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Increases in Cardiac Output Recruit Intrapulmonary Shunt Pathways in the Rat
Author(s) -
Bates Melissa,
Pegelow David,
Fulmer Brendan,
Drezdon Alyssa,
Farrell Emily,
Eldridge Marlowe
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1061.2
Subject(s) - medicine , shunt (medical) , embolization , cardiac output , central venous pressure , inferior vena cava , cardiology , ventricular pressure , blood flow , venous return curve , hemodynamics , anesthesia , blood pressure , surgery , heart rate
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 5×10 5 15μm spheres (3×10 6 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).