Arterialized venous perfusion of composite tissue

The results of our experiment prove that arterialized venous perfusion is a viable means of nourishing complex composite tissue without using the arterial tree. Previous laboratory findings, coupled with the results of this experiment, demonstrate that as long as proximal arterial inflow is ensured, both the arterial and venous trees need not be intact to keep tissue alive. Rather, it seems that the prerequisites for tissue survival are that at least one of the two systems be intact and that there be sufficient inflow and outflow channels available. Whether these channels are arteries or veins is probably not important. The use of properly placed efferent or afferent arteriovenous fistulas allows one system to provide both physiologic functions. Whether the efferent arterial anastomosis stays open over the long term appears to be inconsequential. Survival is ensured by either direct perfusion with oxygen delivery through the venous tree or through the eventual ingrowth of recipient vessels into the flap by way of the delay phenomena. This perfusion technique is ideally suited for tissue with an inadequate arterial tree but with an intact venous system devoid of venous valves (most veins less than 1.5 mm in diameter). A well-vascularized recipient bed capable of providing vessel ingrowth into transferred tissue may be important in the case of delayed arteriovenous fistula occlusion secondary to intimal hyperplasia; therefore, further experimental study of these flaps must be undertaken before arterialized venous flaps can be recommended for placement in recipient sites compromised due to radiation, ischemia, diabetes, or other causes of small vessel disease in the recipient bed. Although efferent arteriovenous fistulas are currently used to provide arterialized venous perfusion in selected cases of end stage arterial occlusive and vasospastic disease, perhaps their greatest role is in the management of tissue transfer with an inadequate arterial tree. Much knowledge must be gained to understand the physiologic principles and requirements for optimal perfusion. Many questions are left unanswered. For example, in those arteriovenous fistulas that narrow or occlude secondary to neointimal hyperplasia or other causes, which channels (veins or arteries?) are used for perfusion during recipient vessel growth? Can intimal hyperplasia be reversed or prevented by drug therapy and would this be advantageous? Can venous valves be made incompetent so that this technique can be used for larger vessels?(ABSTRACT TRUNCATED AT 400 WORDS)