A morphological study of the long-term repair process in experimentally stretched but unruptured arteries and veins.

As many avulsion amputations are incomplete and the vessels remain intact, the immediate pathology and long-term repair process (to 3 months post-injury) of experimentally stretched but unruptured rabbit femoral arteries and veins were examined. In stretched arteries, circumferential skip lesions involving endothelium, internal elastic lamina (IEL) and media occurred frequently and often up to 3 cm from the point of stretch. Medial smooth muscle cells (SMC) were significantly damaged or lost at lesions. Macrophages and neutrophils were found in lesions 1-4 days post-injury. Between 2-4 days, lesions were covered by endothelium and synthetic state SMC appeared in the media. At 1 week, a thin neointima (which persisted to 3 months) covered many lesions. The media at lesions gradually filled with SMC but generally remained disorganised even at 3 months post-injury. Stretching caused tears in vein walls, particularly close to the point of injury. There was no evidence of venous damage or repair in specimens examined 3 weeks and 3 months post-injury.

Lymph node transfer for the treatment of obstructive lymphoedema in the canine model.

The efficacy of transferring vascularised lymph nodes into lymphoedematous limbs was investigated. Stable below-knee lymphoedema was established in one hind limb of 10 dogs. The superficial inguinal lymph node and perinodal tissue from the normal hind limb was moved to the popliteal region of the lymphoedematous leg as a free vascularised transfer. In five dogs lymphaticolymphatic anastomoses between lymphatics of the node and proximal recipient site lymphatics were also performed. Circumferential measurements of the foot, ankle and midleg were obtained preoperatively and postoperatively at 3 and 6 months. These measurements showed postoperative reduction of the lymphoedematous legs compared to controls, with no added benefit from lymphaticolymphatic anastomoses. Technetium 99 scans and lymphangiography demonstrated re-establishment of lymphatic continuity in all recipient legs at 3 and 6 months post-transfer. Histological examination at 3 and 6 months revealed normal architecture in 9 of 10 nodes, although areas of lymphocyte depletion were common. Vascularised lymph node transfer to a lymphoedematous leg re-established lymphatic continuity and resulted in partial reduction of limb size. The addition of lymphaticolymphatic anastomosis to vascularized node transfer is neither necessary nor beneficial.

The long-term fate of microvenous autografts.

Changes in length, external diameter, wall thickness, and morphology were examined in 60 intraarterial vein grafts and 30 intravenous vein grafts inserted in rabbit femoral vessels. Half of each graft type was explored at 6 or 12 months, giving four experimental groups. The overall patency for intraarterial grafts at exploration was 98 percent and for intravenous grafts 100 percent. In comparison with the initial graft length resected, all four groups were significantly shorter at the completion of anastomosis, and three of the four groups also were significantly shorter at exploration. The overall loss in length of grafts varied between 26 and 30 percent of original length. External diameter was significantly increased (from between 133 and 201 percent) in all four groups at exploration compared to the normal femoral vein. Intravenous grafts maintained normal vein morphology to 12 months. Intraarterial grafts were modified by the ingrowth of smooth-muscle cells from the recipient artery, thereby creating a neointima that significantly thickened their walls at both 6 and 12 months.

Changes in the blood biochemistry following experimental flap ischaemia.

The purpose of this study was to elucidate tissue changes occurring within an ischaemic flap by monitoring the blood biochemistry, and to evaluate these changes in relation to ultimate flap viability. A rabbit epigastric free flap was made ischaemic for 4 days at 6 degrees C, then revascularized by anastomosis of its femoral artery and vein. An identical free flap immediately revascularized in another group of rabbits served as a control. The viability of the free flap, as well as various biochemical parameters studied by drawing blood from a catheter in the ear vein, were observed daily. Immediately after the revascularization of ischaemic flaps, there was a 16-fold increase in the plasma levels of creatine kinase (CK) and a smaller but significant 1.5-fold to 2.0-fold increase in lactate dehydrogenase (LDH) and aspartate aminotransferase (AST). In flaps which ultimately failed by 7 days post-ischaemia, the plasma levels of CK, LDH and AST peaked at day 2 post-ischaemia at 68, 13 and 8 times normal respectively, whereas in flaps which survived, the levels of these enzymes recovered to normal by day 3 post-ischaemia. These enzymic changes are probably due to a combination of ischaemic changes in the flap vasculature, ischaemic changes in the flap muscle, and inflammatory changes in the surrounding abdominal tissue. The plasma levels of CK at any time post-ischaemia, and particularly in the first 24 h, were significantly higher in ischaemic flaps which failed compared with those which survived. This parameter is therefore proposed as a possible means of predicting potential flap failure after ischaemic insult, in time to make appropriate surgical intervention.