Introduction:
Asphyxia is the most common cause of cardiac arrest in children, with devastating complications. Asphyxia Cardiac Arrest (ACA) is associated with a generalized systemic inflammatory response, in addition brain injury after cardiac arrest (CA) has been shown to have an inflammatory component. Effective neuroprotective strategies are desperately needed. pGz is a method which moves the body in a repetitive head to foot motion increasing pulsatile shear stress, inducing endothelial nitric oxide (eNO) and increasing microvascular flow to brain, heart and other vital organs. We have shown that pGz applied as a preconditioning (pre-treatment) prior to brain hypoxia ischemia, induces increase in brain anti-apoptotic proteins, and modulated the inflammatory response.
Hypothesis:
The objective of this study was to determine whether pGz post-treatment after ACA, also modifies pro inflammatory brain regulatory proteins.
Methods:
Twelve anesthetized neonatal piglets (weight 2.5-3 kg) were subjected to 30 min of 7% FiO2, followed by 7 min of Apnea and resuscitation with recovery in 21% FiO2. Animals were randomly assigned to; recovery for 3 hr (Hyp-Cont) or recovery with pGz beginning 30min after hypoxia for 3 hr (pGz). Another group(Sham) had surgery and anesthesia but no hypoxia. Protein expression of IL-1β, IL-6, TNFα, eNOS, and p-eNOS in cortex were meassured.
Results:
Hypoxia induced a 38%, 74% and 10% increase from Sham in IL-1β, IL-6, TNFα respectively. In contrast pGz treated animals only had a 4%, 21% increase in IL-1β, IL-6, and a 14% decrease in TNFα from Sham. Activation of eNOS (p-eNOS/eNOS) doubled in pGz treated. Figure [Mean (± SD)*p< 0.01].
Conclusion:
pGz post resuscitation in a piglet model of ACA decreases brain pro-inflammatory regulatory proteins. The latter, taken together with pGz’s induction of anti-apoptotic signaling proteins, suggest that pGz can be a simple, novel neurotherapeutic strategy when applied after cardiac arrest.
TRPC6 is the endothelial calcium channel that regulates leukocyte transendothelial migration during the inflammatory response