INDEPENDENT CONTROL OF MUCOSAL AND TOTAL AIRWAY BLOOD-FLOW DURING HYPOXEMIA

In the larger airways, the blood circulation forms a subepithelial (mucosal) and outer (peribronchial) microvascular network. This raises the possibility that blood flow in these two networks is regulated independently. We used hypoxemia as a stimulus to induce changes in tracheal mucosal blood flow normalized for systemic arterial pressure (Q(tr) n) measured with an inert soluble gas technique and total bronchial blood flow (Q(br)) and normalized Q(br)(Q(brn)) measured with an electromagnetic flow probe in anesthetized sheep. Fifteen minutes of hypoxemia [Po2 40 +/- 7 (SD) Torr] decreased mean Q(tr) n from 1.1 +/- 0.4 to 0.8 +/- 0.4 ml.min-1.mmHg-1.10(2) (-27%; P < 0.05; n = 7) and increased mean Q(br n) from 12.1 +/- 3.2 to 17.1 +/- 5.4 ml.min-1.mmHg-1.10(2) (+41%; P < 0.05; n = 6). The rise in Q(br) correlated with cardiac output (r = 0.68; P < 0.05). Phentolamine pretreatment (0.1 mg/kg iv) blunted the hypoxemia-related decrease of mean Q(tr) n (-8%; P = NS). Tyramine (2.5 mg) applied locally to the trachea decreased mean Q(tr) n significantly after 30 and 45 min by 31 and 19%, respectively (P < 0.05). 6-Hydroxydopamine (0.2 mg 4 times for 1 h locally applied) prevented the hypoxemia-induced as well as local tyramine-induced decrease in mean Q(tr) n (0 and 0%). We conclude that, during arterial hypoxemia, 1) an increase in total airway blood flow is associated with a decrease in airway mucosal blood flow, 2) total airway blood flow correlates with cardiac output, and 3) the decrease in Q(tr) n is at least partly mediated by local catecholamine release. These findings suggest an independent adrenergic regulation of airway mucosal blood flow.