This work is part of a retrospective collection of 179 electronic theses and dissertations (ETDs) from the VCU Libraries pilot ETD system that were designated as available only to VCU users. Please contact us at if you have questions or if you are the author of one of these and would like to release it for online public access.

Non-VCU users: Please talk to your librarian about requesting this thesis through interlibrary loan.

Defense Date


Document Type


Degree Name

Master of Science



First Advisor

Dr. Rakesh C. Kukreja


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.


Part of Retrospective ETD Collection, restricted to VCU only.


© The Author

Is Part Of

VCU University Archives

Is Part Of

VCU Theses and Dissertations

Date of Submission

June 2008