Overview

Oxygen (O2) is a vital requisite for aerobic respiration in both eukaryotic and prokaryotic cells. Therefore, tissues or cell's ability to respond and adapt to oxygen tension is indispensable for the preservation of cellular homeostasis. Indeed, low partial O2 pressure-dependent fluctuations in oxygen levels lead to serious pathophysiological conditions. In general, hypoxia is a state in which the unavailability of sufficient amounts of oxygen at the tissues or cells level results in inadequate oxygen delivery due to low blood supply or low oxygen in the blood (hypoxemia). It can present in acute or chronic forms, in which some tissue can be able to tolerate for a longer duration, other tissues are severely damaged at low oxygen levels. Hypoxia would be a harmful threat to the human who rapidly ascent or resides at high altitudes, causing multifaceted cellular deregulation, leading to severe pathological conditions like acute mountain sickness (AMS) and high-altitude pulmonary edema (HAPE) in humans. Nitric oxide (NO) is a gaseous messenger molecule and plays an essential role in vasodilation. It is synthesized by NO synthase enzymes (eNOS, nNOS, and iNOS) in vascular endothelium and other cell types. Generalized hypoxia was associated with increased oxidative damage and reduction of NO leads to vascular permeability pulmonary edema and instigates the vascular bed damage. However, other circulating cell types (red blood cells (RBCs), mononuclear cells (MNCs), endothelial progenitor cells (EPCs) and platelets) are also involved in NO production in the blood vessels. Various studies have suggested that inhalation of NO has been found to improve arterial oxygenation pulmonary circulation while decreasing arterial pressure in the lungs of HAPE subjects.

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