Pathogenesis of ischemia/reperfusion syndrome

• Main Authors: D E Kutepov, M S Zhigalova, I N Pasechnik
• Format: Article
• Language: Russian
• Published: ECO-vector 2018-08-01
• Series: Kazanskij Medicinskij Žurnal
• Subjects: синдром ишемии-реперфузии; критическая ишемия нижней конечности; активированные формы кислорода; перекисное окисление липидов; миоглобин
• Online Access: https://journals.eco-vector.com/kazanmedj/article/view/9206

Ischemia/reperfusion syndrome is a collective concept that combines various pathological conditions developing against the background of the restoration of the main blood flow in the organ or limb segment, which has long been subjected to ischemia or traumatic amputation. Intensive care physicians often see ischemia/reperfusion syndrome after restoration of blood supply in patients with critical ischemia of the lower limb. The rate of critical ischemia of the lower limbs ranges from 400 to 1000 cases per 1 million of the population. The number of lower limb amputations due to critical lower limb ischemia in economically developed countries is 13.7-32.3 cases per 100,000 of the population. The main etiological factors of critical lower limb ischemia are atherosclerosis of peripheral vessels and vascular complications of diabetes. The pathogenesis of ischemia/reperfusion syndrome is based on a complex of pathophysiological changes resulting from the restoration of blood flow in previously ischemic lower limb. Restoration of blood circulation leads to massive flow into the systemic bloodstream of anaerobic metabolism products, free myoglobin, biologically active substances and inflammatory mediators. The main sources of reperfusion damage are activated forms of oxygen, in particular, superoxide radical О2-, nitric oxide, lipid peroxidation products. In the conditions of primary ischemia, and then tissue reperfusion, excessive production of activated oxygen forms leads to damage of biological structures (lipids, proteins, deoxyribonucleic acid), which causes disruption of normal cell functioning or its death due to necrosis or apoptosis, ion pump dysfunction, adhesion of leukocytes and increased vascular permeability.