Cerebrovascular reactivity can be quantified by correlating blood oxygen level dependent (BOLD) signal intensity with changes in end-tidal partial pressure of carbon dioxide (PCO 2 ). Four 3-min cycles of high and low PCO 2 were induced in three subjects, each cycle containing a steady PCO 2 level lasting at least 60 sec. The BOLD signal closely followed the end-tidal PCO 2 . The mean MRI signal intensity difference between high and low PCO 2 (i.e., cerebrovascular reactivity) was 4.0 ؎ 3.4% for gray matter and 0.0 ؎ 2.0% for white matter. This is the first demonstration of the application of a controlled reproducible physiologic stimulus, i.e., alternating steady state levels of PCO 2 , to the quantification of cerebrovascular reactivity. Cerebral blood flow is generally determined by the metabolic demand of the brain tissue. The capacity for autoregulation can be assessed by measuring hemodynamic responses to a quantifiable stimulus such as a change in partial pressure of carbon dioxide (PCO 2 ). The magnitude of the hemodynamic response relative to the alteration in PCO 2 is termed "cerebrovascular reactivity"; changes in blood oxygen level-dependent (BOLD) signal intensity can be used as an indicator of this reactivity.Our aim was to induce changes in MR signal intensity with changes in end-tidal PCO 2 (PETCO 2 ) by:1. Selecting two easily tolerated levels of PETCO 2 sufficiently different from each other to improve the accuracy in estimating cerebrovascular reactivity by minimizing the effect of noise; 2. Maintaining each PETCO 2 at a steady level long enough to allow stabilization of cerebral blood flow and facilitate correlation of the BOLD signal intensity to a specific PETCO 2 ; and 3. Effecting rapid step changes between steady-state levels of PCO 2 in order to allow multiple measurements of cerebrovascular reactivity within the time available for scanning, thereby minimizing the confounding effect of baseline signal drift typically present in functional imaging data. MATERIALS AND METHODSFollowing institutional ethics approval, we studied one healthy female and two healthy male subjects. The subjects' inspired gas concentrations were supplied via the circuit depicted in schematic form in Fig. 1. Each subject breathed through a mouthpiece (No. 109-P; Vacumed, Ventura, CA) attached to a right angle connector (to enable it to fit inside the MRI head coil). This mouthpiece allows occlusion of the teeth and thus aids in the swallowing of excess saliva while supine. Airway PCO 2 was monitored continuously at the mouth (Capnomac Ultima, Datex Engstrom, Helsinki, Finland) and recorded digitally (Dataq, Akron, OH). Control of PETCO 2Our protocol involved four 3-min cycles of raising and lowering the PETCO 2 . During each cycle the high PETCO 2 level was attained by delivering into the circuit 8% CO 2 in O 2 , at 15 L/min for 10 -15 sec, and maintained at that level by delivering 100% O 2 (the fresh gas flow) at 0.5-2 L/min for the remainder of the 90 sec. The low PETCO 2 was attained by delivering 100% O 2 at ...

The currently recommended prehospital treatment for carbon monoxide (CO) poisoning is administration of 100% O(2). We have shown in dogs that normocapnic hyperpnea with O(2) further accelerates CO elimination. The purpose of this study was to examine the relation between minute ventilation (V E) and the rate of elimination of CO in humans. Seven healthy male volunteers were exposed to CO (400 to 1,000 ppm) in air until their carboxyhemoglobin (COHb) levels reached 10 to 12%. They then breathed either 100% O(2) at resting V E (4.3 to 9.0 L min) for 60 min or O(2) containing 4.5 to 4.8% CO(2) (to maintain normocapnia) at two to six times resting V E for 90 min. The half-time of the decrease in COHb fell from 78 +/- 24 min (mean +/- SD) during resting V E with 100% O(2) to 31 +/- 6 min (p < 0. 001) during normocapnic hyperpnea with O(2). The relation between V E and the half-time of COHb reduction approximated a rectangular hyperbola. Because both the method and circuit are simple, this approach may enhance the first-aid treatment of CO poisoning.