ABSTRACT
Objective To investigate the protective effect and potential mechanisms of hypertonic sodium chloride hydroxyethyl starch solution (HSH) against the cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH).Methods Twenty-four male Sprague-Dawley (SD) rats were randomly assigned to four groups according to the random number table,with 6 rats in each group.The SAH-CVS model was reproduced by injection of the blood twice through the cisterna magna.Rats in both model and HSH treatment groups received 8 mL/kg normal saline (NS) or HSH treatment everyday via caudal vein.Rats in sham group were injected with 1.5 mL/kg NS into cisterna magna followed by 8 mL/kg NS treatment.Rats in normal group received no treatment.Rats were sacrificed to harvest basilar artery after 7 days.The thickness of vessel wall and lumen area were measured using hematoxylin-eosin (HE) staining.The rate of apoptosis of vascular smooth muscle cell (VSMC) was assessed using flow cytometry.Caspase-3 activity was measured by a fluorometric assay.The expressions of Bax and Bcl-2 were determined by Western Blot.Intracellular reactive oxygen species (ROS) was detected by H2DCFDA.Results Compared with normal group,increased thickness of vessel wall (μm:27.72 ± 1.94 vs.18.30 ± 1.10,P＜0.05),decreased lumen area (μm2:26 115 ± 1 991 vs.55 080 ± 2 091,P＜0.05),and elevation of rate of apoptosis of VSMCs [(35.05 ± 5.54) ％ vs.(5.93 ± 1.53) ％,P＜ 0.05] were found in model group.Compared with model group,decreased thickness of vessel wall (μm:22.55 ± 1.50 vs.27.72 ± 1.94,P＜0.05),increase of lumen area (μm2:48 115 ±2 460 vs.26 115 ± 1 991,P＜0.05),and depressed rate of apoptosis of VSMCs [(16.54 ± 5.94) ％ vs.(35.05 ± 5.54) ％,P＜ 0.05] were found in HSH treatment group.Caspase-3 activity,intracellular ROS level,Bax and Bcl-2 expressions in model group were (188.40 ± 19.35)％,(163.50 ± 17.02)％,(208.71 ± 26.04)％ and (44.52 ± 9.61) ％ of those of normal group,and the differences of these parameters between model and normal groups were statistically significant (all P＜0.05).Caspase-3 activity,intracellular ROS level,Bax and Bcl-2 expressions in HSH treatment group were (135.05 ± 19.52)％,(119.44 ± 11.50)％,(139.20 ± 18.04)％ and (85.35 ± 13.12)％ of those of normal group,respectively,and the differences of these parameters between HSH treatment and model groups were statistically significant (all P＜0.05).The differences of all measurements between sham and normal groups were not statistically significant.Conclusion The current results demonstrate that HSH attenuates the SAH-induced CVS,alleviates thickness of vessel wall,and increases lumen area via inhibition of VSMCs apoptosis.
ABSTRACT
@# Neuropathic pain is an intractable pain condition that initiated or caused by a primary lesion or dysfunction in the nervous system. Because the underlying molecular mechanisms of neuropathic pain are largely unknown, routine pharmacologic treatment is often insufficient. It has become a rather tough problem bothering both physicians and patients. Recently, with the development of molecular biology, the study of neuropathic pain stepped into the post-genomic period which is characterized by study of proteome. A number of proteomic studies have been performed using different animal neuropathy models. The Results of these proteomic approaches are summarized in this review to provide a better overview of proteins that are involved in the mechanisms of neuropathic pain. This might allow a better understanding of the pathogenesis of neuropathic pain, and facilitate the discovery of specific therapies and new treatment target.
ABSTRACT
Objective To compare the hemodynamic responses to orotracheal intubation with GlideScope video laryngoscope (GSVL), Macintosh laryngoscope (MDLS) and fiberoptic bronchoscope (FOB) .Methods Sixty ASAⅠorⅡpatients (21 male, 39 female) aged 18-50 yrs weighing 45-90 kg scheduled for elective plastic surgery under general anesthesia with tracheal intubation and mechanical ventilation were randomly divided into 3 groups ( n = 20 each): GSVL group; MDLS group and FOB group. The patients were premedicated with intramuscular scopolamine 0.3 mg. Anesthesia was induced with midazolam 0.05 mg?kg-1 , fentanyl 2?g?kg-1 , propofol 2 mg?kg-1 and vecuronium 0.1 mg?kg-1 and maintained with 1% isoflurane and 60% N2O-40% O2 . Orotracheal intubation was performed at 2 min after intravenous vecuronium. Noninvasive BP and HR were recorded before and after induction of anesthesia, during tracheal intubation and at 1, 2, 3, 4, 5 min after tracheal intubation was completed. The HR and SBP product (RPP) was calculated. Results The intubation time was significantly longer in FOB group than in MDLS group (P