Pathophysiology of ischaemia-reperfusion injury

Vascular ischaemia and reperfusion injury.

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 ...

Ischaemia-Reperfusion-Induced Kidney Injury

Pulmonary ischaemia-reperfusion injury: role of apoptosis.

The central role of lung ischaemia-reperfusion injury in pulmonary dysfunction after cardiac surgery, particularly thoracic organ transplantation, has been well recognised. Lung tissue necrosis after prolonged ischaemia is known to worsen lung function, which was believed to be due largely to adjacent tissue inflammation. Recent studies suggest that lung apoptosis following ischaemia-reperfusio...

Mitochondrial connexin43 as a new player in the pathophysiology of myocardial ischaemia-reperfusion injury.

Connexins are transmembrane proteins whose best known function is to form gap junction channels. Ventricular cardiomyocytes express the connexin isoform Cx43 and are rich in gap junctions essential for the normal propagation of the action potential. In addition to this physiological role, cardiomyocyte gap junctions contribute to the pathophysiology of ischaemia-reperfusion injury, mainly by sy...

the effect of nitroprusside on the renal ischaemia-reperfusion injury

nitric oxide (no) is implicated as an important mediator of, or intermediary in, inflammation, immunity and neurotransmission. in the kidney, no is involved in haemodynamic regulation, control of vascular tone and tubular function. formation of oxygen-derived free radicals (ofr) have been documented in renal ischaemia- reperfusion before. in this study , we investigated the significance of no f...