One of the striking sequelae of arteriovenous communication is the change occurring in the proximal and distal portions of the affected veins, as evidenced by the dilated appearance of the immediate receiving group of venous channels; the intravenous pressure is increased, since the veins receive blood directly from a vessel in which the pressure is higher. The veins assume the anatomic and functional characteristics of arteries and thus become arterialized. The adaptation of the vein to this abnormal strain was studied by Reid,1 who noted the thickening of the vein with firm walls simulating an artery. The intima was thickened and the media hypertrophied, with a new production of elastic tissue in the internal layer. These changes can be explained as an adjustment to altered mechanical conditions. The interposition of the small arteriolar and capillary bed is lacking in the regional circulation, and the blood pressure does not undergo its
BROWN GE. ABNORMAL ARTERIOVENOUS COMMUNICATIONSDIAGNOSED FROM THE OXYGEN CONTENT OF THE BLOOD OF THE REGIONAL VEINS. Arch Surg. 1929;18(3):807–810. doi:10.1001/archsurg.1929.04420040039003
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