Protective effect of dexmedetomidine (DEX) on the lungs of one-lung ventilation (OLV) rat model and its effect on inflammatory factors were investigated. Ninety-two rats were selected and divided into groups A, B, C and D (n=23) according to the principle of similar body weight. OLV rat model was established. Before modeling (15 min), rats in group C were injected with sodium chloride. Rats in group D were injected with DEX at a speed of 5 µg/kg/h. Group A rats were ventilated in both lungs for 2 h. Rats in groups B and C (0.9% sodium chloride injection + OLV) and in group D (DEX + OLV) were subjected to OLV for 2 h and bilateral ventilation for 10 min. Concentrations of interleukin (IL)-6, IL-10 and tumor necrosis factor-α (TNF-α) in lung tissue of rats were detected by ELISA. The malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity in rat lung tissue were detected by radioimmunoassay. Wet weight (W)/dry weight (D) of lung tissue was calculated and indexes of the four groups of rats were compared. Compared with group A, IL-6, TNF-α and MDA concentrations and W/D of lung tissue of rats in groups B, C and D were significantly increased (p<0.05); SOD activity and IL-10 concentration were significantly decreased (p<0.01). Compared with groups B and C, the concentrations of IL-6, TNF-α and W/D in rats of group D were significantly decreased (p<0.01), but IL-10 significantly increased (p<0.01). Compared with groups B and C, the MDA concentration in lung tissue of rats in group D was significantly decreased (p<0.01), but SOD activity significantly increased (p<0.01). DEX can inhibit the production of inflammatory factors in the development and progression of pulmonary inflammation. It can inhibit lipid peroxidation, relieve pulmonary edema, and reduce lung injury after OLV, sin order to protect the lung.
We aimed to investigate whether the cardioprotection of sevoflurane against ischemia/reperfusion (IR) injury is via inhibiting endoplasmic reticulum stress (ERS). The rat in vivo model of myocardial IR injury was induced by ligation of the left anterior descending (LAD) coronary artery. Sevoflurane significantly ameliorated the reduced cardiac function, increased infarct size and elevated troponin I level and lactate dehydrogenase (LDH) activity in plasma induced by IR injury. Sevoflurane suppressed the I/R-induced myocardial apoptosis. The increased protein levels of glucose-regulated protein 78 and C/EBP homologous protein after myocardial I/R were significantly reduced by sevoflurane. The protein levels of phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (PERK), phosphorylated eukaryotic initiation factor 2 (eIF2α) and activating transcription factor 4 (ATF4) were significantly increased in rats with I/R and attenuated by sevoflurane treatment. The phosphorylation of Akt was further activated by sevoflurane. The cardioprotection of sevoflurane could be blocked by wortmannin, a PI3K/Akt inhibitor. Our results suggest that the cardioprotection of sevoflurane against IR injury might be mediated by suppressing PERK/eIF2a/ATF4/CHOP signaling via activating the Akt pathway, which helps in understanding the novel mechanism of the cardioprotection of sevoflurane.
To explore the analgesic effect of dizocine combined with ropivacaine on recurrent neuropathic pain in rat model of peripheral nerve compression. Rats were randomly divided into 5 groups: sham control group (S), peripheral nerve compression model group (M), dizocine group (D), ropivacaine group (R), and combined drug group (DR). Rat peripheral nerve compression model was constructed to observe the symptoms of the rats before and after surgery. Mechanical withdrawal threshold was measured on the 21st day after surgery. The electrophysiological changes of rat peripheral nerve were measured by biopotential recording system, including proximal latency, distal latency, and compound muscle action potential. The incubation period and nerve conduction velocity were further obtained. Histological changes were observed by HE staining and toluidine blue staining. Axon number and myelin damage grade were performed, and the ultrastructure was observed by transmission electron microscopy (TEM). The mechanical withdrawal threshold, nerve conduction velocity, and compound muscle action potential were effectively increased in combination group. However, the proximal latency, distal latency, and incubation period were significantly reduced. Furthermore, dizocine combined with ropivacaine can effectively reduce the degree of myelination. TEM shown that the DR group had the best therapeutic effect, and the histological appearance of the cross section was quite similar to that of the S group. Dizocine combined with ropivacaine has a significant analgesic effect in rat model of peripheral nerve compression.
Anesthetic effects and safety of dexmedetomidine and tramadol, respectively, combined with propofol in ultrasound-guided percutaneous microwave coagulation therapy (PMCT) for hepatocellular carcinoma (HCC) were compared. One hundred and seventy-six patients with HCC, treated by ultrasound-guided PMCT in The Affiliated Hospital of Qingdao University from January 2014 to December 2016, were retrospectively analyzed and divided into two groups: dexmedetomidine group (anesthetized with dexmedetomidine combined with propofol, n=91) and tramadol group (anesthetized with tramadol combined with propofol, n=85). Changes in heart rate (HR), mean arterial pressure (MAP), and oxygen saturation (SpO 2 ) were recorded before oxygen inhalation (T1), intraoperationally (T2), and at 30 min postoperatively (T3), and the recovery time (recorded from the moment the use of anesthetic drugs stopped), hospital stay, visual analogue scale (VAS) score at 48 h after surgery, as well as the adverse reactions in the perioperative period were compared between the two groups. HR and SpO 2 in the dexmedetomidine group at T2 and T3 were significantly lower than those in the tramadol group (P<0.05). HR and SpO 2 at T2 were significantly lower than those at T1 and T3, and HR at T3 was lower than that at T1 (P<0.05). MAP in the dexmedetomidine group at T2 was significantly lower than that in the tramadol group (t=3.836, P<0.001). MAP at T2 was significantly lower than those at T1 and T3, and MAP at T3 was lower than that at T1 (P<0.05). The number of patients with shivering in the dexmedetomidine group was significantly higher than that in the tramadol group (P<0.05). Both tramadol and dexmedetomidine, respectively combined with propofol in PMCT for HCC surgery can achieve satisfactory anesthetic effects. However, tramadol combined with propofol is more effective in stabilizing the vital signs with less side-effects, and is more suitable for PMCT in patients with HCC than dexmedetomidine combined with propofol, which is worth popularizing and applying in clinic.
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