肾上腺素能受体阻滞剂对心肺复苏后家兔心力衰竭影响的实验研究
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摘要
目的目前的研究认为复苏后心肌功能障碍是心肺复苏(CPR)成功后早期导致死亡的主要原因之一。作为心肺复苏的首选药,肾上腺素(AD)在CPR过程中增加冠脉和脑的灌注压促进自主循环恢复(ROSC)的作用已得到广泛的临床验证,但有研究表明AD增加了复苏后心肌功能障碍的严重程度,并认为主要是AD对β和α_1受体激动所致。本研究拟在观察β和α_1肾上腺素能受体阻滞剂联用对家兔心肺复苏后血流动力学和B型脑钠肽(brain natriuretic peptide,BNP)浓度变化,以评价其对复苏后心肌损伤的影响。
方法本实验采用电击致家兔室颤复苏模型,45只健康家兔按随机数字表法分为三组,每组15只,手术对照组(A组)、肾上腺素组(B组)、酒石酸美托洛尔+乌拉地尔组(C组)。在室颤发生前和复苏成功后30min、60min、120min、180min进行血流动力学和血浆BNP浓度指标的测量。
结果复苏后家兔出现不同程度的心功能障碍。与A组比较,B组复苏后心率增快,C组复苏后心率明显低于B组(P＜0.05);B、C组家兔心室压力变化速率(peak first derivative of left ventricular pressure,Peak dp/dt)、左室舒张末压(left ventricle end diastolic pressure,LVEDP)均存在显著差异(P＜0.01),C组peak dp/dt值显著高于B组(P＜0.01);与A组比较,B组和C组LVEDP值在自主循环出现后均有显著增加,而C组与B组比较,LVEDP明显降低(P＜0.05);B、C组BNP值在复苏后较A组明显升高(P＜0.01),并且在整个观察期间均高于基础值,C组BNP值明显低于B组(P＜0.01)。
结论联用β和α_1肾上腺素能受体阻滞剂能在一定程度上改善家兔的复苏后心功能不全,降低血浆中BNP浓度。
Objective Current investigations support the notion that postresuscitation myocardial dysfunction is one of the main causes which lead to deaths after initially successful cardiopulmonary resuscitation(CPR).As the preferred vasopressor agent,adrenaline has been confirmed to improve coronary and cerebral perfusion and enhance the restoration of spontaneous circulation(ROSC) during CPR widely in many clinical settings.However,some evidences showed that adrenaline increased the seveyity of postresuscitation myocardial dysfunction in consequence of itsβandα_1-adrenergic actions during CPR.The present study is to observe the effects ofβ-andα_1-adrenergic blocker on the changes of hemodynamic values and concentration of BNP after rabbits' cardiopulmonary resuscitation.
Methods fourty-five rabbits were randomly allocated to one of 3 groups:sham control groug、adrenaline treatment group、metoprolol+urapidil pretreatment group(n=15,per group).Hemodynamic values and concentration of BNP were measured at different points of before ventricular tachycardia(VF) and 30,60,120,180minutes after CPR.
Results The left cardiac function was significantly reduced in all rabbits.Heart rate(HR) was significantly higher after CPR in B group than in A and C group (P＜0.05).In B and C group,peak first derivative of left ventricular pressure(peak dp/dt) and left ventricle end diastolic pressure(LVEDP) were reduced compared with A group(P＜0.01).The BNP of B and C groups was conspicuous higher compared A group,and the increases could be observed at each postresuscitation time intervals (P＜0.01).The BNP of C group was lower than B group conspicuously(P＜0.01).
Conclusions During cardiopulmonary resuscitationβ-andal-adrenergic blocker can reduce the concentration of BNP and improve postresuscitation myocardial dysfunction.
方法本实验采用电击致家兔室颤复苏模型,45只健康家兔按随机数字表法分为三组,每组15只,手术对照组(A组)、肾上腺素组(B组)、酒石酸美托洛尔+乌拉地尔组(C组)。在室颤发生前和复苏成功后30min、60min、120min、180min进行血流动力学和血浆BNP浓度指标的测量。
结果复苏后家兔出现不同程度的心功能障碍。与A组比较,B组复苏后心率增快,C组复苏后心率明显低于B组(P＜0.05);B、C组家兔心室压力变化速率(peak first derivative of left ventricular pressure,Peak dp/dt)、左室舒张末压(left ventricle end diastolic pressure,LVEDP)均存在显著差异(P＜0.01),C组peak dp/dt值显著高于B组(P＜0.01);与A组比较,B组和C组LVEDP值在自主循环出现后均有显著增加,而C组与B组比较,LVEDP明显降低(P＜0.05);B、C组BNP值在复苏后较A组明显升高(P＜0.01),并且在整个观察期间均高于基础值,C组BNP值明显低于B组(P＜0.01)。
结论联用β和α_1肾上腺素能受体阻滞剂能在一定程度上改善家兔的复苏后心功能不全,降低血浆中BNP浓度。
Objective Current investigations support the notion that postresuscitation myocardial dysfunction is one of the main causes which lead to deaths after initially successful cardiopulmonary resuscitation(CPR).As the preferred vasopressor agent,adrenaline has been confirmed to improve coronary and cerebral perfusion and enhance the restoration of spontaneous circulation(ROSC) during CPR widely in many clinical settings.However,some evidences showed that adrenaline increased the seveyity of postresuscitation myocardial dysfunction in consequence of itsβandα_1-adrenergic actions during CPR.The present study is to observe the effects ofβ-andα_1-adrenergic blocker on the changes of hemodynamic values and concentration of BNP after rabbits' cardiopulmonary resuscitation.
