Stroke, Vol 25, 1760-1764, Copyright © 1994 by American Heart Association
HS Markus, P Vallance and MM Brown
BACKGROUND AND PURPOSE: Prostaglandins are believed to play an important
role in maintenance of cerebral blood flow and possibly in the vasodilatory
response to carbon dioxide. Therefore, the nonsteroidal anti-inflammatory
drugs and aspirin, which inhibit cyclooxygenase, might be expected to
reduce cerebral blood flow and the response to hypercapnia. This could
induce cerebral ischemia in patients with a hemodynamically critical
circulation. It would also interfere with the measurement of
cerebrovascular reserve using carbon dioxide. METHODS: The effect of a
single dose of indomethacin and of two other cyclooxygenase inhibitors
(aspirin and sulindac) on the cerebral circulation was measured using
transcranial Doppler ultrasonography of the middle cerebral artery. Seven
normal adults were studied in each drug group. Resting blood flow velocity
and the responses to hypercapnia and to hyperventilation were measured.
RESULTS: Indomethacin resulted in a fall in basal middle cerebral artery
flow velocity from a mean of 48.9 cm/s to 34.0 cm/s (P < .002). It also
reduced the vasoconstrictor response to hypocapnia (induced by
hyperventilation) from 37.5% to 20.7% (P < .003). There was a
nonsignificant reduction in the vasodilatory response to 8% carbon dioxide
(mean: predrug, 87.7%; postdrug, 61.0%), with marked intersubject
variability. In contrast, basal middle cerebral artery velocity and
vasoconstrictor and vasodilatory responses to changes in carbon dioxide
were unchanged after aspirin or sulindac administration. CONCLUSIONS: The
lack of effect of aspirin on basal cerebral blood flow velocity and on
vasodilatory reserve is reassuring; aspirin will not reduce cerebral blood
flow or the response to a reduced perfusion pressure in patients with
critically impaired cerebral hemodynamics. However, indomethacin should be
avoided in such patients.
ARTICLES
Differential effect of three cyclooxygenase inhibitors on human cerebral blood flow velocity and carbon dioxide reactivity
Division of Clinical Neuroscience, St George's Hospital Medical School, London, UK.
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