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POINT-COUNTERPOINT COMMENTS
Virgen Milagrosa University Foundation
San Carlos City, Pang, Philippines
e-mail: johnberg{at}hawaii.edu
The following letter is in response to Point:Counterpoint: "Chronic hypoxia-induced pulmonary hypertension does/does not lead to loss of pulmonary vasculature" that appears in this issue.
To the Editor: In their initial statement supporting the hypothesized loss of precapillary arteries in chronic hypoxia Rabinovitch, Chesler, and Molthen (6) provide evidence derived from perfusion studies using contrast dyes and other markers. In reply, McLoughlin and McMurtry (5) introduce the problem of artifactual measurements resulting from hypoxic pulmonary vasoconstriction (HPV) of pulmonary arteries. I believe that clarification of how HPV may cause the proposed loss of vessels to occur may contribute to the debate. One way this could happen is through uneven HPV where flow in some vascular channels may become entirely blocked and downstream vessels would appear to be lost through a lack of perfusion. Hultgren (4) initially introduced the concept of uneven HPV in pulmonary arteries to explain the observed patchy distribution of high-altitude pulmonary edema in humans. Anatomically, pulmonary arteries in the adult human lung have a highly variable distribution of smooth muscle (2) consistent with the observed variability of HPV response between individuals. Studies by Dawson et al. (1), using the double-indicator dilution method, showed that hypoxia causes more than a doubling of transit times for infused indicator agents in dog lungs, suggesting that flow rates through parallel channels become more variable with hypoxia. More recently, Hopkins et al. (3), using functional magnetic resonance imaging techniques, provide additional evidence for uneven HPV. It is therefore likely that at least some of the data presented in defense of vessel loss as a cause of pulmonary hypertension may be the result of uneven HPV and artifactual inclusion of HPV-blocked vessels.
REFERENCES
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