Long-term effects of nimodipine on pial microvasculature and systemic circulation in conscious rats

X. Q. Yuan, T. L. Smith, D. S. Prough, D. S. De Witt, J. W. Dusseau, C. D. Lynch, J. M. Fulton, P. M. Hutchins

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Abstract

The chronic cranial window preparation allows repeated measurements of the same pial vessels in unanesthetized rats for several weeks and correlation with 24-h monitoring of hemodynamic variables. Nimodipine (20 mg) or placebo was given via two subcutaneous pellets. Large arterioles dilated 26 and 16%, at hour 1 and days 6-13, respectively (P<0.02). There was an increase in number of small arterioles throughout the whole observation period with the maximal increment of 47% (P<0.05) at days 6-13. Maximal vasodilation with 10% CO2 indicated that the increase in number of small arterioles after administering nimodipine was not caused by the opening of previously closed vessels. The total length of small arterioles and venules increased 47 and 23% at days 6-13, respectively (P<0.001). These increases seem to be caused by the increases in the numbers of vessels, because the average length of the small vessels did not appear to change. This suggests that nimodipine reduces cerebral vascular resistance by causing cerebral microvessel neovascularization. Our data demonstrate that the administration of nimodipine (20 mg) is potent in dilating pial arterioles in the short-term without affecting systemic arterial pressure, and that its long-term effect results in new vessel growth.

Original languageEnglish (US)
Pages (from-to)H1395-H1401
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume258
Issue number5 27-5
StatePublished - Jun 15 1990
Externally publishedYes

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Keywords

  • angiogenesis
  • Brain
  • calcium channel blocker
  • cranial window
  • microcirculation
  • neovascularization

ASJC Scopus subject areas

  • Physiology

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