Hydrogen Sulfide as an Oxygen Sensor – PMC – NCBI

O2-Sensing Tissues

The vast majority of modern-day animals, and especially vertebrates, now depend on O2 and monitoring “sensing” O2 availability is key for survival. O2 sensors can be divided into four “reporting” levels: external, internal, tissue (vascular), and intracellular.

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External chemoreceptors monitor ambient O2. Aquatic vertebrates are especially susceptible to ambient O2 because of the lower solubility (1/30 that of air), low diffusivity (300,000 times slower), 60-fold higher viscosity, and wide swings in O2 availability seasonally, daily, and spatially, even within a few meters (8). Chemoreceptor neuroepithelial cells (NEC) on the external surfaces of fish gills are employed to continuously monitor water partial pressure of oxygen (Po2) (66, 109). Similar neuroepithelial-like cells are found in clusters (neuroepithelial bodies [NEB]) near airway bifurcations in lungs of newborn mammals where they may be important in the transition away from the relatively hypoxic uterine environment during and shortly after birth (72). External O2 sensors other than NEB are relatively uncommon in terrestrial vertebrates. These are replaced by internal O2 sensors that are better suited to monitor blood O2 status and changes in O2 availability (such as in borrows or with increasing altitude) if needed.

The first and second gill arches of fish are heavily invested with internal arterial-facing NEC, and these are the antecedents of glomus cells in the carotid body and aortic arch. The first gill arch and the mammalian carotid body arise from the third embryonic arch, and the second gill arch and aortic bodies arise from the fourth embryonic aortic arch; NEC and type I glomus cells of the carotid body are so similar at the ultrastructural level that there is little doubt of their lineage [reviewed in Jonz and Nurse (66)]. Mammalian adrenal medullary cells and homologous chromaffin cells in fish that line systemic veins secrete catecholamines in response to hypoxemia (119, 138) and may monitor tissue O2 extraction. The adrenal medullary cells may be especially important in monitoring arterial O2 in the newborn until the carotid bodies become fully functional (66).

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The ability of blood vessels themselves to respond to O2 is important in matching perfusion to metabolic demand or in the case of the respiratory organs to maintain normal ventilation/perfusion ratios. It is commonly assumed that to accomplish this, systemic vessels dilate in response to hypoxia and pulmonary vessels constrict (155) but this is obviously not consistent throughout vertebrates or even within mammals (129, 143).

Finally, it is evident that individual cells not only monitor their own O2 status but also have biochemical “contingency plans” to adjust metabolic demand and energy utilization should O2 levels fall. The scope of these contingency plans is highly variable from a few short minutes of survival in highly active mammalian tissues such as the brain and the heart to extended (weeks-months) anoxemia that is tolerated by lower vertebrates such as the crucian carp and turtle (48). Initial sensing and coping mechanisms reflected in response to ischemia/reperfusion injury and pre- and postconditioning are only briefly discussed here in the context of acute O2 sensing. Chronic responses involving metabolic control are described in an excellent review by Clanton et al. (22) and are beyond the scope of the present discussion.