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Role of the Atrial Myocardium in the Pathogenesis of the "Shock Lung"
LCDR Theodore L. Folkerth, MC, USN;
LCDR Eric A. Wahrenbrock, MC, USNR;
LCDR Charles J. Carrico, MC, USNR;
CAPT Max J. Trummer, MC, USN
AMA Arch Surg. 1970;101(3):416-420.
Abstract
Autotransplantation of one lung in dogs has been shown to protect the transplanted lung following hypovolemic shock and reinfusion of blood from the changes of congestive atelectasis referred to as "shock lung." In an attempt to elicit the factor responsible for this protection, ten dogs underwent sectioning and reanastomosis of the left atrial myocardium to interrupt the "throttle valve" or extension of atrial myocardium onto the pulmonary veins. No protection was observed as determined by differential compliance and oxygen uptake, as well as by histologic studies. Our conclusion was that defunctionalization by interruption of the neuromuscular control of the throttle valve surrounding the ostia of the pulmonary veins did not protect against the congestive atelectasis of the shock lung.
Author Affiliations
San Diego, Calif
From the Research Laboratory, Naval Hospital, San Diego, Calif. Dr. Carrico is now with the Department of Surgery, University of Texas Southwestern Medical School, Dallas. Dr. Wahrenbrock is now with the Cardiovascular Research Institute, University of California Medical Center, San Francisco.
Footnotes
Accepted for publication March 9, 1970.
Read before the sectional meeting of the Southern California Chapter of the American College of Surgeons, Coronado, Calif, Jan 17, 1970.
The opinions or assertions contained herein are those of the authors and are not to be construed as official or as reflecting the views of the Navy Department.
Reprint requests to Research Laboratory, Naval Hospital, San Diego, Calif 92134 (Dr. Folkerth).
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