Abstract
1. In spontaneously breathing, anaesthetized rats, a study was made of the effects upon the graded cardiovascular responses to systemic hypoxia (inspiratory fractional O2 concentration, Fi, O2: 0.15, 0.12, 0.08, 0.06) of maintaining arterial CO2 pressure (Pa,CO2) at the air-breathing level by adding CO2 to the inspirate (eucapnic hypoxia), rather than allowing Pa,CO2 to fall (hypocapnia hypoxia). 2. At each Fi,O2, maintenance of eucapnia significantly reduced the increase in respiratory frequency, but significantly accentuated the increase in tidal and minute volume: as a result the fall in Pa,O2 at each Fi,O2 was significantly reduced. 3. Concomitantly, maintenance of eucapnia reduced the increase in heart rate (HR) and fall in arterial pressure (ABP), the effects being significant at Fi,O2 0.08 and/or 0.06. There was also a tendency for the increases in renal and femoral vascular conductances (RVC, FVC) to be reduced; at Fi,O2 0.06 mean increases from control were 2 +/- 10 vs. 16 +/- 7% (eucapnia vs. hypocapnia) for RVC, and 62 +/- 11 vs. 106 +/- 27% for FVC. 4. As maintenance of eucapnia reduced the fall in Pa,O2 at each Fi,O2, the above results were also considered as a function of Pa,O2. Then, maintenance of eucapnia had similar significant effects on the changes in respiration and HR as described above and reduced the mean increase in RVC (16 +/- 11 vs. 23 +/- 10%, at Pa,O2 31 mmHg, which was attained at Fi,O2 0.06 with eucapnia and 0.08 with hypocapnia). However, maintenance of eucapnia had no effect on the falls in ABP and accentuated the mean increase in FVC (74.9 +/- 13 vs. 57 +/- 10% at Pa,O2 31 mmHg). 5. These findings indicate that, in the rat, the hypocapnia that accompanies the hyperventilatory response to systemic hypoxia facilitates the tachycardia and may accentuate the renal vasodilation, but attenuate the hypoxia-induced vasodilatation in skeletal muscle. Possible mechanisms are discussed.
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