Time-dependent alterations in functional and pharmacological arteriolar reactivity after subarachnoid hemorrhage.
OBJECTIVE
Disturbances in cerebral arteriolar function, in addition to large vessel vasospasm, may be responsible for ischemia after subarachnoid hemorrhage. The purpose of this study was to test the hypothesis that subarachnoid hemorrhage alters cerebral microvascular reactivity.


METHODS
An endovascular filament model was used to induce subarachnoid hemorrhage in halothane-anesthetized male Sprague-Dawley rats. We evaluated pial arteriolar responses to sciatic nerve stimulation, topically applied vasoactive agents (adenosine or sodium nitroprusside), and CO(2) inhalation in rats subjected to subarachnoid hemorrhage at 1 to 5 days after insult.


RESULTS
In sham-operated rats, sciatic nerve stimulation evoked a 23.5+/-1.8% increase in arteriolar diameter, which was significantly attenuated to 13.7+/-0.9%, 12.8+/-2.5%, and 18.8+/-2.9% at 24, 48, and 72 hours after subarachnoid hemorrhage, respectively (P<0.05; n> or =7). At 96 and 120 hours after subarachnoid hemorrhage, sciatic nerve stimulation-induced dilation recovered to sham levels. Somatosensory-evoked potentials were unaltered by subarachnoid hemorrhage. Pial vasodilatation to adenosine (10 micromol/L) and sodium nitroprusside (1 micromol/L) were significantly impaired, by 47% and 41%, respectively, at 48 hours after subarachnoid hemorrhage (P<0.05; n=7). In contrast, CO(2) reactivity was unaffected by subarachnoid hemorrhage.


CONCLUSIONS
Pial arteriolar responses to cortical activation may be decreased in the initial 2 to 3 days after experimental subarachnoid hemorrhage.
Britz
Gavin W
GW
Department of Neurological Surgery, University of Washington, Seattle, WA 98122, USA. gbritz@u.washington.edu
Meno
Joseph R
JR
Park
Ik-Seong
IS
Abel
Taylor J
TJ
Chowdhary
Abhineet
A
Nguyen
Thien-Son K
TS
Winn
H Richard
HR
Ngai
Al C
AC
D000241:Adenosine / Q000494:pharmacology; D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000503:physiopathology*; D002545:Brain Ischemia / Q000209:etiology / Q000503:physiopathology; D002245:Carbon Dioxide / Q000494:pharmacology; D002536:Cerebral Arteries / Q000187:drug effects / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000098:blood supply / Q000502:physiology; D004558:Electric Stimulation; D005073:Evoked Potentials, Somatosensory / Q000502:physiology; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012677:Sensation / Q000502:physiology; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000503:physiopathology*; D013346:Subarachnoid Space / Q000187:drug effects / Q000503:physiopathology; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology; D020301:Vasospasm, Intracranial / Q000209:etiology* / Q000503:physiopathology*
D014665:Vasodilator Agents; D002245:Carbon Dioxide; D009599:Nitroprusside; D000241:Adenosine