George H. Crocker

Effects of oleic acid-induced lung injury on oxygen transport and aerobic capacity

We tested the hypothesis that oleic-acid (OA) infusion impairs gas exchange, decreases total cardiopulmonary O2 delivery and lowers maximal aerobic capacity ( [Formula: see text] ). We infused 0.05ml OAkg(-1) (∼3ml) and ∼563ml saline into the right atria of four goats [59.1±14.0 (SD) kg] prior to running them on a treadmill at [Formula: see text] 2-h and 1-d following OA-induced acute lung injury, and with no lung injury. Acute lung injury decreased [Formula: see text] , O2 delivery, arterial O2 concentration and arterial O2 partial pressure compared to no lung injury. The [Formula: see text] positively correlated with O2 delivery and inversely correlated with alveolar-arterial O2 partial pressure difference, suggesting that impaired pulmonary gas exchange decreased O2 delivery and uptake. Results indicate OA infusion may be a useful model for acutely impairing pulmonary gas exchange for exercise studies. Seven OA infusions induced smaller chronic gas exchange and arterial O2 partial pressure changes than acute infusion.

Interactive effects of hypoxia, carbon monoxide and acute lung injury on oxygen transport and aerobic capacity

This study determined how breathing hypoxic gas, reducing circulatory capacitance for O2 by breathing CO, and impairing pulmonary gas exchange by acutely injuring the lungs interact to limit cardiopulmonary O2 delivery, O2 extraction and maximal aerobic capacity (VO2max). Five goats ran on a treadmill at VO2max following oleic-acid induced acute lung injury that impaired pulmonary gas exchange, after partial recovery or with no acute lung injury. Goats breathed normoxic or hypoxic inspired gas fractions (FIO2 0.21 or 0.12) with and without small amounts of CO to maintain carboxyhemoglobin fractions (FHbCO) of 0.02 or 0.30. With the exception of elevated FHbCO with acute lung injury (P=0.08), all combinations of hypoxia, elevated FHbCO and acute lung injury attenuated the reduction in VO2max by 15-27% compared to the sum of each treatments individual reduction in VO2max when administered separately. Simultaneous administration of two treatments attenuated the reduction in VO2max by attenuating the decrease in cardiopulmonary O2 delivery, not synergistically increasing O2 extraction.

Ventilatory response to carbon monoxide during exercise in hypoxia and hypercapnia

We tested if the addition of CO to inspired gases with different inspired O2 and CO2 fractions (FIO2 and FICO2) stimulates ventilation at rest or during submaximal exercise. We measured minute ventilation (VE) in goats breathing combinations of FIO2 ranging from 0.21 to 0.06 and FICO2 from 0 to 0.05, both with and without inspired CO resulting in carboxyhemoglobin fractions (FHbCO) of 0.02 (no CO added), 0.15, or 0.45. We did this while they stood on a treadmill, walked at 1.4, or trotted at 2.5ms-1. Hypoxia, hypercapnia, and exercise, alone and in combination, increased ventilation compared to breathing air at rest. Both elevated FHbCO increased VE compared with ambient FHbCO during exercise (increases of 1.50 and 5.53mls-1kg-1 for FHbCO 0.15 and 0.45, respectively; P=0.035), but not at rest (P=0.958), when the ventilatory effects of FIO2 and FICO2 are factored out. Additionally, FHbCO 0.45 (but not 0.15) increased VE compared to FHbCO 0.02 for all FIO2 and FICO2 when the ventilatory effects of exercise are factored out. Taken together, these data suggest that exercise intensity and FHbCO dose interact to stimulate ventilation during exercise.