title: Manipulation of cerebrovascular resistance during internal carotid artery occlusion by intraarterial verapamil.
abstract: Occlusion of the internal carotid artery (ICA) results in acute cerebral hypotension. We hypothesized that during acute cerebral hypotension, in addition to physiological autoregulation, further arteriolar relaxation is possible by pharmacological means. We tested the feasibility of using intracarotid verapamil, a calcium channel blocker, to decrease the cerebrovascular resistance (CVR) and augment cerebral blood flow (CBF) at low postocclusion distal ICA pressures (PICA). Eleven patients undergoing trial occlusion of ICA were enrolled. Distal ICA or stump pressure, hemispheric CBF, and CVR were determined before and after carotid occlusion. During ICA occlusion, CBF and other physiological variables were determined before and after intracarotid verapamil. Two patients were excluded from the study. Carotid occlusion (n = 9) significantly decreased PICA (mean +/- SD, from 82 +/- 22 to 46 +/- 11 mm Hg, P = 0.001) and CBF (from 42 +/- 11 to 33 +/- 11 mL.100 g-1.min-1, P < 0.05). During occlusion, after intracarotid verapamil (3.9 +/- 1.6 mg), hemispheric CBF tended to increase from 31 +/- 11 to 35 +/- 14 mL.100 g-1.min-1 (P = 0.067). However, the percent increase in CBF after verapamil was a linear function of PICA (y = 1.01 x -32, n = 9, r2 = 0.84, P = 0.006). The decrease in CBF during carotid occlusion suggests that near maximal cerebral autoregulatory vasodilation had occurred, although our results indicate that it may be feasible to further augment CBF by pharmacological means during acute cerebral hypotension.
  
  
  CONCLUSIONS
  When the internal carotid artery is occluded during neurosurgical procedures, there may be a significant reduction in cerebral perfusion. The authors have demonstrated that the intraarterial administration of verapamil increases cerebral blood flow as a linear function of cerebral artery pressure. Intracarotid injection of vasodilators may augment cerebral blood flow during acute cerebral hypotension.
authors.affiliation: Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.
authors.forename: S
authors.initials: S
authors.lastname: Joshi
authors.forename: W L
authors.initials: WL
authors.lastname: Young
authors.forename: J
authors.initials: J
authors.lastname: Pile-Spellman
authors.forename: D H
authors.initials: DH
authors.lastname: Duong
authors.forename: L
authors.initials: L
authors.lastname: Hacein-Bey
authors.forename: M C
authors.initials: MC
authors.lastname: Vang
authors.forename: R S
authors.initials: RS
authors.lastname: Marshall
authors.forename: N
authors.initials: N
authors.lastname: Ostapkovich
authors.forename: T
authors.initials: T
authors.lastname: Jackson
mesh_terms: D000328:Adult; D000368:Aged; D001157:Arterial Occlusive Diseases / Q000503:physiopathology*; D002340:Carotid Artery Diseases / Q000503:physiopathology*; D002343:Carotid Artery, Internal; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009599:Nitroprusside / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects*; D014700:Verapamil / Q000494:pharmacology
chemical_list: D009599:Nitroprusside; D014700:Verapamil