Inducible intrapulmonary arteriovenous pathways during exercise and hypoxia
Exercise-inducible:The reasons that pulmonary gas exchange becomes worse in healthy human subjects during exercise remain unresolved. Previous research, using gas exchange dependent techniques, has ruled out anatomical arteriovenous intrapulmonary shunts as an important contributor to the pulmonary gas exchange inefficiency during exercise. Our current research has challenged that dogma (Lovering et al., J Appl Physiol, 2009) and is re-examining anatomical shunts using non-gas exchange dependent techniques (Laurie et al., J Appl Physiol, 2010; Elliott et al., J Appl Physiol, 2011) to determine whether or not intrapulmonary arteriovenous shunting occurs during exercise in healthy human subjects (Stickland & Lovering, MSSE, 2006).
Hypoxia-inducible: We have demonstrated that hypoxia can induce intrapulmonary arteriovenous shunting in all healthy humans (Laurie et al., J Appl Physiol, 2010; Lovering et al., J Appl Physiol, 2008). The impact of these findings is not yet entirely understood. It is known that intrapulmonary shunting has a negative impact on pulmonary gas exchange efficiency (see above). However, blood flow traveling through these inducible large diameter pathways will bypass the pulmonary capillary filter allowing for potential emboli to enter the systemic circulation that may play a role in the etiology of neurological sequelae associated with high altitude (Stickland & Lovering, MSSE, 2006).
The major goals of this area of research are to: 1) elucidate the mechanism(s) regulating hypoxia-induced intrapulmonary shunting, 2) quantifying the blood flow that travels through these pathways at rest in varying oxygen conditions and 3) determine the role of these pathways in high altitude illnesses such as acute mountain sickness (AMS), high altitude pulmonary (HAPE) and cerebral edema (HACE).Understanding the physiologic role of these inducible intrapulmonary arteriovenous vessels and the mechanisms responsible for their regulation will provide a better understanding of pulmonary gas exchange in health. Also, because the lung acts as a blood filter, understanding the regulation of large diameter pathways within this filter will allow for a better understanding of unexplained embolic phenomena such as transient ischemic attacks (TIAs), myocardial infarction and cryptogenic stroke that occur at sea level as well as those neurological sequelae that occur at high altitudes.
Funding for this work is provided by the Oregon Health & Science University Foundation MRF grant and the Department of Defense.
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