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Objective:To evaluate the effect of flurbiprofen postconditioning on the permeability of blood brain barrier in a rat model of focal cerebral ischemia-reperfusion (I/R) injury.Methods:Eighty healthy male Wistar rats, aged 8-9 weeks, weighing 280-320 g, were divided into 4 groups ( n=20 each) using a random number table method: sham operation group (group Sham), focal cerebral I/R group (group I/R), lipo-microballoons group (group V) and flurbiprofen 10 mg/kg group (group F). Focal cerebral I/R model was established by left middle cerebral artery occlusion for 2 h followed by 24-h reperfusion in anesthetized rats.Flurbiprofen 10 mg/kg (group F), the equal volume of lipo-microballoons (group V) or the equal volume of normal saline (group Sham and group I/R) was injected via the tail vein at the onset of reperfusion.The rats were sacrificed at 24 h of reperfusion, brains were immediately removed, and cerebral tissues were obtained for measurement of brain water content, Evans blue content, expression of matrix metalloproteinase-9 (MMP-9) in ischemic penumbra (by immuno-histochemistry), and expression of phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) and inducible nitric oxide synthase (iNOS) in ischemic penumbra (by Western blot). Results:Compared with Sham group, brain water content and Evans blue content in brain tissues were significantly increased, and the expression of MMP-9, p-p38 MAPK and iNOS in ischemic penumbra was up-regulated in I/R, V and F groups ( P<0.05). Compared with group I/R, brain water content and Evans blue content in brain tissues were significantly decreased, and the expression of MMP-9, p-p38 MAPK and iNOS in ischemic penumbra was down-regulated in group F ( P<0.05), and no significant change was found in the above parameters in group V ( P>0.05). Conclusion:Flurbiprofen postconditioning can decrease the permeability of blood brain barrier during focal cerebral I/R in rats, and the mechanism may be related to inhibiting the activation of p38 MAPK/iNOS signaling pathway and down-regulating the expression of MMP-9.
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Objective To evaluate the efficacy of clemastine fumarate in antagonizing atracuriuminduced release of histamine in the patients undergoing surgery under general anesthesia.Methods Eighty American Society of Anesthesiologists physical status Ⅰ or Ⅱ patients,aged 21-59 yr,with body mass index of 17-26 kg/m2,scheduled for elective modified radical mastectomy,were divided into 2 groups (n=40 each) using a random number table:control group (group C) and clemastine fumarat group (group CF).Clemastine fumarate 2 mg was injected intramuscularly at 20 min before induction of anesthesia.Anesthesia was induced with iv midazolam 0.1 mg/kg,etomidate 0.3 mg/kg,fentanyl 4-6 μg/kg and atracurium 0.8 mg/kg.The patients were mechanically ventilated after insertion of the larygeal mask airway.Anesthesia was maintained with inhalation of 2％ sevoflurane.Before administration of clemastine fumarate,at 20 min after administration,immediately before administration of atracurium,and at 2,5,10 and 20 min after administration of atracurium,arterial blood samples were taken for determination of plasma histamine concentrations,and the peak airway pressure and degree of cutaneous color were recorded.The development of histaminemia and adverse cardiovascular events was assessed.Steward recovery scores and Ramsay sedation scores were recorded at 10 min after removal of the laryngeal mask airway.Results The incidence of histaminemia was 60％ and 8％ in C and CF groups,respectively.Compared with group C,the plasma histamine concentrations,incidence of histaminemia,degree of cutaneous color,and incidence of hypotension and tachycardia were significantly decreased (P＜0.05),and no significant change was found in the peak airway pressure,Steward recovery scores and Ramsay sedation scores in group CF (P＞0.05).Conclusion For atracurium-induced release of histamine in the patients undergoing surgery under general anesthesia,clemastine fumarate 2 mg injected intramuscularly before operation can not only antagonize histamine at H1 level,but also reduce histamine release,and exerts no influence on recovery from anesthesia and produces good antihistamine efficacy.
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BACKGROUND:Internal fixation methods for traditional proximal clavicle fractures and sternoclavicular joint dislocation include Kirschner wire, Kirschner wire with tension band, clavicular hook plate and ordinary T-shaped plate fixation. However, al of these are easy to fal off, damage nerves and blood vessels and affect the fine motion of the sternoclavicular joint. OBJECTIVE:To investigate the therapeutic effects of internal fixation with T-shaped stainless steel locking plate on proximal clavicular fractures and sternoclavicular joint dislocation as wel as to observe the biocompatibility of materials with the host. METHODS: Twelve patients with proximal clavicular fractures and sternoclavicular joint dislocation were enroled at Shanxian Central Hospital from March 2011 to January 2014, including seven cases of proximal clavicular fractures and five cases of sternoclavicular joint dislocation. Al of patients were subject to open reduction and internal fixation with T-shaped locking plate. RESULTS AND CONCLUSION:Al the 12 patients were folowed up for 3-14 months, with an average of 9 months. Al incisions healed wel, with no local eminence. No major substernal blood vessels and organ damage occurred. X-ray films showed that fractures healed without further dislocation and steel plate fracture. At the last folow-up, Rockwood scoring system showed that the excelent rate of shoulder function was 100%. These findings indicate that the internal fixation with stainless steel T-shaped locking plate is reliable and effective in the treatment of proximal clavicle fractures and sternoclavicular joint dislocation, with low risks and satisfactory outcomes, by which, patients can maximize the recovery of shoulder function.
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Objective To investigate the role of high mobility group protein box 1 (HMGB1) in pulmonary vascular remodeling in a rat model of acute lung injury (ALI).Methods Thirty healthy pathogen free male Wistar rats weighing 220-250 g were randomly divided into 3 groups (n =10 each) ∶ group control (group C) ;group LPS (group M) and group LPS + HMGB1 antibody (group H).The animals were anesthetized with intraperitoneal 10％ chloral hydrate 7 ml/kg.ALI was induced with LPS 1 mg/kg infused iv over 30 min in groups M and H.In group H HMGB1 antibody 2 mg/kg was injected iv at 12,24 and 36 h after LPS administration respectively.The animals were sacrificed at 72 h after LPS administration.The left lung was removed for microscopic examination,measurement of the thickness of the medial layer (tunica media) of pulmonary arterioles and determination of the expression of PCNA (by immune-histochemistry) and HMGB1 protein (by Western blotting).Results The medial layer of pulmonary arterioles was significantly thicker and the expression of PCNA and HMGB1 higher in group M than in group C.LPS also induced significant inflammatory cell infiltration within the alveoli and damage to the septa.In group H HMGB1 antibody significantly attenuated the above-mentioned LPS-induced changes.Conclusion HMGB1 may play an important role in the LPS-induced pulmonary vascular remodeling.