Inflammatory Response in Patients under Coronary Artery Bypass Grafting Surgery and Clinical Implications: A Review of the Relevance of Dexmedetomidine Use

Scheme 3

Complex cascade of pathophysiologic phenomena associated with ischemia/reperfusion in CABG. Anaerobic metabolism causes an increase on lactate and reduced pH with transmembrane pump impairment, which lead to an intracellular Ca²⁺ and Na⁺ increases, and consequently cellular edema. Increase on intracellular Ca²⁺ activated phospholipase A2 and calpain, with arachidonic acid degranulate and protein synthesis inhibition. Thus, caspase and neutrophil activation occur with cellular apoptosis. The neutrophils activation induces membrane lesions and more proinflammatory mediators liberation, including nitric oxide, via nitric oxide synthase (NOS) activation and that leads to microvascular damage and endothelial impairment, in a vicious circle.