7) M) given after U-46619 decreased total (RT), precapillary, and postcapillary vascular resistances and increased peak airway pressure. Atropine (20 microM) decreased RT and precapillary and postcapillary vascular resistances and blocked ACh-induced increases in peak airway pressure. The M1-selective agonist McN-A-343 (1.3 x 10(-5) M) decreased RT from 40.27 +/- 2.98 to 29.20 +/- 2.81 cmH2O.l–1.min-100 g lung wt (P = 0.01), and ACh caused no further dilation. The M1-selective antagonist pirenzepine (1.6 x 10(-6) M) blocked ACh-induced vasodilation. The M2-selective antagonist gallamine (7.5 x 10(-7) M) decreased RT from 45.50 +/- 3.19 to 34.86 +/- 1.25 cmH2O.l–1.min.100 g lung wt (P < 0.05), and after gallamine, ACh further decreased RT to 28.59 +/- 1.75 cmH2O.l–1.min.100 g lung wt (P < 0.01). Neither the selective muscarinic agonists nor antagonists affected peak airway pressures. We conclude that ACh-induced vasodilation in isolated rat lungs preconstricted with U-46619 is mediated by M1 receptors. Atropine-induced vasodilation in this model is mediated through the inhibition of the M2 receptor. We postulate that this represents either a blockade of postganglionic receptors, permitting release of vasodilator substances from local nerve terminals, or a direct vasodilatory effect on the vascular smooth muscle.

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MCI-186 (edaravone), a free radical scavenger, attenuates ischemia–reperfusion injury and activation of phospholipase A2 in an isolated rat lung model after 18h of cold preservation

European Journal of Cardio-Thoracic Surgery ◽

10.1016/j.ejcts.2005.12.005 ◽

2006 ◽

Vol 29 (3) ◽

pp. 304-311 ◽

Cited By ~ 16

Author(s):

Y REYES ◽

T SHIMOYAMA ◽

H AKAMATSU ◽

M SUNAMORI

Keyword(s):

Free Radical ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Free Radical Scavenger ◽

Lung Model ◽

Radical Scavenger ◽

Rat Lung ◽

Cold Preservation ◽

Isolated Rat Lung ◽

Isolated Rat

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PGE1, dexamethasone, U-74389G, or Bt2-cAMP as an additive to promote protection by UW solution in I/R injury

Journal of Applied Physiology ◽

10.1152/jappl.1997.83.2.583 ◽

1997 ◽

Vol 83 (2) ◽

pp. 583-590 ◽

Cited By ~ 21

Author(s):

Chi-Huei Chiang ◽

Kang Hsu ◽

Horng-Chin Yan ◽

Horng-Jyh Harn ◽

Deh-Ming Chang

Keyword(s):

Protein Concentration ◽

Lavage Fluid ◽

Lung Model ◽

Rat Lung ◽

Preservation Solution ◽

Uw Solution ◽

Protective Agents ◽

Tnf Α ◽

Isolated Rat Lung ◽

Isolated Rat

Chiang, Chi-Huei, Kang Hsu, Horng-Chin Yan, Horng-Jyh Harn, and Deh-Ming Chang.PGE1, dexamethasone, U-74389G, or Bt2-cAMP as an additive to promote protection by UW solution in I/R injury. J. Appl. Physiol. 83(2): 583–590, 1997.—A method to reduce ischemia-reperfusion (I/R) injury can be an important criterion to improve the preservation solution. Although University of Wisconsin solution (UW) works as a lung preservation solution, its attenuation effect on I/R injury has not been investigated. We attempted to determine whether, by adding various protective agents, modified UW solutions will enhance the I/R attenuation by UW. We examined the I/R injury in an isolated rat lung model. Various solutions, e.g., physiological salt solution (PSS), UW, and modified UW solutions containing various protective agents such as prostaglandin E1, dexamethasone, U-74389G, or dibutyryl adenosine 3′,5′-cyclic monophosphate were perfused individually to evaluate the I/R injury. Isolated rat lung experiments, with ischemia for 45 min, then reperfusion for 60 min, were conducted in a closed circulating system. Hemodynamic changes, lung weight gain (LWG), capillary filtration coefficient ( Kfc), protein content of lavage fluid, concentration of cytokines, and lung histopathology were analyzed. Results showed that the acute I/R lung injury with immediate permeability pulmonary edema was associated with an increase in tumor necrosis factor-α (TNF-α) production. A significant correlation existed between TNF-α and Kfc( r = 0.8, P < 0.0001) and TNF-α and LWG ( r = 0.9, P < 0.0001), indicating that TNF-α is an important cytokine modulating early I/R injury. Significantly lower levels of Kfc, LWG, TNF-α, and protein concentration of lung lavage ( P < 0.05) were found in the UW-perfused group than in the control group perfused with PSS. Modified UW promoted the protective effect of UW to further decrease Kfc, LWG, and TNF-α ( P < 0.05). Histopathological observations also substantiated this evidence. In the UW+U-74389G group, bronchial alveolar lavage fluid contained lowest protein concentration. We conclude that the UW solution attenuates I/R injury of rat lung and that the modified UW solutions further enhance the effect of UW in reducing I/R injury. Among modified solutions, UW+U-74389G is the best. Further investigation of the improved effects of the modified UW solutions would be beneficial in lung transplantation.

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