Experimental Modeling of the Ultra-Necrotic Stage of Critical Ischemia of the Lower Limbs
So far, no experimental model of the necrotic ulcerative stage of critical limb ischemia has been created. Aim. Development of a method for modeling the necrotic ulcerative stage of critical lower limb ischemia. Materials and methods. The experimental study was carried out on 120 rats - males of the "Wistar" line, divided into 4 groups of 30 animals each. In the first group (intact), the level of microcirculation in the muscles of the hind limb was determined. In the second (sham-operated) group, ischemia was not simulated, but the neurovascular bundle of the thigh was isolated and the wound was sutured. In the third group (comparison), the modeling of chronic ischemia of the leg muscles was performed by removing the femoral, popliteal, anterior and posterior tibial arteries. In the fourth (experimental) group, to simulate chronic critical ischemia of the leg muscles, the femoral, popliteal, anterior and posterior tibial arteries and veins were removed, and the peripheral nerve was damaged. In the postoperative period, the dynamics of symptoms of limb ischemia was monitored. Animals were taken out of the experiment, 10 animals in each group by an overdose of anesthesia on the 10th, 21st and 28th days. Before hatching, the level of microcirculation was determined using laser Doppler flowmetry. To study the morphological picture at the same time in the third and fourth groups, the ischemic gastrocnemius muscle of the leg was excised and a standard histological examination was performed. Results. Trophic disorders in animals of the third group developed in 13.3%, and in the experimental group - in 100%. In the experimental group, the level of microcirculation at all periods was significantly less than in the comparison group: on the 10th and 21st by 1.3 times, on the 28th day by 1.2 times, and the area of muscle necrosis was greater by the same days by 21.2%, by 8.2% and by 6.8%. Conclusion. The developed experimental model corresponds to the necrotic ulcerative stage of critical ischemia in humans.