Nimodipine and chronic vasospasm in monkeys

Part I. Clinical and radiological findings

M. Nosko, B. Weir, C. Krueger, D. Cook, S. Norris, T. Overton, D. Boisvert

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

The efficacy of the calcium channel blocker nimodipine in the prevention of chronic cerebral vasospasm (VSP) and delayed ischemia after subarachnoid hemorrhage (SAH) in monkeys was examined in a blind, randomized, placebo-controlled trial. The primate model developed in this laboratory reliably induces chronic cerebral vasospasm and can induce pathologically proven delayed ischemic neurological deficits (DINDs). With standard microsurgical procedures, an average 6.4-ml autologous hematoma was placed directly against the major anterior cerebral vessels in the right basal subarachnoid spaces of 24 monkeys. The monkeys were randomized to one of four groups and were treated orally q8h for 7 days with nimodipine (3, 6, or 12 mg/kg) or placebo. An additional 2 monkeys underwent the surgical procedure without clot placement. Drug administration began between 14 and 20 hours after clot placement. Indices monitored before and after SAH included neurological status, angiographic cerebral vessel caliber, and cerebral blood flow. Significant VSP (25 to 100% reduction in vessel caliber) was present on Day 7 on the clot side in 83% of the animals (P ≤ 0.001). There was no significant difference (P > 0.05) in the incidence of VSP among the four groups. Similarly, there was no significant difference (P > 0.05) in the mean vessel caliber reduction after SAH among the four treatment groups. There was no VSP present on Day 7 in the sham-operated animals. One animal receiving high dose nimodipine (12 mg/kg p.o. q8h) developed a DIND on Day 5 after SAH. A second animal in the 12-mg/kg group developed a transient neurological deficit between Days 4 and 7.

Original languageEnglish (US)
Pages (from-to)129-136
Number of pages8
JournalNeurosurgery
Volume16
Issue number2
StatePublished - 1985
Externally publishedYes

Fingerprint

Nimodipine
Subarachnoid Hemorrhage
Haplorhini
Intracranial Vasospasm
Cerebrovascular Circulation
Placebos
Subarachnoid Space
Calcium Channel Blockers
Hematoma
Primates
Ischemia
Randomized Controlled Trials
Incidence
Pharmaceutical Preparations
Therapeutics

ASJC Scopus subject areas

  • Clinical Neurology
  • Surgery

Cite this

Nosko, M., Weir, B., Krueger, C., Cook, D., Norris, S., Overton, T., & Boisvert, D. (1985). Nimodipine and chronic vasospasm in monkeys: Part I. Clinical and radiological findings. Neurosurgery, 16(2), 129-136.

Nimodipine and chronic vasospasm in monkeys : Part I. Clinical and radiological findings. / Nosko, M.; Weir, B.; Krueger, C.; Cook, D.; Norris, S.; Overton, T.; Boisvert, D.

In: Neurosurgery, Vol. 16, No. 2, 1985, p. 129-136.

Research output: Contribution to journalArticle

Nosko, M, Weir, B, Krueger, C, Cook, D, Norris, S, Overton, T & Boisvert, D 1985, 'Nimodipine and chronic vasospasm in monkeys: Part I. Clinical and radiological findings', Neurosurgery, vol. 16, no. 2, pp. 129-136.
Nosko M, Weir B, Krueger C, Cook D, Norris S, Overton T et al. Nimodipine and chronic vasospasm in monkeys: Part I. Clinical and radiological findings. Neurosurgery. 1985;16(2):129-136.
Nosko, M. ; Weir, B. ; Krueger, C. ; Cook, D. ; Norris, S. ; Overton, T. ; Boisvert, D. / Nimodipine and chronic vasospasm in monkeys : Part I. Clinical and radiological findings. In: Neurosurgery. 1985 ; Vol. 16, No. 2. pp. 129-136.
@article{201d34c54b164fee8c1cc6b351572f11,
title = "Nimodipine and chronic vasospasm in monkeys: Part I. Clinical and radiological findings",
abstract = "The efficacy of the calcium channel blocker nimodipine in the prevention of chronic cerebral vasospasm (VSP) and delayed ischemia after subarachnoid hemorrhage (SAH) in monkeys was examined in a blind, randomized, placebo-controlled trial. The primate model developed in this laboratory reliably induces chronic cerebral vasospasm and can induce pathologically proven delayed ischemic neurological deficits (DINDs). With standard microsurgical procedures, an average 6.4-ml autologous hematoma was placed directly against the major anterior cerebral vessels in the right basal subarachnoid spaces of 24 monkeys. The monkeys were randomized to one of four groups and were treated orally q8h for 7 days with nimodipine (3, 6, or 12 mg/kg) or placebo. An additional 2 monkeys underwent the surgical procedure without clot placement. Drug administration began between 14 and 20 hours after clot placement. Indices monitored before and after SAH included neurological status, angiographic cerebral vessel caliber, and cerebral blood flow. Significant VSP (25 to 100{\%} reduction in vessel caliber) was present on Day 7 on the clot side in 83{\%} of the animals (P ≤ 0.001). There was no significant difference (P > 0.05) in the incidence of VSP among the four groups. Similarly, there was no significant difference (P > 0.05) in the mean vessel caliber reduction after SAH among the four treatment groups. There was no VSP present on Day 7 in the sham-operated animals. One animal receiving high dose nimodipine (12 mg/kg p.o. q8h) developed a DIND on Day 5 after SAH. A second animal in the 12-mg/kg group developed a transient neurological deficit between Days 4 and 7.",
author = "M. Nosko and B. Weir and C. Krueger and D. Cook and S. Norris and T. Overton and D. Boisvert",
year = "1985",
language = "English (US)",
volume = "16",
pages = "129--136",
journal = "Neurosurgery",
issn = "0148-396X",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Nimodipine and chronic vasospasm in monkeys

