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

2008 ◽  
Vol 162 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Sveinung Sørhaug ◽  
Sigurd Steinshamn ◽  
Bjørn Munkvold ◽  
Helge L. Waldum
1988 ◽  
Vol 65 (1) ◽  
pp. 297-305 ◽  
Author(s):  
D. K. Das ◽  
H. Steinberg

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.


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

Peptides ◽  
2002 ◽  
Vol 23 (3) ◽  
pp. 469-478 ◽  
Author(s):  
Ann Tronde ◽  
Eva Krondahl ◽  
Hans von Euler-Chelpin ◽  
Per Brunmark ◽  
Ursula Hultkvist Bengtsson ◽  
...  

2012 ◽  
Vol 112 (11) ◽  
pp. 1915-1920 ◽  
Author(s):  
Melissa L. Bates ◽  
Brendan R. Fulmer ◽  
Emily T. Farrell ◽  
Alyssa Drezdon ◽  
David F. Pegelow ◽  
...  

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.


1981 ◽  
Vol 51 (1) ◽  
pp. 90-98 ◽  
Author(s):  
T. E. Nicholas ◽  
H. A. Barr

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.


1998 ◽  
Vol 275 (6) ◽  
pp. S85
Author(s):  
T C Resta ◽  
L M Eichinger ◽  
R D Russ ◽  
B R Walker

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.


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

1951 ◽  
Vol 167 (3) ◽  
pp. 840-840 ◽  
Author(s):  
Richard W. Lawton ◽  
Doyle Joslin

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."


2012 ◽  
Vol 25 (10) ◽  
pp. 1096-1105 ◽  
Author(s):  
Akihiro Ohsumi ◽  
Fengshi Chen ◽  
Daisuke Nakajima ◽  
Jin Sakamoto ◽  
Tetsu Yamada ◽  
...  

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