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Departments of Neurology (Drs. Ameriso and Fisher) and Medicine (Pulmonary Physiology Laboratory) (Dr. Mohler and M. Suarez), University of Southern California School of Medicine, Los Angeles, CA.
We measured cerebral vasomotor reactivity during normoventilation, hyperventilation (hypocapnia), and breathing of 6% CO2 (hypercapnia) in 20 normal subjects during the hours of 6 to 8 AM, 1 to 3 PM, and 7 to 9 PM. Cerebral vasomotor reactivity was calculated, using transcranial Doppler, as percent change in the mean blood flow velocity of the middle cerebral artery per mm Hg change in end-tidal CO2 during hypocapnia and hypercapnia. Vasomotor reactivity during hypercapnia was lower in the morning (1.72 ± 0.66 %/mm Hg) than in the afternoon (2.34 ± 0.74 %/mm Hg, p < 0.01) and evening (2.31 ± 0.56 %/mm Hg, p < 0.001). Vasomotor reactivity during hypocapnia did not vary significantly during the three periods (2.34 ± 0.59 %/mm Hg in the morning, 2.43 ± 0.51 %/mm Hg in the afternoon, and 2.26 ± 0.52 %/mm Hg in the evening). This reduced morning response to hypercapnia suggests diminished vasodilator reserve during this period, and may be related to the increased stroke risk during the morning hours.
Address correspondence and reprint requests to Dr. Sebastian F. Ameriso, USC School of Medicine, Department of Neurology, Room 5641, 1200 North State Street, Los Angeles, CA 90033.
Supported by Los Angeles County-University of Southern California Medical Center Health Research Association. Computational assistance was provided by NIH MO 1 RR-43.
Received August 27, 1993. Accepted in final form April 5, 1994.
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