T2 - Part I. Clinical and radiological findings

AU - Nosko, M.

AU - Weir, B.

AU - Krueger, C.

AU - Cook, D.

AU - Norris, S.

AU - Overton, T.

AU - Boisvert, D.

PY - 1985

Y1 - 1985

N2 - The efficacy of the calcium channel blocker nimodipine in the prevention of chronic cerebral vasospasm (VSP) and delayed ischemia after subarachnoid hemorrhage (SAH) in monkeys was examined in a blind, randomized, placebo-controlled trial. The primate model developed in this laboratory reliably induces chronic cerebral vasospasm and can induce pathologically proven delayed ischemic neurological deficits (DINDs). With standard microsurgical procedures, an average 6.4-ml autologous hematoma was placed directly against the major anterior cerebral vessels in the right basal subarachnoid spaces of 24 monkeys. The monkeys were randomized to one of four groups and were treated orally q8h for 7 days with nimodipine (3, 6, or 12 mg/kg) or placebo. An additional 2 monkeys underwent the surgical procedure without clot placement. Drug administration began between 14 and 20 hours after clot placement. Indices monitored before and after SAH included neurological status, angiographic cerebral vessel caliber, and cerebral blood flow. Significant VSP (25 to 100% reduction in vessel caliber) was present on Day 7 on the clot side in 83% of the animals (P ≤ 0.001). There was no significant difference (P > 0.05) in the incidence of VSP among the four groups. Similarly, there was no significant difference (P > 0.05) in the mean vessel caliber reduction after SAH among the four treatment groups. There was no VSP present on Day 7 in the sham-operated animals. One animal receiving high dose nimodipine (12 mg/kg p.o. q8h) developed a DIND on Day 5 after SAH. A second animal in the 12-mg/kg group developed a transient neurological deficit between Days 4 and 7.

AB - The efficacy of the calcium channel blocker nimodipine in the prevention of chronic cerebral vasospasm (VSP) and delayed ischemia after subarachnoid hemorrhage (SAH) in monkeys was examined in a blind, randomized, placebo-controlled trial. The primate model developed in this laboratory reliably induces chronic cerebral vasospasm and can induce pathologically proven delayed ischemic neurological deficits (DINDs). With standard microsurgical procedures, an average 6.4-ml autologous hematoma was placed directly against the major anterior cerebral vessels in the right basal subarachnoid spaces of 24 monkeys. The monkeys were randomized to one of four groups and were treated orally q8h for 7 days with nimodipine (3, 6, or 12 mg/kg) or placebo. An additional 2 monkeys underwent the surgical procedure without clot placement. Drug administration began between 14 and 20 hours after clot placement. Indices monitored before and after SAH included neurological status, angiographic cerebral vessel caliber, and cerebral blood flow. Significant VSP (25 to 100% reduction in vessel caliber) was present on Day 7 on the clot side in 83% of the animals (P ≤ 0.001). There was no significant difference (P > 0.05) in the incidence of VSP among the four groups. Similarly, there was no significant difference (P > 0.05) in the mean vessel caliber reduction after SAH among the four treatment groups. There was no VSP present on Day 7 in the sham-operated animals. One animal receiving high dose nimodipine (12 mg/kg p.o. q8h) developed a DIND on Day 5 after SAH. A second animal in the 12-mg/kg group developed a transient neurological deficit between Days 4 and 7.

UR - http://www.scopus.com/inward/record.url?scp=0021984507&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021984507&partnerID=8YFLogxK

M3 - Article

VL - 16

SP - 129

EP - 136

JO - Neurosurgery

JF - Neurosurgery

SN - 0148-396X

IS - 2

ER -