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.
Folkerth TL, Wahrenbrock EA, Carrico CJ, Trummer MJ. Role of the Atrial Myocardium in the Pathogenesis of the "Shock Lung". Arch Surg. 1970;101(3):416–420. doi:10.1001/archsurg.1970.01340270064017
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