4.1 Pharmacokinetic and pharmacodynamic considerations of antioxidant supplementation in AMS As mentioned above, oxidative stress has been proposed as a key contributor to the pathophysiology of AMS, driven by hypobaric hypoxiainduced mitochondrial dysfunction, increased ROS generation, endothelial activation, and neurovascular dysregulation
However, in the agent-level analysis, tirzepatide only demonstrated significant reductions in MACE when compared to placebo, while other endpoints showed favorable but non-significant trends
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This approach not only impacted glucose homeostasis but also produced positive effects on hepatic steatosis, surpassing the outcomes observed with the subcutaneous injection of exenatide [9]