[Effects of Lidocaine on the Rho/ROCK Signal Transduction of the Posterior Basilar Artery in Rabbit SAH].

OBJECTIVE: To observe the expression of Rho/Rho-associated kinase (ROCK) signaling pathway in the basilar artery and the effect of lidocaine on this signaling pathway after subarachnoid hemorrhage (SAH) in rabbits. METHODS: 24 New Zealand white rabbits were randomly divided into sham operation (sham) group, SAH group, and occipital cisterna lidocaine (CD) group. There were 8 rabbits in each group. Intracisternal injection of non-anticoagulant autologous arterial blood (1 mL/kg) were applied to SAH group and CD group animals to establish SAH model, sham normal saline group was injected with 37 ℃ physiological saline (1 mL/kg); after 30 min, CD group was injected with 0.3 mL 2% lidocaine cisterna, SAH group and sham group were injected with saline. After 72 h, food intake and neurologic function damage were measured. The expressions of Rho associated kinase 2 (ROCK2) and myosin light chain (MLC) and calmodulin (CaM) protein in the basilar artery were measured by Western blot. The ROCK2 and MLC and CaM gene expressions were measured by using real-time quantitative PCR. RESULTS: Compared with sham group, reduced food intake, various degrees of neurological impairment, increased ROCK2 mRNA and protein expressions in basal artery, and decreased MLC and CaM expressions were observed in SAH group and CD group (P<0.05). Compared with the SAH group, there was no statistically significant difference in diet intake and neurological damage in the CD group (P>0.05); the mRNA and protein expressions of ROCK2 in the basilar artery decreased, and the expressions of MLC and CaM increased (P<0.05). CONCLUSION: Intracisternal injection of lidocaine may inhibit the transmission of Rho/ROCK signal in the basilar artery and reduce the basilar artery smooth muscle contraction after SAH.

[Neuroprotection Mechanism of Lidocaine in Rabbits with Early Brain Injury Resulted from Subarachnoid Hemorrhage].

OBJECTIVES: To determine the neuroprotection mechanism of lidocaine on early brain injury resulted from subarachnoid hemorrhage. METHODS: Eighteen New Zealand white rabbits were randomly divided into three groups: Sham group, subarachnoid hemorrhage (SAH) group and lidocaine treatment (LD) group. Operations were performed on all animals under anesthesia. Autologous nonheparinized arterial blood (1 mL/kg, body mass) was injected into cisterna magna of rabbits in the SAH and LD groups, while saline (1 mL/kg, body mass) was given to rabbits in the sham group. Thirty minutes later, intravenous injection of 0.6 mL 20 mg/mL lidocaine was given to those in the LD group, and intravenous injection of 0.6 mL saline was given to those in the Sham and SAH groups. Food intake and neurological impairments of the rabbits were assessed 72 h after the induction of SAH. The protein and mRNA experssions of Caspase-3 and cytochrome-c (Cyt-c) in hippocampus tissues were detected using real-time PCR (RT-PCR) and Western blot. RESULTS: Rabbits in the SAH and LD groups had lower food intake and higher mRNA and protein expressions of Caspase-3 and Cyt-c than those in the sham groups, which was accompanied with varying degrees of neurological impairments. No significant differences in food intake and neurological impairments were found between the SAH and LD groups (P >0.05). However, rabbits in the LD group had lower levels of mRNA and protein expressions of Caspase-3 and Cyt-c than those in the SAH group (P <0.05). CONCLUSION: The neuroprotection mechanism of lidocaine on early brain injury in rabbits with subarachnoid hemorrhage may be associated with inhibition of mitochondrial pathway and downregulated mRNA and protein expressions of Caspase-3 and Cyt-c in brain tissues.

[Comparison of Two Methods of Lidocaine Administrating for Neuroprotection in Rabbit Model of Subarachnoid Hemorrhage].

OBJECTIVES: To compare the neuroprotection effect of two methods of Lidocaine administration in rabbit model of subarachnoid hemorrhage. METHODS: Forty New Zealand white rabbits were randomly divided into sham group, subarachnoid hemorrhage group (SAH), Lidocaine intravenous injection group (L1), and Lidocaine intracisternal administration group (L2). The rabbits were given general anaesthesia, then 1.5 mL autologous nonheparinized arterial blood was injected into cisterna magna to establish SAH model, while 1.5 mL saline was used in sham group. Thirty minutes later, the rabbits in L1 and L2 group respectively received 0.3 mL 2% Lidocaine administration of intravenously and intracisternally injection. All animals were sacrificed at 72 h after SAH. The samples of basilar artery and hippocampus tissue were processed for morphometric analysis. At pre-operation and 72 h after SAH, the level of interleukin-6 (IL-6) in serum was measured. HE staining and C fos immunohistochemical staining were performed in L1 and L2 groups. Artery area and artery diameter of basal arteries, normal neuron density and C-fos positive cell in hippocampus were measured at 72 h after SAH. RESULTS: The baseline level of IL-6 was not significant different in four groups (P>0.05). The level of IL-6 at 72 h after SAH was significantly higher than that at pre-operation in SAH, L1 and L2 groups (P<0.05), while the level of IL-6 in SAH and L1 group was higher than that in L2 group (P<0.05). Compared to sham and L2 group, the cross-section area and diameter of basal artery were smaller in SAH and L1 group, while the normal neuron density of hippocampus was less (P<0.05). CONCLUSIONS: Intracisternal administration of Lidocaine could provide neuroprotection in rabbit model of subarachnoid hemorrhage.

[The effect of Xuebijing injection on immune regulation in SIRS patients].

OBJECTIVE: To investgate the effect of Xuebijing Injection on immune regulation in patients with systemic inflammatory response syndrome (SIRS). METHODS: 56 SIRS patients admitted to the ICU of Guizhou Provincial Hospital from January 2013 to December 2013 were included in this study. The patients were randomly divided into a control (C) and a treatment (T) group. Patients in C group received routine treatment; while patients in T group received additional Xuebijing Injection 50 mL Bid. The following indicators were recorded and compared between the two groups before and 4 and 7 days after treatments: CD4+, CD8+, CD4+/CD8+, monocytes CD14+/human leukocyte antigen-DR (HLA-DR), score of acute physiology and chronic health evaluation II (APACHE II), heart rate, white blood cells, body temperature, respiration rate, and MODS (7 d after treatment only). RESULTS: No differences were found between the two groups before treatments (P > 0.05). T Group had higher levels of CD4+, CD8, CD4+/CD8+ and monocytes CD14+/HLA-DR than C group at 4 and 7 d after treatments (P < 0.05). T group also had higher levels of improvement in vital indicators compared with C group (P < 0.05). No significant difference in incidence of multiple organ dysfunction syndrome (MODS) was found between the two groups (P > 0.05). CONCLUSION: Xuebijing Injection can regulate immune function of patients with SIRS.