安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
Acta Universitatis Medicinalis Anhui
2015年
10期
1430-1433
,共4页
陈军喜%孙坚%管细红%贾宝辉%夏芝辉%闫智杰%吴丽丽
陳軍喜%孫堅%管細紅%賈寶輝%夏芝輝%閆智傑%吳麗麗
진군희%손견%관세홍%가보휘%하지휘%염지걸%오려려
卡维地洛%脓毒症%氧化应激%心脏功能
卡維地洛%膿毒癥%氧化應激%心髒功能
잡유지락%농독증%양화응격%심장공능
carvedilol%sepsis%oxidative stress%cardiac function
目的 明确早期脓毒症大鼠心脏变化特点及卡维地洛的预先干预作用. 方法 40 只SD大鼠随机分为脓毒症组( S组)、脓毒症卡维地洛预先干预组( CS组)、卡维地洛对照组(C组)和生理盐水对照组(N组),CS组和C组给予卡维地洛10 mg/( kg·d)灌胃,4周后S组和CS组大鼠尾静脉注射脂多糖(LPS)20 mg/kg制备脓毒症模型,C组和N组注射等容量生理盐水,24 h后检测各组大鼠心率、血压、血清磷酸激酸激酶( CK)、磷酸激酸激酶同工酶( CK-MB)、N末端脑钠肽前体( NT-proBNP )浓度,心肌中超氧化物歧化酶( SOD)、丙二醛( MDA)和三磷酸腺苷( ATP)的含量,观察心肌形态学改变. 结果 卡维地洛可使正常大鼠心率减慢,心肌MDA含量下降、SOD含量升高. LPS可使大鼠心率增快,血清CK、CK-MB、NT-proBNP浓度和心肌MDA含量升高,心肌SOD和ATP含量降低;卡维地洛预先干预可减轻LPS所致大鼠的这些变化. 4 组大鼠血压和心肌形态学变化差异无统计学意义. 结论 早期脓毒症大鼠心率增快,心肌氧化应激,心脏功能受损,心肌能量生成减少. 卡维地洛可增强大鼠抗氧化应激能力,卡维地洛预先干预可改善脓毒症心肌能量代谢和心脏功能,可能与其抗氧化应激作用有关.
目的 明確早期膿毒癥大鼠心髒變化特點及卡維地洛的預先榦預作用. 方法 40 隻SD大鼠隨機分為膿毒癥組( S組)、膿毒癥卡維地洛預先榦預組( CS組)、卡維地洛對照組(C組)和生理鹽水對照組(N組),CS組和C組給予卡維地洛10 mg/( kg·d)灌胃,4週後S組和CS組大鼠尾靜脈註射脂多糖(LPS)20 mg/kg製備膿毒癥模型,C組和N組註射等容量生理鹽水,24 h後檢測各組大鼠心率、血壓、血清燐痠激痠激酶( CK)、燐痠激痠激酶同工酶( CK-MB)、N末耑腦鈉肽前體( NT-proBNP )濃度,心肌中超氧化物歧化酶( SOD)、丙二醛( MDA)和三燐痠腺苷( ATP)的含量,觀察心肌形態學改變. 結果 卡維地洛可使正常大鼠心率減慢,心肌MDA含量下降、SOD含量升高. LPS可使大鼠心率增快,血清CK、CK-MB、NT-proBNP濃度和心肌MDA含量升高,心肌SOD和ATP含量降低;卡維地洛預先榦預可減輕LPS所緻大鼠的這些變化. 4 組大鼠血壓和心肌形態學變化差異無統計學意義. 結論 早期膿毒癥大鼠心率增快,心肌氧化應激,心髒功能受損,心肌能量生成減少. 卡維地洛可增彊大鼠抗氧化應激能力,卡維地洛預先榦預可改善膿毒癥心肌能量代謝和心髒功能,可能與其抗氧化應激作用有關.
목적 명학조기농독증대서심장변화특점급잡유지락적예선간예작용. 방법 40 지SD대서수궤분위농독증조( S조)、농독증잡유지락예선간예조( CS조)、잡유지락대조조(C조)화생리염수대조조(N조),CS조화C조급여잡유지락10 mg/( kg·d)관위,4주후S조화CS조대서미정맥주사지다당(LPS)20 mg/kg제비농독증모형,C조화N조주사등용량생리염수,24 h후검측각조대서심솔、혈압、혈청린산격산격매( CK)、린산격산격매동공매( CK-MB)、N말단뇌납태전체( NT-proBNP )농도,심기중초양화물기화매( SOD)、병이철( MDA)화삼린산선감( ATP)적함량,관찰심기형태학개변. 결과 잡유지락가사정상대서심솔감만,심기MDA함량하강、SOD함량승고. LPS가사대서심솔증쾌,혈청CK、CK-MB、NT-proBNP농도화심기MDA함량승고,심기SOD화ATP함량강저;잡유지락예선간예가감경LPS소치대서적저사변화. 4 조대서혈압화심기형태학변화차이무통계학의의. 결론 조기농독증대서심솔증쾌,심기양화응격,심장공능수손,심기능량생성감소. 잡유지락가증강대서항양화응격능력,잡유지락예선간예가개선농독증심기능량대사화심장공능,가능여기항양화응격작용유관.
Objective Trying to demonstrate the characteristics of early septic rats ' hearts changes and the ad-vanced intervention effects of carvedilol. Methods 40 SD rats were randomly divided into 4 groups: sepsis group ( S group ) , carvedilol-advanced-intervention sepsis group ( CS group ) , carvedilol group ( C group ) and control group(N group). The S and CS groups were injected lipopolysaccharide (LPS) (20mg/kg) into caudal vein to in-duce sepsis, the C and N groups were injected with the same volume of normal saline. The carvedilol had been o-rally administered 10 mg/kg once a day for 4 weeks prior to the injection of LPS in C and CS groups. The S and N groups were administered normal saline instead. After 24 hours, the items including heart rate, blood pressure, and the concentrations of serum creatine kinase ( CK ) , creatine kinase isoenzyme-MB ( CK-MB ) , amino-terminal pro-brain natriuretic peptide (NT-proBNP),superoxide dismutase(SOD), malondialdehyde(MDA),andadenosine triphosphate( ATP) in myocardium were detected and compared, and the morphological changes of myocardium were observed. Results Carvedilol could slow down heart rate, decrease myocardial MDA concentration and in-crease myocardial SOD concentration in normal rats. LPS could increase rats' heart rate and concentrations of ser-um CK,CK-MB,NT-proBNP and MDA in myocardium, and it also could decrease concentrations of SOD and ATP in myocardium. Carvedilol-advanced-intervention could reduce the effect of the LPS in the rats. Conclusion Sep-sis in early stage could induce the rises of heart rate, oxidative stress, damages of cardiac function, and reduction of myocardial energy generation of the rats. However, carvedilol can enhance the ability of antioxidant of the rats. Carvedilol-advadanced intervention of sepsis could ameliorate myocardial energy metabolism and cardiac function that may be related to the antioxidant property of carvedilol.