Реализация ишемии и реперфузии в хирургии магистральных артерий нижних конечностей

Objectives. To study the molecular mechanisms of endogenic angioprotectors of stress-limiting system NO-heat shock proteins HSP70 and vascular endothelial growth factor system (VEGF) as a long-term adaptation variant to ischemia in lower limb reconstructive surgery. Methods. According to the design the study is considered to be an open, prospective, in parallel groups, includes 40 patients with the obliterating lower limb atherosclerosis. The patients were divided into 4 groups according to the degree of the lower limb ischemia and the methods of operation: the 1 st group 10 patients according to Fontaine classification system (IIb-III stages) and the 2 nd group 10 patients (IV stage) who had undergone reconstructive surgery with polytetrafluroethylene graft (PTFE); the 3 rd group 10 patients with cardiogenic nonvalvular embolism of lower extremity arteries undergone urgent embolectomy; group 4 10 patients (IIb stage) without arterial reconstruction due to poor distal runoff or patient's refusal to be operated on. Results. In ischemia/reperfusion realization HSP70 dynamics was comparable in all patients undergone arterial reconstruction, i.e. stress reaction to damage was similar regardless of the extent of ischemia. Increased secretion of the studied metabolites may be regarded as a protective mechanism to ischemic/reperfusion injury. Increased secretion of the studied metabolites is considered as a kind of defense mechanism in the implementation of ischemia/repersusion and their reduction in the postoperative period is largely due to the degree of circulatory compensation. Intraoperative endothelial injury deteriorated the course of the endothelial dysfunction by activating NO synthesis. Conclusion. Stress-inducible NO and HSP70 systems combined with endothelial growth factor form a kind of “shield” which timely limits the impact of the damaging ischemic/reperfusion factors.