Abstract 12145: Remote Ischemic Preconditioning Regulates Post-resuscitation Microcirculation via A KAtp Channel-dependent Mechanism in a Rat Model of Cardiac Arrest
Introduction: Remote ischemic preconditioning (RIPC) provides potent protection to tissue microcirculation against ischemic-reperfusion injury. However, the underlying microvascular mechanism of RIPC is not fully understood. The present study investigated whether the protective effects of RIPC on microcirculation and myocardial function after cardiopulmonary resuscitation (CPR) are related to KATP channel activation.
Hypothesis: RIPC-induced activation of the KATP channel would result in improved microcirculation and myocardial function following resuscitation.
Methods: Twenty-four male Sprague-Dawley rats were randomized into three groups (n=8 for each group): RIPC, RIPC with KATP channel blocker, and control. Remote ischemic preconditioning was induced by four cycles of 5 min of limb ischemia followed by 5 minutes of reperfusion. Ventricular fibrillation was induced and untreated for 8 min followed by 8 min of CPR. The animals were monitored for 6 h and observed for an additional 66 h. Sublingual microcirculation was assessed by a sidestream dark-field imaging device, and myocardial function was measured by echocardiography at baseline, 30 min, 1 h, 2 h, 4 h, and 6h post-resuscitation.
Results: At 30 min and subsequent intervals post-resuscitation, both perfused vessel density and microcirculatory flow index were significantly greater in the RIPC group than in the control group (P< 0.05). Compared with the control group, a significantly higher ejection fraction, myocardial performance index, and greater duration of survival were observed in the RIPC group (P < 0.05). Pretreatment with the KATP channel blocker (glibenclamide) significantly reversed the microvasucular and myocardial protective effects of RIPC (P< 0.05) (Figure 1, 2).
Conclusions: In a rat model of CPR, the beneficial effect of RIPC on sublingual microcirculation and cardiac function with improved survival was related, at least in part, to the activation of KATP channel.
Author Disclosures: S. Zhao: None. Z. Tang: None. J. Wang: None. Z. Yang: None. F. Chen: None. M.A. Peberdy: None. J.P. Ornato: None. W. Tang: None.
- © 2016 by American Heart Association, Inc.