Ischemia-Reperfusion Injury

Abstract

Ischemia-reperfusion injury forms the basis of tissue damage and cellular apoptosis in many pathologic and traumatic processes. The tissue damage follows a natural progression of cellular and metabolic events initiated by an ischemic episode. Ischemia causes intracellular/extracellular changes principally resulting in increased intracellular calcium, pH changes, and adenosine triphosphate depletion that end in cell death if the process is not interrupted. This interruption takes the form of reperfusion, characterized by a "flushing" of tissues with toxic metabolites, principally reactive oxygen species. The immediate effect is mitochondrial pore permeability, complement activation, cytochrome release, cytokine activation, inflammation, edema, neutrophil platelet adhesion, capillary plugging, and thrombosis. This sets the stage for the long recognized "no-reflow" phenomenon and progressive tissue death. Current recognition of cellular "cross-talk" and molecular events have introduced new logical strategies to sequentially combat the events occurring in relation to ischemia-reperfusion injury. These include mechanical preconditioning and pharmacological preconditioning and postconditioning strategies. It is likely that success in reversing or limiting tissue damage will be found in a sequential multitargeted approach using a combination of these strategies-clinical trials in this regard are sorely needed.

Predictive value of ischaemia‐modified albumin in spermatogenesis in an experimental testicular torsion model

“…In this study, a significant decrease in terms of sperm parameters and significant increase in terms of FSH levels were found following an average of 69-hr torsion in the orchiectomy group than in the detorsion group, in which no significant difference was observed compared with the control group. Ischaemia/reperfusion injury is caused by reactive oxygen radicals produced following reperfusion in tissues exposed to ischaemia (Widgerow, 2014 TA B L E 4 Evaluation of the correlation between Johnsen score and study parameters in 4-hr T/D group in testicular torsion patients who underwent orchiectomy and detorsion. While only the testicular damage that occurred due to the time lag until treatment was previously considered in testicular torsion cases, recent studies have shown that ischaemia/reperfusion injury occurring following detorsion also has an effect on testicular function and infertility.…”

“…While only the testicular damage that occurred due to the time lag until treatment was previously considered in testicular torsion cases, recent studies have shown that ischaemia/reperfusion injury occurring following detorsion also has an effect on testicular function and infertility. Ischaemia/reperfusion injury is caused by reactive oxygen radicals produced following reperfusion in tissues exposed to ischaemia (Widgerow, 2014 in testicular torsion patients who underwent orchiectomy and detorsion. In this study, no significant difference was observed among hormone profiles, and sperm morphology and motility were significantly higher in the post-torsion orchiectomy group than in the detorsion group (Arap et al, 2007).…”

<p>Postconditioning Protection Against Myocardiocyte Anoxia/Reoxygenation Injury From Penehyclidine Hydrochloride</p>

“…As a result, a large amount of reactive oxygen species (ROS) was generated, inflammatory response was activated, calcium overload ensued and mitochondrial permeability transition pore (MPTP) was activated. 29 Mitochondria played the central role of cell death and apoptosis. With MPTP opening, mitochondria starts to swell and inner membrane begins to depolarize.…”

Silencing LncRNA AK139328 protects vascular endothelial cells from ischemia-reperfusion injury by increasing PI3K/Akt signaling

“…I/R injury causes tissue damage, complement activation, cytochrome release, cytokine activation, inflammation, edema, neutrophil platelet adhesion, capillary plugging, and thrombosis [34]. Spinal cord ischemia triggered local edema, vasospasm, free radicals, calcium influx into the axons, and loss of potassium from the intercellular space [35].…”