No abstract

Background:We aimed to investigate the effect of electroacupuncture at Zusanli (ST36) and Sanyinjiao (SP6) on adrenocortical function in patients with etomidate anesthesia. Material/Methods:We randomly divided 80 patients who underwent elective surgery into 4 groups: group etomidate (ETO), group etomidate + electroacupuncture (ETO+EA), group etomidate + sham acupuncture (ETO+SEA), and group propofol (PRO). The patients in group ETO, ETO+EA, and ETO+SEA were induced with etomidate and sufentanil and maintained with intravenous infusion of etomidate and remifentanil. Group PRO was induced with propofol and sufentanil and maintained with propofol and remifentanil. Group ETO+EA received electro-acupuncture stimulation at Zusanli and Sanyinjiao throughout the operation, while group ETO+SEA received electro-acupuncture stimulation at non-acupoints. We recorded the values of MAP, HR, BIS, CVP, cortisol, ACTH, epinephrine, norepinephrine, and arterial blood gas during the perioperative period. Results:Cortisol concentrations were significantly higher at all times except T0 in group ETO+EA compared with group ETO. The ACTH concentrations were lower in group ETO+EA than that in group ETO at point T3. Conclusions:Electroacupuncture at ST 36 and SP 6 can mitigate the adrenal cortical inhibition induced by etomidate and can reduce the secretion of catecholamines during surgery.

BACKGROUND: Due to the lack of efficient neuroprotective therapies, the ischemia-reperfusion (I/R) injury is a major medical problem urgently needed to be further studied. OBJECTIVE: To investigate the neuro-protective effects of propofol-dexmedetomidine (dex) combination on I/R-induced cerebral injury and potential mechanisms. METHODS: Sprague-Dawley rats were randomized to sham-operated, I/R, I/R plus propofol, I/R plus dex, and I/R plus propofoldex combination group. I/R insult was induced by 2 h middle cerebral artery occlusion (MCAO) followed by 24 h reperfusion; Drugs were administered 20 min before the onset of ischemia and continued for another 2 h. Functional outcomes, the expression of Superoxide dismutase (SOD), Methane Dicarboxylic Aldehyde (MDA), Tumor necrosis factor-␣ (TNF-␣), Interleukin-1␤ (IL-1␤), caspase-3 and protein kinase B (AKT) were tested. RESULTS: Propofol-dex combination significantly mitigates I/R-induced neurological deficits in model rats compared to dex or propofol infusion alone. The decreased activity of SOD was significantly reversed following co-administration of propofol and dex, along with the down-regulated MDA content. Perioperative treatment with propofol and dex significantly suppressed I/R-up regulated TNF-␣ and IL-1␤ expressions, ameliorated AKT1 expression and caspase-3 activity. CONCLUSION: Propofol-dex combination exerted a stronger neuro-protection against I/R injury when compared with propofol or dex alone.

Little is known about the effects of the development of type 2 diabetes on glutamate homeostasis in the spinal cord. Therefore, we quantified the extracellular levels of glutamate in the spinal cord of Zucker diabetic fatty (ZDF) rats using in vivo microdialysis. In addition, protein levels of glutamate transporter-1 (GLT-1) in the spinal cord of ZDF rats were measured using Western blot. Finally, the effects of repeated intrathecal injections of ceftriaxone, which was previously shown to enhance GLT-1 expression, on the development of mechanical allodynia and hyperalgesia as well as on basal extracellular level of glutamate and the expression of GLT-1 in the spinal cord of ZDF rats were evaluated. It was found that ZDF rats developed mechanical hyperalgesia and allodynia, which were associated with increased basal extracellular levels of glutamate and attenuated levels of GLT-1 expression in the spinal cord, particularly in the dorsal horn. Furthermore, repeated intrathecal administrations of ceftriaxone dose-dependently prevented the development of mechanical hyperalgesia and allodynia in ZDF rats, which were correlated with enhanced GLT-1 expression without altering the basal glutamate levels in the spinal cord of ZDF rats. Overall, the results suggested that impaired glutamate reuptake in the spinal cord may contribute to the development of neuropathic pains in type 2 diabetes.