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Reperfusion injury in peripheral vascular disease

Reperfusion injury in peripheral vascular disease 97 Reperfusion injury in peripheral vascular disease SAGE Publications, Inc.1994DOI: 10.1177/1358836X9400500202 MA Green Queen Elizabeth Hospital, Birmingham, UK CP Shearman Queen Elizabeth Hospital, Birmingham, UK Address for correspondence: CP Shearman, Department of Vascular Surgery, Queen Elizabeth Hospital, Birmingham B15 2TH, UK. Introduction Atheromatous peripheral vascular disease commonly results in tissue ischaemia and the aim of most therapeutic intervention is the restoration of blood flow. Following periods of acute ischaemia it is now generally recognized that most damage occurs not during the period of ischaemia itself, but paradoxically on reperfusion of the tissue with oxygenated bloody 1 Reperfusion initiates a complex, inter-related series of biochemical and cellular reactions which exacerbate the local damage and also mediate remote injury to other organs. Activated neutrophils appear to be important mediators of the resultant injury, neutrophil depletion prior to reperfusion reducing the subsequent tissue damage,2 and vascular endothelium the common target, becoming more permeable. These events are clinically apparent following reperfusion of a large mass of ischaemic tissue such as the gut or leg and are a major cause of morbidity and mortality.3,4 It appears, however, that even relatively mild episodes of ischaemia followed by reperfusion may have similar, less pronounced adverse http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Vascular Medicine SAGE

Reperfusion injury in peripheral vascular disease

Abstract

97 Reperfusion injury in peripheral vascular disease SAGE Publications, Inc.1994DOI: 10.1177/1358836X9400500202 MA Green Queen Elizabeth Hospital, Birmingham, UK CP Shearman Queen Elizabeth Hospital, Birmingham, UK Address for correspondence: CP Shearman, Department of Vascular Surgery, Queen Elizabeth Hospital, Birmingham B15 2TH, UK. Introduction Atheromatous peripheral vascular disease commonly results in tissue ischaemia and the aim of most therapeutic intervention is the restoration of blood flow. Following periods of acute ischaemia it is now generally recognized that most damage occurs not during the period of ischaemia itself, but paradoxically on reperfusion of the tissue with oxygenated bloody 1 Reperfusion initiates a complex, inter-related series of biochemical and cellular reactions which exacerbate the local damage and also mediate remote injury to other organs. Activated neutrophils appear to be important mediators of the resultant injury, neutrophil depletion prior to reperfusion reducing the subsequent tissue damage,2 and vascular endothelium the common target, becoming more permeable. These events are clinically apparent following reperfusion of a large mass of ischaemic tissue such as the gut or leg and are a major cause of morbidity and mortality.3,4 It appears, however, that even relatively mild episodes of ischaemia followed by reperfusion may have similar, less pronounced adverse
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