| Research Abstract |
Methods:
Animal model :
After anesthetized with halothane, adult Spraugue-Dawley rats were ventilated with air/O2
Femoral artery and vein were cannulated for measurement of MAP and blood gas analysis and for infusion, drawing blood, and administration of drugs, respectively. Furthermore, a probe of laser Doppler was inserted in close to dura matter through a small burr hole in the right parietal bone to measure regional cerebral blood flow. Regional cerebral blood flow was repetedly measured at stepwise change of MAP (40-160mmHg). Static cerebral autoregulation (SCAR) was assessed with % change of regional cerebral blood flow at MAP of lOOmmHg.
(1) SCAR was evaluated during isoflurane or midazolam + fentanyl anesthesia.
(2) SCAR was evaluated during normo, hypo, or hypercapnia.
(3) SCAR was evaluated during normothermia or brain moderate hypothermia (33-34℃).
(4) Incomplete brain ischemia was induced with ligation of bilateral carotid arteries for 5min. SCAR was evaluated during normothermia or brain moderate hypothermia (33-34℃) in the post-ischemic rats.
Results and Conclusions
SCAR was significantly impaired during isofllurane, but not during midazolam + fentanyl anesthesia.
Hypercapnia significantly impaired SCAR, in contrast, hypocapnia hyper-regulated SCAR. Moderate brain hypothermia significantly impaired SCAR as compared with normothermia.
SCAR was significantly impaired in the post ischemic rats as compared with the normal rats. However, inducing brain moderate hypothermia, does not cause further aggravation of SCAR in the post ischemic rats.
In summary, during brain moderate hypothermic therapy, combined sedation of midazolam and opiods and maintaining normocapnic state are preferable. Although moderate hypothermia itself does impair cerebral autoregulation, however, inducing the moderate hypothermia in the post cerebral ischemia may not cause further aggravation of SCAR.
|
