Abstract: Ischaemia reperfusion (I/R) injury is a physiological phenomenon whereby hypoxic tissue damage can be perpetuated by tissue reperfusion; this can occur in the setting of pathology or as a surgical complication. Naturally, tissues sensitive to hypoxic episodes such as the brain, heart, kidney, liver and lung tissue are most often affected. Current treatments for I/R injury focus of limiting the pathological response to reperfusion through ischemic preconditioning (IPC) and medications that mimic the IPC response. Anesthetic preconditioning (APC) and anesthetic postconditioning (APoC) can produce protective responses similar to IPC, thus modulating the effects of I/R injury, with a far longer impact on organ systems than their sedative or analgesic effects. The pathological process and molecular mechanism of I/R injury involve calcium overload, mitochondrial dysfunction, oxidative stress, inflammation, autophagy, and other key signaling pathways. However, how anesthetics are involved remains to be further investigated. Elucidating its underlying mechanism is vital to prevent perioperative I/R injury and benefit our patients. Importantly, the protective mechanisms differ between the types of anesthetics and between types of tissue. Understanding the differences can lead to more informed clinical decisions. Here, we systematically review and compare the molecular mechanisms that can explain how inhalational and intravenous anesthesia regulate I/R injury and provide a comprehensive analysis of recent basic clinical studies for APC and APoC in the context of different organ I/R injury.
Lucas et al. (Thu,) studied this question.