Methods fourty-five rabbits were randomly allocated to one of 3 groups:sham control groug、adrenaline treatment group、metoprolol+urapidil pretreatment group(n=15,per group).Hemodynamic values and concentration of BNP were measured at different points of before ventricular tachycardia(VF) and 30,60,120,180minutes after CPR.
Results The left cardiac function was significantly reduced in all rabbits.Heart rate(HR) was significantly higher after CPR in B group than in A and C group (P＜0.05).In B and C group,peak first derivative of left ventricular pressure(peak dp/dt) and left ventricle end diastolic pressure(LVEDP) were reduced compared with A group(P＜0.01).The BNP of B and C groups was conspicuous higher compared A group,and the increases could be observed at each postresuscitation time intervals (P＜0.01).The BNP of C group was lower than B group conspicuously(P＜0.01).
Conclusions During cardiopulmonary resuscitationβ-andal-adrenergic blocker can reduce the concentration of BNP and improve postresuscitation myocardial dysfunction.
引文
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14 武建军,李利华.心肌缺血及再灌注损伤时心脏α_1肾上素能受体的变化及其临床意义.军医进修学院学报,1997;18:287-290
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38 Tang W,Weil MH,Sum S,et al.Low energy biphasic waveform defibrillation reduces the severity of postresuscitation myocardial dysfunction[J].Crit Care Med,2000;28(ll suppl):N222-4
39 Kern KB,Hilwig RW,Rhee KH,Berg RA.Myocardial dysfunction after resuscitation from cardiac arrest: an example of global myocardial stunning.J Am Coil Cardiol ,1996;28(1):232-240
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2 Thel MC,O' C onn or CM.Cardiopulmonary resuscitation:historical perspective to recent investigations[J].Am Heart J,1999,137(1):39-48.
3 Cooper S,EvansC.Resuscittion predictor scoring scale for in hospital cardiac arrests[J].Emerg Med J,2003,20(1):6-9
4 Herlitz J,Bang A.Gunnarsaon J,et al.Factors associated with survival to hospital discharge among patients hospitalised alive after out of hospital cardiac arrest:change in outcome over 20 years in the community of G(o|¨)teborg,Sweden[J].Heart,2003,89(1):25-30
5 Kloner RA,Arimie RB,Kay GL,et al.Evidence for stunned myocardium in humans:a 2001 update[J].Coron Artery Dis,2001;12(5):349-56
6 Carden DL,Neil Granger D.Pathophysiology of ischemia-reperfusion injury 2000;190:255-266
7 Pioer HM,Garcia-Dorado D,Ovize M.A fresh look at reperfusion injury.Cardiovasc Res 1998;38(2):291-300
8 Carcia-Dorado D,Theroux P,Desco M,et al.Cell-to-cell interaction:a mechanism to explain wave-from progression of myocardial necrosis[J].Am J physiol 1989;256(5 pt 2):H1266-73
9 Gilbert EM,Olsen SL,Renlund OG,,et al.Beta-adrenergic receptor regulation and left ventricular function in idiopathic dilated cardiomyopathy.Am J Cardiol,1993,71(9):23C-29C
10 Kern KB,Elchisak MA,Sanders AB,et al.Plasma catecholamines and resuscitation from prolonged cardiac arrest[J].Crit Care Med,1989,17(8):786-791
11 Tam LB,Benjanin Ⅱ,Clark WA,et al.Beta-adrenergic receptor desensitization may serve a carcdioprotective role.Cardiovasc Res,1992,26:608
12 Terzic A,PuceatM,VassortG,et al.Cardiac α_1 adrenoceptors:an overview.Pharmacol Rev,1993;45:147-175
13 Vargas HM,Gorman AJ.Vascular alpha-1 adrenergic receptor subtypes in the regulation of arterial pressure[J].Life Sci,1995;57(25):2291-2308
14 武建军,李利华.心肌缺血及再灌注损伤时心脏α_1肾上素能受体的变化及其临床意义.军医进修学院学报,1997;18:287-290
15 武建军,李利华,张颖丽,等.大鼠心跳骤停期间心脏和肾脏α_1肾上腺素能受体的变化.中华医学杂志,1996;11(6):456-458
16 Corr PB,Shayman JA,Kramer JB,et al.Increased alpha-adrenergic receptors in ischemic cat myocardium:a potential mediator of electrophysiological derangements[J].J Clin Invest,1981;67(4):1232-1236
