Abstract
The respiratory response to sustained hypoxia reflects the net effect of the peripheral chemoreceptor excitation and the central depression. To obtain a pure depressant effect of central hypoxia (alv. PO2, 35-75 mmHg) on respiration, the recipient cat's carotid bodies were vascularly isolated and bilaterally perfused with blood from a donor cat. Cats were anesthetized, vagotomized, paralyzed, and artificially ventilated. Alv. PCO2 was kept at a normal value (iso- and normocapnia) throughout the experiment. The minute integrated phrenic nerve activity (Min. PNA) was used as an indication of inspiratory activity. The Min. PNA at which the recipient and donor cats were both breathing room air (central normoxia and peripheral chemoreceptor normoxia) was taken as 100% (control), and Min. PNA expressed as a percentage of the control was measured in a series of three experiments (A, B, and C): experiment A (normoxia-hypoxia; central normoxia and peripheral chemoreceptor hypoxia), experiment B (hypoxia-hypoxia; central hypoxia and peripheral chemoreceptor hypoxia), and experiment C (hypoxia-normoxia; central hypoxia and peripheral chemoreceptor normoxia). At alv. PO2 of about 50 mmHg, Min. PNA was 169.7 +/- 23.6% (mean +/- SD) in experiment A, 127.3 +/- 22.0% in experiment B, and 71.6 +/- 17.3% in experiment C. Thus, a pure depressant effect of normocapnic hypoxia (alv. PO2 of 50 mmHg) was 42.4% (= 169.7-127.3) or 28.4% (= 100-71.6). At alv. PO2 of about 40 mmHg, Min. PNA was 185.2 +/- 16.8% in experiment A, 146.2 +/- 19.0% in experiment B, and 54.8 +/- 15.2% in experiment C. Thus, a pure depressant effect of normocapnic hypoxia (alv. PO2 of 40 mmHg) was 39.0% (= 185.2-146.2) or 45.2% (= 100-54.8). From these results, we concluded that a pure depressant effect of normocapnic central hypoxia (alv. PO2, 40-50 mmHg) was 28-45% and this was affected by a stimulating drive from the peripheral chemoreceptors.
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