High-altitude physiology: Understanding molecular, pharmacological and clinical insights

Abstract

Acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE), and high-altitude cerebral edema (HACE) are three common forms of altitude sickness. These conditions can be life-threatening, with symptoms like fatigue, dizziness, and headaches. Ascending to high elevations increases the likelihood of developing these conditions, with some individuals adapting quickly while others need to descend. Early acclimatization is beneficial for avoiding AMS and HACE, but it takes weeks to months to improve job performance and performance at high altitudes. HAPE is a leading cause of mortality from altitude sickness, characterized by foamy mucus, coughing, and difficulty breathing. Treatment is most effective when it is administered quickly, with mild cases resolving with additional time spent at altitude. Oxygen therapy and chemicals such as acetazolamide, spironolactone, and dexamethasone are used to restore fluid balance and prevent complications. Genes and environmental factors influence genetic reactions to low oxygen levels at high altitudes. This review explores pharmacological interventions currently used or under investigation, such as acetazolamide, dexamethasone, and novel HIF stabilizers. By integrating molecular insights with pharmacological data, we aim to provide a comprehensive understanding of altitude-related illnesses. Studying altitude sickness is highly relevant not only for climbers and high-altitude workers but also for broader medical contexts like hypoxia-related diseases. This manuscript aims to bridge the gap between basic science and clinical practice, facilitating improved strategies for management and prevention of high-altitude disorders.