Main Article Content
By Akiva Kirschner, Biomedical Engineering
Advisor: Jack Rubinstein
Presentation ID: PM_B10
Abstract: Remote ischemic preconditioning (RIPC) is a process via which brief bouts of vascular occlusion prompt a systemic response that protects distal tissues and organs from subsequent ischemic insults. Our laboratory has recently observed that non-occlusive binding (NOB) of the arm can induce the RIPC phenotype in healthy males through either attenuation of circulating cytokines and improvement of vascular function. This finding was prompted by the observation that Jewish men bind on their arm a religious device commonly known as tefillin that produces NOB of the arm for approximately thirty minutes daily. We developed a mouse model in order to mimic the NOB phenotype to study the time-dependency and mechanism of the observed effect and to link these changes to infarct size. Non-occlusive rubber bands were placed on the left forearm of C57BL mice for 30 minutes daily for varying time periods up to 8 days. At the conclusion of each period mice were either subjected to blood draws for phenotype analysis or surgically induced ischemia/reperfusion injury. We found that mice that were treated for 1 to 8 days had smaller infarct size and many (but not all) of the established biomarkers of the RIPC phenotype changed, with the acute (single use) showing the most dramatic effects. In summary, NOB of a mouse results in an RIPC phenotype that was similar to the observed changes in humans and furthermore these changes were associated with significantly decreased infarct size.