BACKGROUND： Serum high sensitive C-reactive protein （hs-CRP）, which regards as a high sensitive mark of systemic inflammatory response syndrome, can provide a lot of valuable information for the treatment and progn...BACKGROUND： Serum high sensitive C-reactive protein （hs-CRP）, which regards as a high sensitive mark of systemic inflammatory response syndrome, can provide a lot of valuable information for the treatment and prognosis of cerebrovascular disease. OBJECTIVE： To observe the differences of blood glucose, lipid, homocysteine and previous disease history among patients with acute cerebral infarction at various levels of hs-CRP and compare changes of hs-CRP of patients with various degrees of neurologic impairment. DESIGN： Contrast observation. SETTING： Department of Neurology, Shenzhou Hospital, Shenyang Medical College. PARTICIPANTS： A total of 102 patients with acute cerebral infarction were selected from Department of Neurology, Shenzhou Hospital of Shenyang Medical College from February 2005 to September 2006, including 55 males and 47 females aged from 55 to 86 years. All accepted patients met the diagnostic criteria of cerebral infarction established by the Fourth National Cerebrovascular Disease Academic Meeting and were diagnosed with CT or MRI examination. All patients provided the confirmed consent. Based on clinical criteria of neurologic impairment established by the Fourth National Cerebrovascular Disease Academic Meeting, patients were randomly divided into mild group （0 - 15 points, n =46）, moderate group （16 - 30 points, n =38） and severe group （31 - 45 points, n =18）. In addition, based on hs-CRP level within 72 hours, patients were divided into normal group （hs-CRP ≤3 mg/L, n =53） and increasing group （hs-CRP 〉 3 mg/L, n =-49）. METHODS： ① 2 mL venous blood was selected from hospitalized patients in the next morning to separate serum. Quantitative measurement of hs-CRP was dealt with Latex Enhnced Turbidimetric Immunoassay （LETIA）. ②Fasting venous blood was colleted from hospitalized patients in the next morning to measure numeration of white blood cells, fibrinogen, blood glucose, total cholesterol （TC）, triacylglycerol （TG）, high density lipoprotein cholesterol （HDL-C）, low density lipoprotein cholesterol （LDL-C） and homocysteine. ③Measurement data were compared with t test or analysis of variance. MAIN OUTCOME MEASURES： ①Comparisons of serum biochemical indexes among patients with various levels of hs-CRP; ②comparisons of risk factors among patients with various levels of hs-CRP; ③comparisons of levels of hs-CRP among patients with various degrees of clinical neurologic impairment. RESULTS： A total of 102 patients were involved in the final analysis. ①Plasma fibrinogen and numeration of leucocytes were more in the increasing group than those in the normal group （t =4.39, 3.54, P 〈 0.01）; while, there were no significant differences of blood glucose, TC, TG, HDL-C, LDL-C and homocysteine between the two groups （P 〉 0.05）. ② Percentage of patients with hypertension and diabetes mellitus （DM） was higher in the increasing group than the normal group （ Х^2=3.98, 4.23, P 〈 0.05）; while, percentage of patients with smoking in the increasing group was not significantly different from that of patients in the normal group （P 〉 0.05）. ③Level of hs-CRP of patients with severe neurologic impairment was higher than that of patients with moderate neurologic impairment （t =2.273, P 〈 0.05）; that of patients with moderate neurologic impairment was higher than that of patients with mild neurologic impairment （t =2.586, P 〈 0.05）; that of patients with severe neurologic impairment was obviously higher than that of patients with mild neurologic impairment （t = 4.913, P 〈 0.01）. CONCLUSION： ① With the increase of hs-CRP, plasma fibrinogen and numeration of leucocytes of patients with acute cerebral infarction is increased, especially, they are increased remarkably among patients who have history of diabetes mellitus and hypertension. ②Increase of level of hs-CRP can be regarded as one of marks to evaluate severity of acute stroke.展开更多
