Ischaemia-reperfusion (I/R) injury is a complex process involving microvascular dysfunction, inflammatory responses, and oxidative stress. Reperfusion of ischaemic tissues can lead to microvascular dysfunction, characterized by impaired endothelium-dependent dilation, enhanced fluid filtration, and leukocyte plugging in capillaries. Activated endothelial cells produce more oxygen radicals and less nitric oxide, leading to the release of inflammatory mediators and increased adhesion molecule biosynthesis. Risk factors such as hypercholesterolaemia, hypertension, and diabetes exacerbate these microvascular alterations. Reperfusion can also activate endothelial cells in remote organs, leading to leukocyte-dependent microvascular injury and multiple organ dysfunction syndrome (MODS). Adaptational responses, such as ischaemic preconditioning, offer protection against subsequent ischaemia. There are two types of preconditioning: acute, which is protein synthesis-independent, and delayed, which requires protein synthesis. The mechanisms of preconditioning involve the activation of kinases such as protein kinase C and the transcription factor NF-κB. The protective effects of preconditioning are mediated by the modulation of oxidative stress, adhesion molecule expression, and inflammatory responses. The role of nitric oxide, superoxide, and other oxidants in I/R injury is significant, as they contribute to endothelial dysfunction and vascular permeability. The inflammatory mediators released during I/R can activate leukocytes and endothelial cells, leading to vascular injury and organ dysfunction. The study of I/R injury has led to the identification of potential therapeutic targets, including the modulation of oxidant stress, adhesion molecules, and inflammatory responses. The understanding of the pathophysiology of I/R injury is crucial for the development of effective therapeutic strategies to prevent and treat I/R-induced microvascular injury.Ischaemia-reperfusion (I/R) injury is a complex process involving microvascular dysfunction, inflammatory responses, and oxidative stress. Reperfusion of ischaemic tissues can lead to microvascular dysfunction, characterized by impaired endothelium-dependent dilation, enhanced fluid filtration, and leukocyte plugging in capillaries. Activated endothelial cells produce more oxygen radicals and less nitric oxide, leading to the release of inflammatory mediators and increased adhesion molecule biosynthesis. Risk factors such as hypercholesterolaemia, hypertension, and diabetes exacerbate these microvascular alterations. Reperfusion can also activate endothelial cells in remote organs, leading to leukocyte-dependent microvascular injury and multiple organ dysfunction syndrome (MODS). Adaptational responses, such as ischaemic preconditioning, offer protection against subsequent ischaemia. There are two types of preconditioning: acute, which is protein synthesis-independent, and delayed, which requires protein synthesis. The mechanisms of preconditioning involve the activation of kinases such as protein kinase C and the transcription factor NF-κB. The protective effects of preconditioning are mediated by the modulation of oxidative stress, adhesion molecule expression, and inflammatory responses. The role of nitric oxide, superoxide, and other oxidants in I/R injury is significant, as they contribute to endothelial dysfunction and vascular permeability. The inflammatory mediators released during I/R can activate leukocytes and endothelial cells, leading to vascular injury and organ dysfunction. The study of I/R injury has led to the identification of potential therapeutic targets, including the modulation of oxidant stress, adhesion molecules, and inflammatory responses. The understanding of the pathophysiology of I/R injury is crucial for the development of effective therapeutic strategies to prevent and treat I/R-induced microvascular injury.