scholarly journals Time to move away from an oxygen-centric model of pulmonary infarction? – Authors' reply

Author(s):  
Dennis McGonagle ◽  
Charlie Bridgewood ◽  
James F M Meaney
Keyword(s):  
2021 ◽  
Vol 9 (9) ◽  
Author(s):  
Kyoko Gocho ◽  
Shinnosuke Kitazawa ◽  
Shinya Matsushita ◽  
Nobuyuki Hamanaka

1960 ◽  
Vol 198 (3) ◽  
pp. 543-546 ◽  
Author(s):  
S. A. Kabins ◽  
J. Fridman ◽  
J. Neustadt ◽  
G. Espinosa ◽  
L. N. Katz

A localized pulmonary infarction was produced by injecting a starch suspension into the pulmonary artery wedge position of one lung lobe in pentobarbitalized dogs, and the effect of three so-called antiserotonins on the ensuing pulmonary edema was determined. Edema was inhibited in the nonembolized lung lobes in 88% of the B.A.S. (1-benzyl-2-methyl-5-methoxytryptamine HCl), 45% of the DHE (dihydroergotamine), and 12% of the BOL (2-brom- d-lysergic acid diethylamide) dogs. Reasons are given for assuming that the actions of B.A.S. and DHE are due to their antiadrenergic rather than to any antiserotonin properties which they may have. Serotonin, therefore, at most has a slight role in the pulmonary edema formation caused by starch emboli. It is postulated that the emboli by producing an infarct and setting up a reflex mediated through the sympathetic nervous system, cause the release in turn of catecholamines and of histamine, the latter being immediately responsible for the capillary permeability change leading to pulmonary edema.


CHEST Journal ◽  
1991 ◽  
Vol 99 (2) ◽  
pp. 298-300 ◽  
Author(s):  
Romain Kessler ◽  
Philippe Fraisse ◽  
Denis Krause ◽  
Francis Veillon ◽  
André Vandevenne

1988 ◽  
Vol 47 (10) ◽  
pp. 869-872 ◽  
Author(s):  
H S Howe ◽  
M L Boey ◽  
K Y Fong ◽  
P H Feng

1972 ◽  
Vol 14 (2) ◽  
pp. 181-188 ◽  
Author(s):  
Joe I. Miller ◽  
Edgar G. Harrison ◽  
Philip E. Bernatz
Keyword(s):  

The Lancet ◽  
1927 ◽  
Vol 210 (5442) ◽  
pp. 1289-1290
Author(s):  
Richard Massingham

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