ischaemiásreperfúziós

Ischaemicreperfusion refers to the damage that occurs when blood supply returns to an area of tissue that has previously been deprived of oxygen. This condition, also known as reperfusion injury, is a complex biological process. It arises from the restoration of blood flow to tissues that have suffered ischaemia, which is a state of inadequate blood supply. While reperfusion is essential for salvaging threatened tissue and promoting healing, it can paradoxically lead to further cellular and tissue damage.

The underlying mechanisms of ischaemicreperfusion injury are multifaceted and involve several biological pathways. When oxygen and nutrients are absent during ischaemia, cells begin to malfunction. Upon reperfusion, the sudden influx of oxygen can trigger the formation of reactive oxygen species (ROS), also known as free radicals. These unstable molecules can damage cellular components like lipids, proteins, and DNA. Furthermore, reperfusion can activate inflammatory processes. Immune cells are recruited to the injured area, releasing inflammatory mediators that contribute to tissue damage. Endothelial cells lining the blood vessels can also be activated, leading to increased permeability and microvascular dysfunction.

The consequences of ischaemicreperfusion injury vary depending on the affected organ and the duration of the ischaemic period. It is a significant factor in the pathophysiology of various clinical conditions, including myocardial infarction (heart attack), stroke, and organ transplantation. Strategies to mitigate ischaemicreperfusion injury often focus on limiting the initial ischaemia, optimizing reperfusion protocols, and employing pharmacological interventions to reduce oxidative stress and inflammation.