Cerebrovascular Response to Acute Decreases in Arterial PO2

The purpose of these studies was to examine the time course of the cerebrovascular response to acute hypoxia in unanesthetized ponies. An electromagnetic flow transducer chronically placed on the internal carotid artery of the pony allowed continuous recording of internal carotid artery blood flow (ICBF) which has been shown to be representative of cerebral blood flow (CBF). The ponies were subjected to three levels of acute isocapnic hypoxia (P a O 2 = 62, 44, and 39 mm Hg for hypoxia level I, II, and III, respectively), and the temporal and steady-state cerebrovascular response was examined. ICBF increased significantly at all three hypoxia levels (8, 25, and 40% at hypoxia I, II, and III, respectively). This increase was rapid in the two most severe levels of hypoxia, beginning within 45 s, and was complete within 90 s. The increase lagged behind the reduction in P a O 2 by 24–28 s. During the very mild level of hypoxia (I), no such rapid increase in flow was observed; rather, the increase occurred only after 5 min of hypoxia. Microsphere (15 μm diameter) measurements from six ponies during the most severe level of hypoxia (III) demonstrated that CBF increased 38%. Noncerebral tissues known to be vascularly connected to the circle of Willis, and thus capable of receiving blood flow via the internal carotid artery, either did not change or increased so slightly during hypoxia that their effect on ICBF was minimal. These data imply that mediators of the cerebrovascular response to hypoxia must be capable of sensing hypoxia and affecting cerebrovascular smooth muscle within seconds. The slower time course in mild hypoxia suggests other mechanisms may be involved when P a O 2 is greater than 50 mm Hg.