BACKGROUND： Brief exposure to the anesthetic sevoflurane results in delayed neuroprotection, However, few studies have addressed delayed neuroprotection after preconditioning with a single administration of sevoflura...BACKGROUND： Brief exposure to the anesthetic sevoflurane results in delayed neuroprotection, However, few studies have addressed delayed neuroprotection after preconditioning with a single administration of sevoflurane. OBJECTIVE： To explore the relationship between a single preconditioning administration of sevoflurane and reactive oxygen species production and protein kinase C-epsilon （PKC-ε ） translocation. DESIGN, TIME, AND SETTING： The randomized, controlled, animal experiment was conducted at the Central Laboratory, Xiangya Hospital, Central South University, China from November 2007 to April 2008. MATERIALS： A total of 120 healthy, male, Sprague Dawley rats were equally and randomly assigned into five groups： sham operation, ischemia/reperfusion, sevoflurane, 2-mercaptopropionylglycine （2-MPG, a selective reactive oxygen species scavenger） ＋ sevoflurane （MPG ＋ sevoflurane）, and MPG. Sevoflurane （Baxter, USA） and MPG （Sigma, USA） were used in this study. METHODS： Intervention consisted of three procedures. （1） MPG injection： a selective reactive oxygen species scavenger, MPG （20 mg/kg）, was infused into the rat caudal vein in the MPG and MPG ＋ sevoflurane groups. （2） Sevoflurane preconditioning： 30 minutes following MPG injection, rats in the sevoflurane and MPG ＋ sevoflurane groups breathed a mixed gas of 2.4% sevoflurane and 97.6% oxygen for 60 minutes. Rats in the sham operation, ischemia/reperfusion, and MPG groups breathed 100% pure oxygen for 60 minutes. （3） IschemiaJreperfusion： 24 hours after sevoflurane or pure oxygen preconditioning, middle cerebral artery occlusion models were established in the ischemia/reperfusion, sevoflurane, MPG ＋ sevoflurane, and MPG groups. Following 2 hours ischemia/6 hours and 24 hours reperfusion, the carotid artery was separated, but the middle cerebral artery was not occluded, in the sham operation group. MAIN OUTCOME MEASURES： In the ischemic hemisphere, PKC-ε translocation in the rat parietal cortex was measured by Western blot analysis. Infarct volume was calculated using the TTC assay. Neurological deficits were evaluated in rats using a scoring system of 8 points. RESULTS： After 6 hours reperfusion, the ratio of PKC-ε in membrane/（cytosol ＋ membrane） was significantly less in the sham operation group than in the ischemia/reperfusion, sevoflurane, MPG ＋ sevoflurane）, and MPG groups （P 〈 0.05）. The ratio of PKC-ε in membrane/（cytosol ＋ membrane） was significantly greater in the sevoflurane group than in the sham operation, ischemia/reperfusion, MPG ＋ sevoflurane, and MPG groups （P 〈 0.05）. No significant differences were observed in the ischemiaJreperfusJon, M PG ＋ sevoflurane, and MPG groups （P 〉 0.05）. Following 24 hours reperfusion, the ratio of PKC-ε in membrane/（cytosol ＋ membrane） was significantly less in the sham operation group than in the ischemia/reperfusion, sevoflurane, MPG ＋ sevoflurane, and MPG groups （P 〈 0.05）. No significant differences were detected in the ischemia/reperfusion, sevoflurane, MPG ＋ sevoflurane, and MPG groups （P 〉 0.05）. Compared with the ischemia/reperfusion, MPG ＋ sevoflurane, and MPG groups, infarct volume was significantly smaller, and neurological deficits were significantly improved, in the sevoflurane group （P 〈 0.05）. No significant differences in infarct volume and neurological deficits were observed among the ischemia/reperfusion, MPG ＋ sevoflurane, and MPG groups （P 〉 0.05）. Infarcts or neurological deficits were not detected in the sham operation group. CONCLUSION： A single preconditioning administration of sevoflurane reduced infarct volumes and improved neurological deficits in ischemic rats. Delayed neuroprotection may be mediated by reactive oxygen species and correlated to PKC- ε activation.展开更多
