Fig. 2
From: Pathophysiology and clinical consequences of arterial blood gases and pH after cardiac arrest
Effect of oxygen on microglia, cardiomyocytes, and lung epithelial cells. Microglia: hypoxic neurons have an anaerobic metabolism with increased intracellular Ca2+ intake; persistent hypoxia generates reduction of ATP and further energetic failure. Hyperoxia can disrupt microglia function by increasing free radicals. Hyperoxia increases input resistance to antioxidant and decrease membrane conductance (K+ channel) and stimulates firing of putative central CO2/H+ chemoreceptors neurons. Cardiomyocytes: effects of anoxia on cellular energetic turnover and on intra- and extracellular environments and its effect on cardiac function. In hyperoxia, O2 radical free and reduction of nitric oxide can eventually lead to coronary vasoconstriction. In the lung epithelium, hypoxia induces pulmonary vascular remodeling, with resident vascular cell activation, monocytes/fibrocytes recruitment, and persistent vasoconstriction structural remodeling. Hyperoxia exposure stimulates p53 to activate miR34a in a positive feedback loop, with consequent abnormal cell proliferation, apoptosis, impaired alveolarization, and cell death