Intrapulmonary arteriovenous anastomoses (IPAVS) directly connect the arterial and venous circulations in the lung, bypassing the capillary network. Here, we used solid, latex microspheres and isolated rat lung and intact, spontaneously breathing rat models to test the hypothesis that IPAVS are recruited by alveolar hypoxia. We found that hypoxia recruits IPAVS in the intact rat, but not the isolated lung. IPAVS are at least 70 μm in the rat and, interestingly, appear to be recruited when the mixed venous Po(2) falls below 22 mmHg. These data provide evidence that large-diameter, direct arteriovenous connections exist in the lung and are recruitable by hypoxia in the intact animal.
Using an intact, spontaneously breathing, instrumented rat model, we investigated the effects of progressive embolization and pulmonary blood flow on intrapulmonary shunt pathway (IPAVs) recruitment. We hypothesized that progressive embolization and increased regional flow would recruit IPAVs in a dose‐dependent manner. We injected six boluses of 5×105 15μm spheres (3×106 total) in 0.4 or 0.8 mL aliquots via the inferior vena cava and harvested the kidney to assess transpulmonary passage of spheres. Spheres bypassed the lungs in 1/3 rats and 3/3 rats injected with 0.4 and 0.8 mL, respectively. The shunt fraction increased in a dose‐dependent manner with progressive embolization. Interestingly, right ventricular systolic pressure (RVSP) rose in the rats receiving 0.4mL injections (28±4 to 36±15 mmHg), but not in animals receiving 0.8 mL (24±3 mmHg vs 24±1mmHg). The transiently higher cardiac output associated with the larger volume injections may recruit and distend the pulmonary vasculature, including IPAVs, resulting in lower RVSP and greater sphere passage. These data suggest that increased pulmonary blood flow is important for IPAV recruitment. Further studies are needed to better define the mechanical and mediator‐based mechanisms regulating IPAVs and their importance in determining pulmonary vasculature pressure.This research was supported by a grant from the NIH (5R01HL086897‐02).
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