Vascular ischaemia and reperfusion injury.
نویسندگان
چکیده
Although restoration of blood flow to an ischaemic organ is essential to prevent irreversible tissue injury, reperfusion per se may result in a local and systemic inflammatory response that may augment tissue injury in excess of that produced by ischaemia alone. Cellular damage after reperfusion of previously viable ischaemic tissues is defined as ischaemia-reperfusion (I-R) injury. I-R injury is characterized by oxidant production, complement activation, leucocyte-endothelial cell adhesion, platelet-leucocyte aggregation, increased microvascular permeability and decreased endothelium-dependent relaxation. In its severest form, I-R injury can lead to multiorgan dysfunction or death. Although our understanding of the pathophysiology of I-R injury has advanced significantly in the last decade, such experimentally derived concepts have yet to be fully integrated into clinical practice. Treatment of I-R injury is also confounded by the fact that inhibition of I-R-associated inflammation might disrupt protective physiological responses or result in immunosuppression. Thus, while timely reperfusion of the ischaemic area at risk remains the cornerstone of clinical practice, therapeutic strategies such as ischaemic preconditioning, controlled reperfusion, and anti-oxidant, complement or neutrophil therapy may significantly prevent or limit I-R-induced injury in humans.
منابع مشابه
Reperfusion strategies in the management of extremity vascular injury with ischaemia.
BACKGROUND Extremity injury with ischaemia is the most common pattern of vascular trauma and is a challenge for surgeons who must make decisions about the timing and mechanism of limb reperfusion. In modern military conflicts, effective use of limb tourniquets and rapid transport of the injured have increased the number of casualties who reach a medical service with potentially survivable vascu...
متن کاملExploring the role of dimethylarginine dimethylaminohydrolase-mediated reduction in tissue asymmetrical dimethylarginine levels in cardio-protective mechanism of ischaemic postconditioning in rats
Objective(s): Reperfusion of ischaemic myocardium results in reduced nitric oxide (NO) biosynthesis by endothelial nitric oxide synthase (eNOS) leading to endothelial dysfunction and subsequent tissue damage. Impaired NO biosynthesis may be partly due to increased levels of asymmetrical dimethylarginine (ADMA), an endogenous inhibitor of eNOS. As dimethylarginine dimet...
متن کاملShort-interval postconditioning protects the bowel against ischaemia–reperfusion injury in rats
Objective Acute mesenteric ischaemia leads to intestinal damage. Restoration of blood flow results in further damage to tissue, which is called reperfusion injury. This study aimed to investigate the protective effects of short-interval postconditioning and to determine the optimal interval for reperfusion in an experimental rat model of intestinal ischaemia. Methods Forty adult male Wistar rat...
متن کاملLocally targeted cytoprotection with dextran sulfate attenuates experimental porcine myocardial ischaemia/reperfusion injury.
AIMS Intravascular inflammatory events during ischaemia/reperfusion injury following coronary angioplasty alter and denudate the endothelium of its natural anticoagulant heparan sulfate proteoglycan (HSPG) layer, contributing to myocardial tissue damage. We propose that locally targeted cytoprotection of ischaemic myocardium with the glycosaminoglycan analogue dextran sulfate (DXS, MW 5000) may...
متن کاملPreclinical research Locally targeted cytoprotection with dextran sulfate attenuates experimental porcine myocardial ischaemia/reperfusion injury
Aims Intravascular inflammatory events during ischaemia/reperfusion injury following coronary angioplasty alter and denudate the endothelium of its natural anticoagulant heparan sulfate proteoglycan (HSPG) layer, contributing to myocardial tissue damage. We propose that locally targeted cytoprotection of ischaemic myocardium with the glycosaminoglycan analogue dextran sulfate (DXS, MW 5000) may...
متن کاملAerosolized PGE1, PGI2 and nitroprusside protect against vascular leakage in lung ischaemia-reperfusion.
High permeability oedema is an important feature in lung injury secondary to ischaemia-reperfusion. This study investigated the influence of aerosolized prostaglandin E1 (PGE1), prostaglandin I2 (PCI2) and the nitric oxide (NO)-donor, sodium nitroprusside (SNP) on microvascular barrier function in pulmonary ischaemia-reperfusion. Buffer-perfused rabbit lungs were exposed to 180 or 210 min of wa...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- British medical bulletin
دوره 70 شماره
صفحات -
تاریخ انتشار 2004