17 吴皎辉,韩启德,王宪,等.大鼠心肌缺血与重灌时α_1肾上腺素受体及其亚型的改变.中国病理生理杂志,1991;7:122-125
18 潘胜军,周兆年.急性低氧对肺动脉、肾动脉及肠系膜动脉平滑肌张力的影响.中国应用生理学杂志,1995;11(4):299-303
19 Norman A,Paradis,Michadl I Rose,et al.The effect of global ischemia and reperfusion on the plasma levels of vasoactive peptides.The neuroendocrine response to cardiac arrest and resuscitation.Resuscitation,1993,26(3):261-269
20 Belardinelli L,Linder J,Berne R.The cardiac effects of adenosine.Prog Cardiovasc Dis,1989,32:73
21 Tang W,Weil MH,Sum S,et al.Epinephrine increases the severity of postresuscitation myocardial dysfunction[J].Circulation,1995;92(10):3089-3093
22 Linder KH,Prengel AW,Pfenninger EG,et al.Vasopressin improves vital organ blood flow during closed-chest cardiopulmonary resuscitation in pig.Circulation,1995;91(1):215-221
23 Mulligan KA,McKnite SH,Linder KH,et al.Synergistic effects of vasopressin plus epinephrine during cardiopulmonary resuscitation[J].Resuscitation,1997,35(3):265-271
24 Viskin S,Belhassen B,Roth A,et al.Aminophylline for bradyasystolic cardiac arrest refraotory to atropine and epinephrine.Ann Intern Med,1993;118(4):279-281
25 Weil MH,Tang W.CPR Resuscitation of the Arrested Heart,北京:科学出版社2001.第一版:179-190
26樊寻梅。心肺复苏的最新进展-第六届WOLF CREEK会议纪要。,2001;12(10):404
27 Tang W,Weil MH,Sun S,et al.Progressive myocardial dysfunction after cardiac resuscitation.Crit Care Med,1993;21(7):1046-1050
28 Gazmuri RJ,Weil MH,Bisera J,et al.Myoocardial dysfunction after successful resuscitation from cardiac arrest.Crit Care Med,1996;24(6):992-1000
29 Kern KB,Hilwig RW,Rhee KH,Berg RA.Myocardial dysfunction after successful resuscitation from cardiac arrest;an example of global myocardial stunning.J Am Coil Cardiol,1996;28(1):232-240
30 Tresch DD,Keelan MH Jr,Siegel R,et al.Long-term survival after prehospital sudden cardiac death.Am Heart J 1984 Jul;108(1):1-5
31 Brain Resuscitation Clinical Trial Π Study Group:A randomized clinical trial of calcium entry blocker aadministration to comatose survivors of cardiac arrest.Design,methods,and patient characteristics.Control Clin Trials 1991Aug;12(4):525-45
32 Kern KB,Postresuscitation myocardial dysfunction[J].Cardiol Clin 2002;20:89-101
33 Guest TM,Ramanatham AV,Tuteur PG,et al.Myocardial injury in critically ill patients-a frequently unrecognized complication[J].JAMA,1995;273(24):1945-1949
34 Von Planta I,Weil MH,Von Planta M,et al.Cardiopulmonary resuscitation in the rat[J].J Appl Physiol,1988;65(6):2641-2647
35 李树岩,李淑梅。不同剂量肾上腺素对犬心脏骤停复苏时平均动脉压及血清肌钙蛋白T含量的影响,中国危重病急救医学,1997,9(8):462-463
36 Xie J,Weil MH,Sun S,et al.High-energy defibrillation increases the severity of postresuscitation myocardial dysfunction[J].Circulation,1997;96(2):683-688
37 Tang W,Weil MH,Sum S,et al.The effects of biphasic and conventional monophasic defibrillation on postresuscitation myocardial function[J].J Am Coll Cardiol,1999;34(3):815-822
38 Tang W,Weil MH,Sum S,et al.Low energy biphasic waveform defibrillation reduces the severity of postresuscitation myocardial dysfunction[J].Crit Care Med,2000;28(ll suppl):N222-4
39 Kern KB,Hilwig RW,Rhee KH,Berg RA.Myocardial dysfunction after resuscitation from cardiac arrest: an example of global myocardial stunning.J Am Coil Cardiol ,1996;28(1):232-240
40 Laurent I,Spaulding C,Monchi M,et al.Transient shock after successful resuscitation:Clinical evidence for post-cardiac arrest myocardial stunning.J Am Coil Cardiol,2000;35(suppl A):399A
41 James T.Niemann,Daniel Garner,Roger J.Lewis.Tumor necrosis factor-a is associated with early postresuscitation myocardial dysfunction[J].Crit Care Med,2004;32(8):1753-1758
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