Search

To evaluate the reliability of noninvasive oximeters during exercise in patients with cystic fibrosis (CF), we studied 9 patients during exercise tests, using 3 devices (Hewlett-Packard 47201A, Biox-Ohmeda 3700, Nellcor [...]

Cystic fibrosis (CF) is a disease that causes the abnormal formation of fibrous tissue (a dense, inelastic tissue similar to scar tissue) in the lungs. The presence of fibrous tissue in the lungs causes them to become stiff, making breathing difficult, and reduces the exchange of oxygen and carbon dioxide across lung membranes so that less oxygen gets into the blood. Patients with CF have difficulty in exercising because their ability to breathe is impaired, and they cannot get enough oxygen to the exercising muscles. The effect of air containing a higher-than-normal oxygen concentration (oxygen supplementation) on the ability to exercise was evaluated in 36 patients with CF. Patients exercised on exercise bicycles while breathing normal air (21 percent oxygen) or hyperoxic air, with 30 percent oxygen. When exercise was performed while breathing hyperoxic air, the concentration of oxygen in the subjects' blood was higher than when exercise was performed while breathing normal air. However, breathing hyperoxic air did not increase the ability to exercise harder. When exercise was performed, either at peak levels or at submaximal levels, breathing hyperoxic air reduced the rate of breathing and heart rate when compared with breathing normal air. It is concluded that breathing hyperoxic air allows patients with CF to exercise at maximum levels with less work required by the lungs and heart. (Consumer Summary produced by Reliance Medical Information, Inc.)

Curtis, Scott E., Thomas A. Walker, W. E. Bradley, and Stephen M. Cain. Raising P50increases tissue PO2in canine skeletal muscle but does not affect critical O2extraction ratio.J. Appl. Physiol.83(5): 1681–1689, 1997.—Affinity of hemoglobin (Hb) for O2determines in part the rate of O2diffusion from capillaries to myocytes by altering capillary PO2. We hypothesized that a decrease in Hb O2affinity (increased P50) would increase capillary and tissue PO2(PtiO2) and improve O2consumption during ischemia. To test this hypothesis, blood flow to the pump-perfused left hindlimb of 18 anesthetized and paralyzed dogs was progressively decreased over 90 min while hindlimb O2consumption and O2delivery (Q˙o2) and PtiO2were measured at the muscle surface. ArterialPO2was maintained at 150 ± 10 Torr in all dogs. We increased P50by 12.3 ± 0.9 (SE) Torr in nine dogs with RSR-13, an allosteric modifier of Hb. This decreased arterial O2saturation to 90–92% but increased mean PtiO2from 35.5 ± 11.6 to 44.1 ± 15.2 (SD) Torr (P< 0.05) with no change in controls (n= 9). O2extraction ratio at criticalQ˙o2was 74 ± 2% in controls and 79 ± 1% in RSR-13-treated dogs (P= not significant). PtiO2was 30–40% higher in the RSR-13-treated group at anyQ˙o2above critical but did not differ between groups below criticalQ˙o2. Perfusion heterogeneity and convergence of the dissociation curves near criticalQ˙o2may have mitigated any effect of increased P50on O2diffusion. Still, increasing P50by 12 Torr with RSR-13 significantly increased PtiO2atQ˙o2values above critical.

Raising P₅₀ increases tissue PO₂ in canine skeletal muscle but does not affect critical O₂ extraction ratio. J. Appl. Physiol. 83(5): 1681-1689, 1997.—Affinity of hemoglobin (Hb) for O₂ determines in part the rate of O₂ diffusion from capillaries to myocytes by altering capillary PO₂. We hypothesized that a decrease in Hb O₂ affinity (increased P₅₀) would increase capillary and tissue PO₂ (Pti_O2) and improve O₂ consumption during ischemia. To test this hypothesis, blood flow to the pump-perfused left hindlimb of 18 anesthetized and paralyzed dogs was progressively decreased over 90 min while hindlimb O₂ consumption and O₂ delivery (&Qdot;O₂) and Pti_O2 were measured at the muscle surface. Arterial PO₂ was maintained at 150 ± 10 Torr in all dogs. We increased P₅₀ by 12.3 ± 0.9 (SE) Torr in nine dogs with RSR-13, an allosteric modifier of Hb. This decreased arterial O₂ saturation to 90-92% but increased mean Pti_O2 from 35.5 ± 11.6 to 44.1 ± 15.2 (SD) Torr (P &lt; 0.05) with no change in controls (n = 9). O₂ extraction ratio at critical &Qdot;O₂ was 74 ± 2% in controls and 79 ± 1% in RSR-13-treated dogs (P = not significant). Pti_O2 was 30-40% higher in the RSR-13-treated group at any &Qdot;O₂ above critical but did not differ between groups below critical &Qdot;O₂. Perfusion heterogeneity and convergence of the dissociation curves near critical &Qdot;O₂ may have mitigated any effect of increased P₅₀ on O₂ diffusion. Still, increasing P₅₀ by 12 Torr with RSR-13 significantly increased Pti_O2 at &Qdot;O₂ values above critical.