Floor plan - 2013 Annual Meeting - American Association for Hand ...

ASRM SCIENTIFIC PAPER PRESENTATION: RESEARCH II
Changes in the Nitric Oxide Pathway During Free Flap Failure
Institution where the work was prepared: R Adams Cowley Shock Trauma Center, Baltimore, MD, USA
Rachel Bluebond-Langner, MD1; Suhail K. Mithani, MD1; Hunter C. Champion, MD, PhD2; Eduardo D. Rodriguez1;
(1)R Adams Cowley Shock Trauma Center, (2)Johns Hopkins School of Medicine
INTRODUCTION:
Despite advances in microsurgery, free flap failure or flap salvage re-exploration range from 5-20%. Nitric Oxide (NO) has been shown
to play a role in free flap failure and up-regulation of NO has been targeted with varying success. The purpose of this study was to look
at changes in the NO pathway, specifically the downstream effector of NO and cyclic guanosine monophosphate (cGMP).
MATERIALS AND METHODS
Twenty Sprague-Dawley rats underwent harvest of a free flap based on the inferior epigastric vessels. In ten rats (group 1) the flap was
havested, stored sterile for 20 minutes to simulate warm ischemia time and then anastomosed to the femoral vessels under the microscope
using 10-0 nylon. To simulate flap failure, in ten rats (group 2) the flap was raised, arterial anastomosis performed and the vein was occluded
with 10-0 nylon for 12 hours and then released. Rats were euthanized at three days. Serum, flap tissue and vascular pedicle were collected.
cGMP levels were measured in the serum and tissue. eNOS, iNOS, arginase and PDE-5 activity was measured in the flap tissue.
RESULTS:
All flaps in group 1 survived and 85% of flaps in group 2 survived. PDE5 activity in flaps that survived increased by 17% compared to
controls, while flaps that failed had 59%* increased activity. eNOS activity was halved in free flap tissue compared with controls, and
reduced an additional 2 fold* in free flap failure. iNOS activity was comparable in free flaps compared to controls, but doubled in free
flap failure*. Arginase activity increased modestly in flaps which survived compared to controls; however, activity increased almost 2 fold
in flaps which failed. cGMP levels were 20%* higher in the vascular pedicles and plasma of free flaps that survived compared with those
that failed. (*=p