Zeitschriften

Journal of Molecular Medicine -     

Zeitschriften

Journal of Molecular Medicine -     

Zeitschriften

Journal of Molecular Medicine -     

THE HISTOPATHOLOGY OF PROGRESSIVE MUSCULAR DYSTROPHY AS REVEALED BY ULTRAVIOLET PHOTOMICROGRAPHY

1. In a series of rats subjected to hemorrhage and shock a high negative correlation was found between the portal and peripheral venous oxygen saturations and the arterial blood pressure on the one hand, and the blood amino nitrogen levels on the other, and a high positive correlation between the portal and the peripheral oxygen saturations and between each of these and the blood pressure. 2. In five cats subjected to hemorrhage and shock the rise in plasma amino nitrogen and the fall in peripheral and portal venous oxygen saturations were confirmed. Further it was shown that the hepatic vein oxygen saturation falls early in shock while the arterial oxygen saturation showed no alteration except terminally, when it may fall also. 3. Ligation of the hepatic artery in rats did not affect the liver''s ability to deaminate amino acids. Hemorrhage in a series of hepatic artery ligated rats did not produce any greater rise in the blood amino nitrogen than a similar hemorrhage in normal rats. The hepatic artery probably cannot compensate to any degree for the decrease in portal blood flow in shock. 4. An operation was devised whereby the viscera and portal circulation of the rat were eliminated and the liver maintained only on its arterial circulation. The ability of such a liver to metabolize amino acids was found to be less than either the normal or the hepatic artery ligated liver and to have very little reserve. 5. On complete occlusion of the circulation to the rat liver this organ was found to resist anoxia up to 45 minutes. With further anoxia irreversible damage to this organ''s ability to handle amino acids occurred. 6. It is concluded that the blood amino nitrogen rise during shock results from an increased breakdown of protein in the peripheral tissues, the products of which accumulate either because they do not circulate through the liver at a sufficiently rapid rate or because with continued anoxia intrinsic damage may occur to the hepatic parenchyma so that it cannot dispose of amino acids.     

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