文摘BACKGROUND： Serum high sensitive C-reactive protein （hs-CRP）, which regards as a high sensitive mark of systemic inflammatory response syndrome, can provide a lot of valuable information for the treatment and prognosis of cerebrovascular disease. OBJECTIVE： To observe the differences of blood glucose, lipid, homocysteine and previous disease history among patients with acute cerebral infarction at various levels of hs-CRP and compare changes of hs-CRP of patients with various degrees of neurologic impairment. DESIGN： Contrast observation. SETTING： Department of Neurology, Shenzhou Hospital, Shenyang Medical College. PARTICIPANTS： A total of 102 patients with acute cerebral infarction were selected from Department of Neurology, Shenzhou Hospital of Shenyang Medical College from February 2005 to September 2006, including 55 males and 47 females aged from 55 to 86 years. All accepted patients met the diagnostic criteria of cerebral infarction established by the Fourth National Cerebrovascular Disease Academic Meeting and were diagnosed with CT or MRI examination. All patients provided the confirmed consent. Based on clinical criteria of neurologic impairment established by the Fourth National Cerebrovascular Disease Academic Meeting, patients were randomly divided into mild group （0 - 15 points, n =46）, moderate group （16 - 30 points, n =38） and severe group （31 - 45 points, n =18）. In addition, based on hs-CRP level within 72 hours, patients were divided into normal group （hs-CRP ≤3 mg/L, n =53） and increasing group （hs-CRP 〉 3 mg/L, n =-49）. METHODS： ① 2 mL venous blood was selected from hospitalized patients in the next morning to separate serum. Quantitative measurement of hs-CRP was dealt with Latex Enhnced Turbidimetric Immunoassay （LETIA）. ②Fasting venous blood was colleted from hospitalized patients in the next morning to measure numeration of white blood cells, fibrinogen, blood glucose, total cholesterol （TC）, triacylglycerol （TG）, high density lipoprotein cholesterol （HDL-C）, low density lipoprotein cholesterol （LDL-C） and homocysteine. ③Measurement data were compared with t test or analysis of variance. MAIN OUTCOME MEASURES： ①Comparisons of serum biochemical indexes among patients with various levels of hs-CRP; ②comparisons of risk factors among patients with various levels of hs-CRP; ③comparisons of levels of hs-CRP among patients with various degrees of clinical neurologic impairment. RESULTS： A total of 102 patients were involved in the final analysis. ①Plasma fibrinogen and numeration of leucocytes were more in the increasing group than those in the normal group （t =4.39, 3.54, P 〈 0.01）; while, there were no significant differences of blood glucose, TC, TG, HDL-C, LDL-C and homocysteine between the two groups （P 〉 0.05）. ② Percentage of patients with hypertension and diabetes mellitus （DM） was higher in the increasing group than the normal group （ Х^2=3.98, 4.23, P 〈 0.05）; while, percentage of patients with smoking in the increasing group was not significantly different from that of patients in the normal group （P 〉 0.05）. ③Level of hs-CRP of patients with severe neurologic impairment was higher than that of patients with moderate neurologic impairment （t =2.273, P 〈 0.05）; that of patients with moderate neurologic impairment was higher than that of patients with mild neurologic impairment （t =2.586, P 〈 0.05）; that of patients with severe neurologic impairment was obviously higher than that of patients with mild neurologic impairment （t = 4.913, P 〈 0.01）. CONCLUSION： ① With the increase of hs-CRP, plasma fibrinogen and numeration of leucocytes of patients with acute cerebral infarction is increased, especially, they are increased remarkably among patients who have history of diabetes mellitus and hypertension. ②Increase of level of hs-CRP can be regarded as one of marks to evaluate severity of acute stroke.
