Intravenous rosuvastatin for acute stroke treatment: an animal study

Stroke. 2008 Feb;39(2):433-8. doi: 10.1161/STROKEAHA.107.492470. Epub 2007 Dec 27.

Abstract

Background and purpose: Statins exert rapid cholesterol-independent vasoprotective effects. Here, we tested whether postevent treatment with intravenously (i.v.) administered rosuvastatin improves acute stroke outcome in mice.

Methods: 129/SV wild-type mice were subjected to 1-hour filamentous middle cerebral artery occlusion (MCAo), followed by reperfusion, and were postevent treated with i.v. or intraperitoneal (i.p.) rosuvastatin given up to 6 hours after MCAo (dose range 0.02 to 20 mg kg(-1) body weight).

Results: Rosuvastatin, when administered i.v., significantly reduced lesion size when given up to 4 hours after MCAo and in doses as low as 0.2 mg kg(-1). In contrast, i.p. administration provided protection only when given directly on reperfusion at a dose of 20 mg kg(-1) but not at lower doses or later time points. Lesion protection was evident as late as 5 days after brain ischemia and was associated with functional improvements in the pole-test and wire-hanging test (2.0 mg kg(-1) dose). Neuroprotection with i.v. rosuvastatin was achieved with peak plasma concentrations <0.5 ng ml(-1) (ie, with 0.2 mg kg(-1)) and was associated with increased levels of phosphorylated Akt kinase and endothelial nitric oxide synthase in the vasculature.

Conclusions: Rosuvastatin, given intravenously at pharmacologically relevant concentrations, protects from focal brain ischemia up to 4 hours after an event. In our opinion, the development of an intravenous statin formulation is warranted for acute stroke trials with statins in humans.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Animals
  • Aorta / enzymology
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Fluorobenzenes / blood
  • Fluorobenzenes / pharmacology*
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / blood
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology*
  • Infarction, Middle Cerebral Artery / drug therapy*
  • Infarction, Middle Cerebral Artery / pathology
  • Injections, Intravenous
  • Mice
  • Mice, Inbred Strains
  • Nitric Oxide Synthase Type II / metabolism
  • Nitric Oxide Synthase Type III
  • Phosphorylation / drug effects
  • Proto-Oncogene Proteins c-akt / metabolism
  • Pyrimidines / blood
  • Pyrimidines / pharmacology*
  • Recovery of Function / drug effects
  • Reperfusion Injury / drug therapy*
  • Reperfusion Injury / pathology
  • Rosuvastatin Calcium
  • Sulfonamides / blood
  • Sulfonamides / pharmacology*

Substances

  • Fluorobenzenes
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • Pyrimidines
  • Sulfonamides
  • Rosuvastatin Calcium
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase Type III
  • Nos3 protein, mouse
  • Proto-Oncogene Proteins c-akt