Effect of dexmedetomidine postconditioning on cardiac function after cardiac arrest-cardiopulmonary resuscitation in swine

Objective To evaluate the effect of dexmedetomidine postconditioning on cardiac function after cardiac arrest-cardiopulmonary resuscitation in swine. Methods Twenty-eight healthy male white swine, weighing 33-41 kg, were divided into 4 groups (n=7 each) using a random number table: sham operation group (group S), cardiac arrest-cardiopulmonary resuscitation group (group CA-CPR), low-dose dexmedetomidine postconditioning group (group LDP) and high-dose dexmedetomidine postconditioning group (group HDP). Ventricular fibrillation was electrically induced and left untreated for 8 min, and then cardiopulmonary resuscitation was initiated and continued for 5 min.At 5 min after successful resuscitation, dexmedetomidine was infused via the femoral vein at a loading dose of 0.25 μg/kg followed by an infusion of 0.25 μg·kg-1·h-1 for 6 h in group LDP, and dexmedetomidine was infused via the femoral vein at a loading dose of 0.50 μg/kg followed by an infusion of 0.50 μg·kg-1·h-1 for 6 h in group HDP.The equal volume of normal saline was given in S and CA-CPR groups.At 1, 3, 6 and 24 h after resuscitation, stroke volume (SV) and global ejection fraction (GEF) were measured using PiCCO, and the concentration of cardiac troponin I (cTnI) in serum was also measured by enzyme-linked immunosorbent assay.At 24 h after resuscitation, the animals were sacrificed, hearts were removed and myocardial tissues were obtained for determination of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) contents (by enzyme-linked immunosorbent assay), malondialdehyde (MDA) content (by thiobarbituric acid method), and superoxide dismutase (SOD) activity (using xanthine oxidase method). Results Compared with group S, the SV and GEF were significantly decreased, the cTnI concentration in serum and contents of TNF-α, IL-6 and MDA in myocardial tissues were increased, and the activity of SOD in myocardial tissues was decreased in CA-CPR, LDP and HDP groups (P<0.05). Compared with group CA-CPR, the SV and GEF were significantly increased, the cTnI concentration in serum and contents of TNF-α, IL-6 and MDA in myocardial tissues were decreased, and the activity of SOD in myocardial tissues was increased in LDP and HDP groups (P<0.05). Compared with group LDP, the SV and GEF were significantly increased, the cTnI concentration in serum and contents of TNF-α, IL-6 and MDA in myocardial tissues were decreased, and the activity of SOD in myocardial tissues was increased in group HDP (P<0.05). Conclusion Dexmedetomidine postconditioning can improve cardiac function after cardiac arrest-cardiopulmonary resuscitation in swine, and the mechanism may be related to inhibiting inflammatory responses and oxidative stress responses. Key words: Dexmedetomidine; Heart arrest; Cardiopulmonary resuscitation; Ventricular function