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Defense Date
2005
DOI
https://doi.org/10.25772/PBXA-9H33
Document Type
Thesis
Degree Name
Master of Science
Department
Physiology
First Advisor
Dr. Rakesh C. Kukreja
Abstract
Rho Kinase (Rho-K) has been implicated in the pathophysiology of many deleterious conditions and its inhibition was shown to ameliorate these compromising effects. It is unclear; however, whether inhibition of Rho-K would decrease infarct size in hearts after ischemia/reperfusion. Adult ICR mice were randomized to 1 of 4 treatments: saline, fasudil (Rho-K inhibitor (10 mg/kg i.p.), Fasudil+L-NAME (Nitric Oxide synthase inhibitor, 15 mg/kg), and L-NAME. Hearts were isolated, perfused in Langendorff mode and subjected to 30 min stabilization before 30 min ischemia and 60 min reperfusion. Left ventricular (LV) function was monitored. Hearts were stained and infarct size measured. Fasudil reduced infarct size as compared with control hearts; however, this protective effect was abolished by L-NAME. LV function mirrored these trends. The loss of cardioprotection after L-NAME administration indicates that cardioprotection by Rho-K inhibition is mediated through nitric oxide-dependent pathway. Furthermore, Fasudil administration at and throughout reperfusion showed similar cardioprotection.
Rights
© The Author
Is Part Of
VCU University Archives
Is Part Of
VCU Theses and Dissertations
Date of Submission
June 2008
VCU Only:
Off Campus Download
Comments
Part of Retrospective ETD Collection, restricted to VCU only.