Cerebral pressure-flow and metabolic responses to sustained hypoxia: effect of CO2

Abstract

This study was designed to determine the role of CO2 in the cerebral hemodynamic, metabolic, and fluid shift responses in a conscious sheep model of acute mountain sickness (AMS). Ewes were instrumented chronically with left ventricular, aortic, inferior vena cava, sagittal sinus, and epidural catheters and exposed to 96 h of hypoxia in an environmental chamber in two groups: 1) hypocapnic [HH; n = 12; arterial PO2 (PaO2) = 40 Torr, arterial PCO2 (PaCO2) = 27 Torr] and 2) eucapnic (EH; n = 9; PaCO2 = 40 Torr, PaCO2 = 37 Torr). AMS, estimated from food and water intakes and behavior, occurred in 9 of 12 HH and 9 of 9 EH sheep. Intracranial pressure (Picp) and the pressure gradient between Picp and sagittal sinus (Psag) increased in AMS sheep only. Total and regional cerebral blood flows, except in the choroid plexus (Qcp), were elevated significantly (P < 0.05) throughout hypoxia in all sheep; cerebral blood flow was greater in EH sheep (P < 0.05). Qcp decreased in HH (P < 0.05) but remained unchanged in EH sheep. Cerebral O2 and glucose uptakes were not altered in either group. Brain edema, reflected by elevated wet-to-dry tissue weight ratios (P < 0.0001), occurred only in AMS sheep. We conclude 1) AMS is associated with cerebral edema and normal brain aerobic metabolism, 2) decreased Qcp and increased Picp-Psag gradients during HH likely compensate the increased intracranial volume in AMS, and 3) CO2 supplementation at constant PaO2 did not reduce AMS, Picp, or brain tissue edema.

Cerebral blood flow during hypoxic hypoxia with plasma-based hemoglobin at reduced hematocrit

“…Others have reported no change in blood flow to choroid plexus during hypoxic hypoxia (7,21,42). The reduction in blood flow that we observed during hypoxia may be related to vasopressin-and ANG IImediated constriction (7,8,25).…”

“…Interestingly, the increase in CBF during anemia is approximately the same as the increase in CBF during hypoxic hypoxia at equivalent reductions in Ca O 2 (20). With hypoxic hypoxia, the increase in CBF compensates for the decrease in Ca O 2 , thereby maintaining cerebral O 2 transport (CBF ϫ Ca O 2 ) to the cerebral microcirculation (20,22,42). With anemia, cerebral O 2 transport generally is well preserved (1,16,20), although small decreases have also been reported (6,37).…”

Effects of 8h of eucapnic and poikilocapnic hypoxia on middle cerebral artery velocity and heart rate in humans

“…In general, there appears to be first a period of time over which cerebral blood flow increases, which is then followed by a subsequent decrease in CBF over a number of days (Severinghaus et al 1966;Huang et al 1987). The study by Huang et al (1987) Yang, Bergo, Krasney & Krasney (1994) seem to show little difference in the time course for CBF between sheep exposed to 96 h of eucapnic hypoxia and sheep exposed to the same period of poikilocapnic hypoxia, although the overall level of CBF was lower in the poikilocapnic sheep compared with the eucapnic sheep. In that study, values for CBF were obtained at 1 and 6 h into the exposure as well as at 24 h intervals, and in respect of these times, our findings may be considered as consistent with their results.…”

Association between laparoscopic abdominal surgery and postoperative symptoms of raised intracranial pressure

“…It is well documented that cerebral arteriolar tone is exquisitely sensitive to levels of CO 2 [14], with hypercapnia leading to vasodilation, and thus to increased cerebral blood volume. It also is known that CO 2 used during insufflation is absorbed from the peritoneum [9] However, E T CO 2 levels are maintained fairly constant by the anesthetist during surgery, which intuitively renders the CO 2 absorption theory unconvincing for any possible rise in ICP.…”

“…Some volatile anesthetic agents are believed to reduce the autoregulatory capacity of the brain [1,14], thus allowing small increases in intracranial volume to produce significant increases in ICP.…”