The occurrence of cell-infiltrated intimal lesions at the confluence of many small tributaries with canine jugular and femoral veins suggested that these areas (confluences) might (1) differ structurally from the rest of the receiving vein and (2) serve as initiation sites for thrombi. To explore these possibilities, the number of tributaries was determined by careful blunt dissection, and the architecture of confluences was studied by light and scanning and transmission electron microscopy. In addition to confluences formed by a named tributary (omobrachial), canine jugular veins averaged 11 confluences formed with small (0.2 to 2.5 mm diameter) unnamed tributaries that had not been previously described. Femoral veins averaged eight confluences of which four were formed with small unnamed tributaries. Double-leafed valves were found at 90% of jugular and 76% of femoral vein confluences. Previously such valves were described only at the confluence of superficial with deep leg veins. Corrosion casts of iliac, saphenous, azygous, costocervical, and maxillary veins as well as cranial and caudal vena cava demonstrated a similar pattern of tributaries and valves.

The three structures (receiving vein, tributary, valves) that formed the confluence differed, necessitating considerable modification as they approached the area of fusion. Jugular and femoral vein walls contained 5 to 10 layers of smooth muscle, abundant collagen, and a small amount of elastin. Tributary walls contained 0 to 2 discontinuous smooth muscle cell layers, limited collagen, and no elastin. As receiving veins approached a confluence, the thickness decreased by 15 to 77% except at valve attachment sites, which were thickened. A cluster of smooth muscle cells formed the junction of valve leaflets with vein. Endothelium was continuous over the luminal surface of all three structures. Calculations showed that these small-valved tributaries make only a small contribution to venous return. On the other hand, there is considerable information to support the concept that local attenuation of the vein wall would lead to localized vessel dilation, resulting in rupture of the endothelium and basement membrane.