Question

A mountain climber ascends to an altitude where the partial pressure of oxygen in the atmosphere is very low.

1. What happens to levels of erythropoietin in the blood after a period of time at high elevations?

2.How does a low concentration of oxygen in the alveoli affect the state of contraction of pulmonary arterioles?

3.Explain why pulmonary edema is a symptom of altitude sickness

Answer 1

1. Upon exposure to high altitude, there will be a latent period of 6 hours followed by a rapid increase in erythropoietin, and a secondary fall to a level of approximately twice normal. The increased erythropoietin stimulus will also reflected in a shortened marrow radio iron transit time. Elevated erythropoietin will be associated with an increased iron uptake within 24 hours of the stimulus, suggesting a direct action of erythropoietin on hemoglobin synthesis by the existing marrow population.
2. . Oxygen sensors located in the pulmonary vasculature detect the drop of alveolar oxygen tension and lead to vasoconstriction of small pulmonary arteries and pulmonary veins. The response of smooth-muscle cells in the pulmonary vasculature to acute hypoxia begins within seconds and involves inhibition of voltage-dependent potassium channels, membrane depolarization, and calcium entry through L-type calcium channels. Moreover, hypoxia up-regulates transient receptor potential channels, leading to additional calcium entry through receptor and store-operated calcium-channels. Whether a constitutively decreased mRNA expression of voltage-dependent potassium channels or an acquired transcriptional defect of the voltage-dependent potassium channels protein expression is at the origin of HAPE susceptibility remains to be determined.

3. HAPE mainly occurs due to exaggerated hypoxic pulmonary vasoconstriction and elevated pulmonary artery pressure. The HAPE is a high permeability type of edema occurring also due to leaks in the capillary wall (‘stress failure’). High altitude pulmonary edema (HAPE) is the abnormal accumulation of plasma and some red cells in the lung due to a breakdown in the pulmonary blood-gas barrier, triggered by hypobaric hypoxia. This breakdown develops from a number of maladaptive responses to the hypoxia encountered at higher altitudes, including poor ventilatory response, increased sympathetic tone, exaggerated and uneven pulmonary vasoconstriction (pulmonary hypertension), inadequate production of endothelial nitric oxide, and overproduction of endothelin, many of which are genetically determined. The end result is a patchy accumulation of extravascular fluid in the alveolar spaces that impairs respiration and can, in severe cases, prove fatal.