title: The effect of caffeine on dilated cerebral circulation and on diagnostic CO2 reactivity testing.
abstract: Reduction of cerebral blood flow by caffeine has been shown in multiple studies. However, the effect of this substance on pathologically dilated cerebral vessels is not clearly defined. The aim of this study was to investigate the effect of caffeine on an already dilated cerebral circulation and specify if these vessels are still able to constrict as a consequence of caffeine stimulation. A second aim of this study was to compare results of cerebral vasomotor CO(2) reactivity testing with and without caffeine ingestion. Seventeen healthy adult volunteers had vasomotor reactivity tested before and thirty minutes after ingestion of 300 mg of caffeine. Each vasomotor reactivity test consisted of velocity measurements from both middle cerebral arteries using transcranial Doppler ultrasound during normocapnia, hypercapnia, and hypocapnia. Hemodynamic data and end-tidal CO(2) (etCO(2)) concentration were also recorded. The vasomotor reactivity (VMR) and CO(2) reactivity were calculated from a measured data pool. At a level of etCO(2)=40 mmHg the resting velocity in the middle cerebral artery (V(MCA)) dropped from 70.7+/-22.8 cm/sec to 60.7 +/- 15.4 cm/sec 30 minutes after caffeine stimulation (14.1% decrease, p<0.001). During hypercapnia of etCO(2)=50 mmHg there was also a significant decline of V(MCA) from 103.1+/-25.4 to 91.4+/-21.8 cm/sec (11.3%, p<0.001). There was not a statistically significant reduction of V(MCA) during hypocapnia. Calculated VMR and CO(2) reactivity before and after caffeine intake were not statistically significant. The presented data demonstrate a significant decrease in cerebral blood flow velocities after caffeine ingestion both in a normal cerebrovascular bed and under conditions of peripheral cerebrovascular vasodilatation. These findings support the important role of caffeine in regulation of CBF under different pathological conditions. Despite significant reactive vasodilatation in the brain microcirculation, caffeine is still able to act as a competitive antagonist of CO(2) on cerebral microvessels. The fact that caffeine may decrease CBF despite significant pathological vasodilatation offers the possibility of therapeutic manipulation in patients with traumatic vasoparalysis. For routine clinical testing of CO(2) reactivity it is not necessary to insist on pre-test dietary restrictions.
authors.affiliation: Department of Neurological Surgery, School of Medicine, University of Washington, Seattle, Washington, USA. drmartinblaha@yahoo.com
authors.forename: Martin
authors.initials: M
authors.lastname: Blaha
authors.forename: Vladimir
authors.initials: V
authors.lastname: Benes
authors.forename: Colleen M
authors.initials: CM
authors.lastname: Douville
authors.forename: David W
authors.initials: DW
authors.lastname: Newell
mesh_terms: D000328:Adult; D002110:Caffeine / Q000008:administration & dosage* / Q000378:metabolism; D002245:Carbon Dioxide; D000697:Central Nervous System Stimulants / Q000008:administration & dosage* / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D005260:Female; D006801:Humans; D006935:Hypercapnia / Q000139:chemically induced* / Q000175:diagnosis*; D008297:Male; D008875:Middle Aged; D020768:Middle Cerebral Artery / Q000000981:diagnostic imaging; D017585:Ultrasonography, Doppler, Transcranial / Q000379:methods
chemical_list: D000697:Central Nervous System Stimulants; D002245:Carbon Dioxide; D002110:Caffeine