RESPONSE OF UPPER AIRWAY AND CHEST-WALL MUSCLES TO SELECTIVE BRAIN-STEM HYPOXIA IN THE NEWBORN

In animals with intact peripheral chemosensory afferents, hypoxia diff erentially affects upper airway (UA) and chest wall muscles. To determ ine the contribution of brain stem (BS) hypoxia to the response of UA and chest wall muscles during early life, we perfused the BS through a vertebral artery intermittently with blood from an extracorporeal cir cuit in nine newborn piglets (age 1-5 days). BS perfusions were perfor med with hypoxemic blood (arterial PO2 32 +/- 6 to 38 +/- 8 Torr) with different levels of BS PCO2 (28 +/-2, 37 +/- 4, and 56 +/- 5 Torr) wh ile systemic normocapnic hyperoxia was maintained (arterial PCO2 36 +/ - 3 to 40 +/- 6 Torr, arterial PO2 345 +/- 73 to 392 +/- 37 Torr). Ele ctromyograms (EMGs) of alae nasi (AN), external intercostal (EI), and diaphragm (DIA) were recorded. Normocapnic hypoxia of the BS induced a sustained increase in AN EMG (P < 0.01, analysis of variance) and dep ression of EI and DIA EMGs without a transient increase. These contras ting responses were also observed during hypocapnic and hypercapnic hy poxia of the BS and were not affected by inputs from the peripheral ch emoreceptors or rostral cerebral structures that were not exposed to h ypoxia. We conclude that, despite eliciting the known central respirat ory depression, BS hypoxia causes an increase in the respiratory drive to an UA airway muscle. Thus, BS hypoxia elicits a selective rather t han a generalized respiratory muscle depression. The respiratory muscl es with high energy expenditure (DIA and EI) are depressed while UA mu scles are stimulated or disinhibited. This response is independent of the level of BS arterial PCO2.