title: Acute effects of nimodipine on cerebral vasculature and brain metabolism in high grade subarachnoid hemorrhage patients.
abstract: BACKGROUND
  Nimodipine is the only medication shown to improve outcomes after aneurysmal subarachnoid hemorrhage (SAH). Preliminary theories regarding the mechanism by which it prevents vasospasm have been challenged. The acute physiologic and metabolic effects of oral Nimodipine have not been examined in patients with poor-grade SAH.
  
  
  METHODS
  This is an observational study performed in 16 poor-grade SAH patients undergoing multimodality monitoring who received oral Nimodipine as part of routine clinical care. A total of 663 doses of Nimodipine were observed. Changes in physiologic measurements including MAP, CPP, ICP, P(bt)O(2), and CBF were examined.
  
  
  RESULTS
  Administration of oral Nimodipine was associated with a 1.33 mmHg decrease in MAP (P < 0.001) and a 1.22 mmHg decrease in CPP (P < 0.001). When administration of Nimodipine was associated with MAP decreases, P(bt)O(2) (1.03 mmHg; P < 0.001) and CBF (0.39 ml/100 g/min; P = 0.002) also decreased.
  
  
  CONCLUSIONS
  Despite CPP targeted therapy with vasopressor medication, oral Nimodipine was associated with a decrease in MAP and CPP. When Nimodipine administration was associated with a decrease in MAP, there were concomitant drops in P(bt)O(2) and CBF. These findings suggest that MAP support after oral Nimodipine may be important to maintain adequate CBF in patients with poor-grade subarachnoid hemorrhage.
authors.affiliation: Division of Neurocritical Care, The Neurologic Institute of New York, Columbia University College of Physicians and Surgeons, Milstein Hospital Building 8 Center, 177 Fort Washington Ave, New York, NY 10032, USA.
authors.forename: H Alex
authors.initials: HA
authors.lastname: Choi
authors.forename: Sang-Bae
authors.initials: SB
authors.lastname: Ko
authors.forename: Huahiou
authors.initials: H
authors.lastname: Chen
authors.forename: Emily
authors.initials: E
authors.lastname: Gilmore
authors.forename: Amanda M
authors.initials: AM
authors.lastname: Carpenter
authors.forename: Danielle
authors.initials: D
authors.lastname: Lee
authors.forename: Jan
authors.initials: J
authors.lastname: Claassen
authors.forename: Stephan A
authors.initials: SA
authors.lastname: Mayer
authors.forename: J Michael
authors.initials: JM
authors.lastname: Schmidt
authors.forename: Kiwon
authors.initials: K
authors.lastname: Lee
authors.forename: E Sander
authors.initials: ES
authors.lastname: Connelly
authors.forename: Myunghee
authors.initials: M
authors.lastname: Paik
authors.forename: Neeraj
authors.initials: N
authors.lastname: Badjatia
mesh_terms: D000328:Adult; D000368:Aged; D001921:Brain / Q000098:blood supply* / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000008:administration & dosage*; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D003422:Critical Care / Q000379:methods; D004734:Energy Metabolism / Q000187:drug effects; D005260:Female; D006706:Homeostasis / Q000187:drug effects; D006801:Humans; D008297:Male; D017551:Microdialysis; D008875:Middle Aged; D009553:Nimodipine / Q000008:administration & dosage*; D010100:Oxygen / Q000378:metabolism; D012189:Retrospective Studies; D013345:Subarachnoid Hemorrhage / Q000188:drug therapy*; D055815:Young Adult
chemical_list: D002121:Calcium Channel Blockers; D009553:Nimodipine; D010100:Oxygen