Lung vascular responses and VA/Q matching after chronic hypoxia in neonatal piglets.
We hypothesized that exposure of neonatal swine to chronic alveolar hypoxia (CH) would cause increased PVR, blunt acute hypoxic vasoconstriction, and increase VA/Q mismatch. After exposure to either normobaric alveolar hypoxia (FIO2 = 0.10) or room air for 2 weeks, animals were anesthetized and ventilated first with room air and then with hypoxic gas (FIO2 = 0.12). PVR, and pressure-flow (P/Q) relations were measured between 15-100% of baseline cardiac output. VA/Q matching was measured by the multiple inert gas elimination technique. During room air breathing, the mean PVR and P/Q slope in the CH animals was significantly greater than in the control (C) animals. P/Q intercepts were similar and near the origin for both groups. The absolute PVR and P/Q slope were greater for CH compared to C animals during acute alveolar hypoxia. The fractional increase in PVR and P/Q slope in the response to acute hypoxia was similar for both groups. PaO2, intrapulmonary shunt, and SDQp (an index of VA/Q heterogeneity) were similar for both groups. We conclude that CH in neonatal swine causes pulmonary hypertension, but does not attenuate acute hypoxic pulmonary vasoconstriction, nor VA/Q matching.
Gibson
R L
RL
Department of Pediatrics University of Washington School of Medicine, Seattle 98195.
Davis
C B
CB
Standaert
T A
TA
Truog
W E
WE
Redding
G J
GJ
D000818:Animals; D001835:Body Weight; D006439:Hemodynamics; D006976:Hypertension, Pulmonary / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology*; D008168:Lung / Q000098:blood supply* / Q000503:physiopathology; D011652:Pulmonary Circulation; D011659:Pulmonary Gas Exchange; D012119:Respiration; D013552:Swine; D014655:Vascular Resistance; D014692:Ventilation-Perfusion Ratio