[Intracerebral steal after acetazolamide administration].
Occlusion or high grade stenosis of the internal carotid artery may be asymptomatic depending on the collateral patterns in the circle of Willis and the reserve capacity of the microvascular (arteriolar) system. The distensibility of the cerebral arterioles may be described quantitatively by the vasomotor reactivity. We present three patients with severe stenosis of an internal carotid artery associated with more severe stenosis or occlusion of the contralateral internal carotid artery. We continuously measured blood flow velocity in both middle cerebral arteries by transcranial Doppler ultrasound in rest and for 20 minutes after IV administration of 1 g acetazolamide. Arterial blood pressure was determined with tonometry, end-tidal CO2 was determined by a capnometer. In resting condition the anterior communicating artery, the posterior communicating artery and the ophthalmic artery supplied collateral blood flow towards the side of the more severe internal carotid artery disease. Blood flow velocity decreased after acetazolamide administration in all patients in the middle cerebral arteries on the side of the more severe occlusive carotid disease, while increased on the contralateral side. We assume that the exhausted arteriolar system on the more severely affected side was not able to further dilate and the open collateral system could have driven blood towards the other side with preserved reserve capacity. The reduced blood flow velocity in the middle cerebral arteries after acetazolamide may reflect this intracerebral steal phenomenon.
Vastagh
Ildikó
I
Semmelweis Egyetem, Neurológiai Klinika, Budapest. ildiko@neur.sote.hu
Pozsár
Melinda
M
Folyovich
András
A
Debreczeni
Róbert
R
Pálvölgyi
László
L
Bereczki
Dániel
D
Szirmai
Imre
I
D000086:Acetazolamide / Q000008:administration & dosage / Q000494:pharmacology*; D000368:Aged; D000927:Anticonvulsants / Q000494:pharmacology; D001783:Blood Flow Velocity / Q000187:drug effects*; D001785:Blood Gas Monitoring, Transcutaneous; D001794:Blood Pressure; D002257:Carbonic Anhydrase Inhibitors / Q000494:pharmacology; D002343:Carotid Artery, Internal / Q000187:drug effects* / Q000503:physiopathology*; D016893:Carotid Stenosis / Q000188:drug therapy* / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D005260:Female; D006801:Humans; D007275:Injections, Intravenous; D008297:Male; D008875:Middle Aged; D020768:Middle Cerebral Artery / Q000187:drug effects* / Q000503:physiopathology; D012720:Severity of Illness Index; D017585:Ultrasonography, Doppler, Transcranial; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000494:pharmacology*
D000927:Anticonvulsants; D002257:Carbonic Anhydrase Inhibitors; D014665:Vasodilator Agents; D000086:Acetazolamide