TY - JOUR

T1 - МОЛЕКУЛЯРНЫЕ И КЛЕТОЧНЫЕ МЕХАНИЗМЫ ПОВРЕЖДЕНИЯ РЕНАЛЬНОЙ ПАРЕНХИМЫ ПРИ ТЕПЛОВОЙ ИШЕМИИ ПОЧКИ

AU - Popov, S V

AU - Guseinov, R G

AU - Martov, A G

AU - Muratov, T M

AU - Tabynbaev, N B

PY - 2017

Y1 - 2017

N2 - Warm ischemia of the renal parenchyma is a forced feature of laparoscopic partial nephrectomy. It is accompanied by oxygen deprivation of the organ and followed by re-oxygenation, which can cause additional damage to the renal tissue. This damage can result in acute functional and structural disorders of individual parts of the nephron, increasing the risk for a renal dysfunction. Timely diagnosis of the dysfunction is vital for the success of the treatment. The article provides an overview of current scientific data on the mechanisms of ischemic and reperfusion injuries at the molecular-cellular level and describes the current methods of their detection. Experimental and clinical study of the molecular-cellular mechanisms of ischemic-reperfusion injury of the renal tissue made it possible, first, to determine the main targets of alteration (cytolemma, mitochondria, lysosomes), and second, to establish its consequences, among which the most important are hypoergosis, DNA damage, simultaneous activation of intracellular systems of the suicidal program and induction of electrical breakdown of membranes of target nephrocytes; thirdly, to reveal the range of possibilities for limiting the consequences of hypoxia and/or re-oxygenation, among which interference in the metabolism of purines, measures ensuring the preservation of colloid osmotic pressure inside and outside the cell and membrane stabilization, antioxidant defense and inhibition of cysteine proteinases, etc. However, despite the advances in understanding the pathogenesis of cell damage, including ischemic-hypoxic injury, the problem of intraoperative ischemia-reperfusion safety remains relevant.

AB - Warm ischemia of the renal parenchyma is a forced feature of laparoscopic partial nephrectomy. It is accompanied by oxygen deprivation of the organ and followed by re-oxygenation, which can cause additional damage to the renal tissue. This damage can result in acute functional and structural disorders of individual parts of the nephron, increasing the risk for a renal dysfunction. Timely diagnosis of the dysfunction is vital for the success of the treatment. The article provides an overview of current scientific data on the mechanisms of ischemic and reperfusion injuries at the molecular-cellular level and describes the current methods of their detection. Experimental and clinical study of the molecular-cellular mechanisms of ischemic-reperfusion injury of the renal tissue made it possible, first, to determine the main targets of alteration (cytolemma, mitochondria, lysosomes), and second, to establish its consequences, among which the most important are hypoergosis, DNA damage, simultaneous activation of intracellular systems of the suicidal program and induction of electrical breakdown of membranes of target nephrocytes; thirdly, to reveal the range of possibilities for limiting the consequences of hypoxia and/or re-oxygenation, among which interference in the metabolism of purines, measures ensuring the preservation of colloid osmotic pressure inside and outside the cell and membrane stabilization, antioxidant defense and inhibition of cysteine proteinases, etc. However, despite the advances in understanding the pathogenesis of cell damage, including ischemic-hypoxic injury, the problem of intraoperative ischemia-reperfusion safety remains relevant.

KW - Animals

KW - Apoptosis

KW - Calcium/metabolism

KW - Calpain/metabolism

KW - Cell Hypoxia

KW - Free Radicals/metabolism

KW - Humans

KW - Intracellular Space/metabolism

KW - Kidney/blood supply

KW - Parenchymal Tissue/metabolism

KW - Proteolysis

KW - Reperfusion Injury/etiology

KW - Warm Ischemia/adverse effects

M3 - Обзорная статья

C2 - 28952698

SP - 79

EP - 84

JO - УРОЛОГИЯ

JF - УРОЛОГИЯ

SN - 1728-2985

IS - 4

ER -