Intrapulmonary arteriovenous anastomoses (IPAVA) allow large diameter particles of venous origin to bypass the pulmonary capillary bed and embolize the systemic arterial circulation. IPAVA have been routinely observed in healthy humans with exercise,
hypoxia, and
catecholamine infusion, but the mechanism by which they are recruited is not well-defined. We hypothesized that
beta-adrenergic receptor stimulation recruits IPAVA and that receptor blockade would limit
hypoxia-induced IPAVA recruitment. To test our hypothesis, we evaluated the transpulmonary passage of
microspheres in intact rats and isolated rats lung infused with the
beta-adrenergic receptor agonist isoproterenol. We also evaluated IPAVA recruitment in intact rats with
hypoxia and the
beta-adrenergic receptor blocker
propranolol. We found that IPAVA are recruited in the intact rat by
isoproterenol and their recruitment by
hypoxia can be minimized by
propranolol, suggesting a role for the
adrenergic system in the recruitment of IPAVA by
hypoxia. IPAVA recruitment is completely abolished by ventilation with 100%
oxygen.
Isoproterenol also recruits IPAVA in isolated rat lungs. The fact that
isoproterenol can recruit IPAVA in isolated lungs, without increased pulmonary flow, suggests that elevated cardiac output is not required for IPAVA recruitment.