Comparison of Cardioprotective Effects of Propofol versus Sevoflurane in Pediatric Living Donor Liver Transplantation.

BACKGROUND Our study compared the myocardiac protective effect of propofol vs. sevoflurane in pediatric patients receiving living donor liver transplantation (LDLT) surgery. MATERIAL AND METHODS We randomly and equally divided 120 children who underwent LDLT into a sevoflurane group and a propofol group. Preoperative, intraoperative, and postoperative data were collected and compared between the 2 groups. The concentrations of cTnI, CK-MB, IL-6, TNF-alpha, and HMGB1 at 5 min after induction (T0), 30 min in the anhepatic period (T1), and 3 h after reperfusion (T2), and at the end of surgery (T3) were measured. RESULTS There was no statistically significant difference in the characteristics of children in the 2 groups. Compared with T0, the levels of IL-6 and TNF-alpha at T1, T2, and T3 were higher, while the HMGB1 at T2 and T3 were higher (P<0.05). A similar trend for IL-6, TNF-alpha, and HMGB1 at different time points in the 2 groups was observed. Compared with T0, the cTnI and CK-MB at T2 and T3 were significantly higher (P<0.05), but there was no significant difference at different time points in the 2 groups. For the adverse events, there was no significant difference between the 2 groups. CONCLUSIONS Our study shows that the cardioprotective effect in pediatric patients undergoing living donor liver transplantation is similar with propofol and sevoflurane anesthesia.

Effect of sevoflurane and propofol on acute kidney injury in pediatric living donor liver transplantation.

BACKGROUND: Acute kidney injury (AKI) is the primary cause of morbidity and mortality after major abdominal surgery. However, little is known about the effect of anesthetics on the development of AKI after pediatric liver transplantation (LT). This study aimed to compare the effects of propofol and sevoflurane anesthetics on postoperative AKI after LT surgery. METHODS: A total of 120 pediatric patients scheduled for pediatric LT were randomly assigned to receive either continuous infusion of propofol or inhalation of sevoflurane. Serum creatinine (Scr), inflammatory medium and oxidative stress factors and renal biomarkers were measured before surgery (T1), 5 min after anhepatic phase (T2), 10 min after ischemia reperfusion (T3), 2 h after ischemia reperfusion (T4), 24 h after surgery (T5), and 3 d after surgery (T6) to evaluate the effects of anesthetics on the development of postoperative AKI. RESULTS: The incidence of AKI was lower in patients receiving sevoflurane than those receiving propofol. The mean arterial pressure was changed slightly in sevoflurane group. The inflammatory factors of interleukin-18, tumor necrosis factor-α, and the levels of neutrophil gelatinase-associated lipocalin (NGAL) were lower in sevoflurane group, while no oxidative stress factors [hydrogen peroxide (H2O2), malondialdehyde and superoxide dismutase)] and interleukin-10 showed differences between the groups. CONCLUSIONS: Anesthesia with sevoflurane may be associated with a modest decrease in the incidence of AKI when compared with propofol. Further clarification with relevance to such association is warranted.

Spinal CXCL5 contributes to nerve injury-induced neuropathic pain via modulating GSK-3ß phosphorylation and activity in rats.

BACKGROUND: Neuroinflammation is identified to be crucial in the development of neuropathic pain, whereas definite molecular mechanisms remain obscure. Recently, chemokine CXCL5 is manifested to participate in the inflammatory process of central nervous system, however, little is known about the potential effect of spinal CXCL5 on pathogenesis of pain. This study investigated whether and how CXCL5 and its receptor CXCR2 regulated neuropathic pain in a rat model of chronic constriction injury (CCI) of the sciatic nerves. METHODS: Recombinant CXCL5, a neutralizing antibody against CXCL5, selective CXCR2 antagonist SB225002 and GSK-3ß inhibitor TDZD-8 were injected intrathecally. PWT and PWL were documented to assess mechanical allodynia and thermal hyperalgesia. Simultaneously, levels of CXCL5 and CXCR2 in spinal dorsal horn were measured by RT-qPCR after nociceptive testing. Western blot was utilized to evaluate spinal GSK-3ß expression and phosphorylation. RESULTS: We found that CCI engendered rapid and long-lasting mechanical allodynia and thermal hyperalgesia, which was accompanied by dramatical rise of spinal CXCL5 and CXCR2 expression. CCI also caused an increase of pGSK-3ß (Tyr216) and a decrease of pGSK-3ß (Ser9) without affecting total protein level of GSK-3ß. Moreover, spinal blockage of CXCL5/CXCR2 pathway attenuated neuropathic pain and inhibited the enhancement of GSK-3ß activity. Also, intrathecal delivery of exogenous CXCL5 dose-dependently induced nociceptive hypersensitivity in naïve rats, which was prevented by the supplemental addition of TDZD-8. CONCLUSION: These present findings indicate that up-regulation of spinal CXCL5 and CXCR2 is involved in neuropathic pain after nerve injury, through regulating GSK-3ß activity in rats.

The effects of electroacupuncture treatment on the postoperative cognitive function in aged rats with acute myocardial ischemia-reperfusion.

Many literatures have proven that postoperative cognitive dysfunction (POCD) was very common in old patients after the injury of acute myocardial ischemia-reperfusion (AMIR) clinically such as the off-pump coronary artery bypass surgery (OPCAB) without definite mechanism; however, reports on the animal experiments were rarely seen. We hypothesized that AMIR could contribute to cognitive dysfunction, and this severe injury might be impeded by EA via hindering neuroinflammation and oxidative stress response as well as modulating the balance of the autonomic nervous system. The aged male Sprague Dawley rats were randomly assigned into three experimental groups: sham (sham operation), AMIR, and EA (electroacupunture treatment, acupoints GV20 and ST36+AMIR) groups. The survival rate, heart rate variability analysis, examination of pathology within the hippocampal CA1, oxidative stress, systemic inflammation and the behavior testing were evaluated by their corresponding methods. The results showed that the rats subjected to AMIR had lower survival rates, higher malondialdehyde (MDA), decreased superoxide dismutase (SOD) activity, more microglial activation, and presented evidence of severe brain injury and cognitive dysfunction on the 1st, 3rd, 7th days after reperfusion compared to sham-operated controls. Most important of all, the above damages induced by the AMIR were significantly improved by the EA treatment. Our findings indicated that EA treatment could be a neuroprotective therapy for the cognitive dysfunction induced by the AMIR event, which might be attributablefor balancing the autonomic nervous system, inhibiting the neuronic apoptosis, hindering microglial activation, attenuating oxidative stress and restraining the central and peripheral inflammation reactions.