ABSTRACT
Objective@#To evaluate the effects of sevoflurane on microglial polarization after traumatic brain injury (TBI) in rats.@*Methods@#Seventy-two healthy adult male Sprague-Dawley rats, weighing 230-250 g, were divided into 3 groups (n=24 each) using a random number table method: sham operation group (group Sham), group TBI, and TBI plus sevoflurane anesthesia group (group TBI+ Sevo). TBI models were established by using Feeney′s method in TBI and TBI+ Sevo groups, 30 min later 2.4% sevoflurane was inhaled for 1 h once a day for 3 consecutive days in TBI+ Sevo group, while pure oxygen was inhaled instead in Sham and TBI groups.At 1, 3, 7 and 14 days after establishing the model, 6 rats were selected, the neurological function was evaluated with the modified neurologic severity score (mNSS), and tail venous blood samples were taken for determination of tumor necrosis factor-a (TNF-α), interleukin-1beta (IL-1β) and IL-6 concentrations by enzyme-linked immunosorbent assay.The rats were then sacrificed, the limbic cortical tissues of brain contusion lesion were taken for determination of cell apoptosis (by TUNEL) and expression of microglial marker Iba-1, microglial M1 phenotypic marker CD86 and microglial M2 phenotypic marker CD206 (by Western blot).@*Results@#Compared with group Sham, the mNSS score, apoptosis rate of cortical cells, expression of Iba-1, CD86 and CD206, and concentrations of serum TNF-α, IL-1β and IL-6 were significantly increased in TBI and TBI+ Sevo groups (P<0.05). Compared with TBI group, the mNSS score, apoptosis rate of cortical cells, expression of Iba-1 and CD86 and concentrations of serum TNF-α, IL-1β and IL-6 were significantly decreased, and the expression of CD206 was up-regulated in TBI+ Sevo group (P<0.05).@*Conclusion@#The mechanism by which sevoflurane anesthesia reduces TBI may be related to promoting microglial polarization and inhibiting systemic inflammatory response in rats.
ABSTRACT
Objective To evaluate the effects of sevoflurane on microglial polarization after traumatic brain injury (TBI) in rats.Methods Seventy-two healthy adult male Sprague-Dawley rats,weighing 230-250 g,were divided into 3 groups (n=24 each) using a random number table method:sham operation group (group Sham),group TBI,and TBI plus sevoflurane anesthesia group (group TBI+Sevo).TBI models were established by using Feeney's method in TBI and TBI+Sevo groups,30 min later 2.4％sevoflurane was inhaled for 1 h once a day for 3 consecutive days in TBI+Sevo group,while pure oxygen was inhaled instead in Sham and TBI groups.At 1,3,7 and 14 days after establishing the model,6 rats were selected,the neurological function was evaluated with the modified neurologic severity score (mNSS),and tail venous blood samples were taken for determination of tumor necrosis factor-a (TNF-α),interleukin-1beta (IL-1β) and IL-6 concentrations by enzyme-linked immunosorbent assay.The rats were then sacrificed,the limbic cortical tissues of brain contusion lesion were taken for determination of cell apoptosis (by TUNEL) and expression of microglial marker lba-1,microglial M1 phenotypic marker CD86 and microglial M2 phenotypic marker CD206 (by Western blot).Results Compared with group Sham,the mNSS score,apoptosis rate of cortical cells,expression of Iba-1,CD86 and CD206,and concentrations of serum TNF-α,IL-1β and IL-6 were significantly increased in TBI and TBI+Sevo groups (P＜0.05).Compared with TBI group,the mNSS score,apoptosis rate of cortical cells,expression of Iba-1 and CD86 and concentrations of serum TNF-α,IL-1β and IL-6 were significantly decreased,and the expression of CD206 was up-regulated in TBI+Sevo group (P＜0.05).Conclusion The mechanism by which sevoflurane anesthesia reduces TBI may be related to promoting microglial polarization and inhibiting systemic inflammatory response in rats.
ABSTRACT
To discuss the cause of positive atropine test and the possible reason for false positive atropine test, providing a certain aids for for clinical diagnosis and treatment. Eighty patients, conducted atropine test due to sinus bradycardia, with Positive results from January 2010 to June 2013, were selected. Sinus heart rate were calculated and the changes in heart Arnie were observed by tracing electrocardiogram. Esophageal electrophysiological examination and atropine test were aimantrated. SPSS 10.0 statistical software was adopted and x2 test was applied for comparison. The positive results of atropine test and results of esophageal electrophysiological examination in different ages showed that as age grows, false maise rate of atropine test was significantly reduced, presenting statistically significant difference [x2=6.2821, p<0.05]; The positive results of atropine test and results of esophageal electrophysiological examination in different heart rates showed that false positive rate of atropine test on those with bradycardia was smaller than those with significant bradycardia. presenting statistically significant difference [x2=5.1792, p<0.05]. Simple sinus bradycardia is mostly caused by the increase of vagus nerve tension, almost negative in atropine test. Sick sinus syndrome [SSS] leads to aboornucry in pacemaking and conduction induced by organic lesions in sinus nodes. Moreover, as the disease progresses, r able to cause severe and persistent sinus bradycardia, almost positive in atropine test. Therefore, to identify the increase in vagus nerve tension or sinus bradycardia induced by SSS has a crucial clinical significance. Furthermore, the false positive and false negative profiles in atropine test can easily lead to misdiagnosis and mistreatment in clinic