文摘BACKGROUND： Brief exposure to the anesthetic sevoflurane results in delayed neuroprotection, However, few studies have addressed delayed neuroprotection after preconditioning with a single administration of sevoflurane. OBJECTIVE： To explore the relationship between a single preconditioning administration of sevoflurane and reactive oxygen species production and protein kinase C-epsilon （PKC-ε ） translocation. DESIGN, TIME, AND SETTING： The randomized, controlled, animal experiment was conducted at the Central Laboratory, Xiangya Hospital, Central South University, China from November 2007 to April 2008. MATERIALS： A total of 120 healthy, male, Sprague Dawley rats were equally and randomly assigned into five groups： sham operation, ischemia/reperfusion, sevoflurane, 2-mercaptopropionylglycine （2-MPG, a selective reactive oxygen species scavenger） ＋ sevoflurane （MPG ＋ sevoflurane）, and MPG. Sevoflurane （Baxter, USA） and MPG （Sigma, USA） were used in this study. METHODS： Intervention consisted of three procedures. （1） MPG injection： a selective reactive oxygen species scavenger, MPG （20 mg/kg）, was infused into the rat caudal vein in the MPG and MPG ＋ sevoflurane groups. （2） Sevoflurane preconditioning： 30 minutes following MPG injection, rats in the sevoflurane and MPG ＋ sevoflurane groups breathed a mixed gas of 2.4% sevoflurane and 97.6% oxygen for 60 minutes. Rats in the sham operation, ischemia/reperfusion, and MPG groups breathed 100% pure oxygen for 60 minutes. （3） IschemiaJreperfusion： 24 hours after sevoflurane or pure oxygen preconditioning, middle cerebral artery occlusion models were established in the ischemia/reperfusion, sevoflurane, MPG ＋ sevoflurane, and MPG groups. Following 2 hours ischemia/6 hours and 24 hours reperfusion, the carotid artery was separated, but the middle cerebral artery was not occluded, in the sham operation group. MAIN OUTCOME MEASURES： In the ischemic hemisphere, PKC-ε translocation in the rat parietal cortex was measured by Western blot analysis. Infarct volume was calculated using the TTC assay. Neurological deficits were evaluated in rats using a scoring system of 8 points. RESULTS： After 6 hours reperfusion, the ratio of PKC-ε in membrane/（cytosol ＋ membrane） was significantly less in the sham operation group than in the ischemia/reperfusion, sevoflurane, MPG ＋ sevoflurane）, and MPG groups （P 〈 0.05）. The ratio of PKC-ε in membrane/（cytosol ＋ membrane） was significantly greater in the sevoflurane group than in the sham operation, ischemia/reperfusion, MPG ＋ sevoflurane, and MPG groups （P 〈 0.05）. No significant differences were observed in the ischemiaJreperfusJon, M PG ＋ sevoflurane, and MPG groups （P 〉 0.05）. Following 24 hours reperfusion, the ratio of PKC-ε in membrane/（cytosol ＋ membrane） was significantly less in the sham operation group than in the ischemia/reperfusion, sevoflurane, MPG ＋ sevoflurane, and MPG groups （P 〈 0.05）. No significant differences were detected in the ischemia/reperfusion, sevoflurane, MPG ＋ sevoflurane, and MPG groups （P 〉 0.05）. Compared with the ischemia/reperfusion, MPG ＋ sevoflurane, and MPG groups, infarct volume was significantly smaller, and neurological deficits were significantly improved, in the sevoflurane group （P 〈 0.05）. No significant differences in infarct volume and neurological deficits were observed among the ischemia/reperfusion, MPG ＋ sevoflurane, and MPG groups （P 〉 0.05）. Infarcts or neurological deficits were not detected in the sham operation group. CONCLUSION： A single preconditioning administration of sevoflurane reduced infarct volumes and improved neurological deficits in ischemic rats. Delayed neuroprotection may be mediated by reactive oxygen species and correlated to PKC- ε activation.
