肿瘤坏死因子-α对心脏交感神经节的影响

目的探究肿瘤坏死因子-α(TNF-α)对心脏交感神经节的影响。方法 14只成年犬随机分为两组:实验组7只,将0.1ml TNF-α(0.1mg/ml)分别局部微量注射进入左侧心脏交感神经节(LSG)、右侧心脏交感神经节(RSG);对照组7只,将同等量的生理盐水分别局部微量注射进入LSG和RSG。电压递增式高频电刺激(频率20Hz,脉宽0.1ms)作用于LSG、RSG可分别引起血压升高、心率加快,以最大收缩压(SBP)改变代表LSG功能,以心率变化代表RSG功能。微电极固定在LSG、RSG之后,使用labChart Pro软件记录并分析神经活性的频率和振幅。分别记录基础状态和干预30min后LSG、RSG的神经功能和活性。结果与基础状态相比,实验组30min后LSG和RSG功能及神经活性显著升高(P0.05),而对照组以上指标未见显著性改变(P0.05)。30min后,实验组LSG、RSG功能和神经活性均明显高于对照组(P0.05)。结论 TNF-α可显著增强心脏交感神经节的功能和活性。     

星状神经节切除对压力超负荷致心力衰竭大鼠的影响

目的观察切除左侧星状神经节(left stellate ganglion, LSG)或右侧星状神经节(right stellate ganglion, RSG)对大鼠心力衰竭的影响及区别。方法取雄性SD大鼠30只, 采用随机数字表法分为对照组、LSG组、RSG组3组, 每组各10只。3组均行腹主动脉缩窄术, 建立压力超负荷心力衰竭大鼠模型;LSG和RSG组分别通过手术钝性分离并切除LSG或RSG, 对照组不做此处理。记录3组大鼠术前、术后30 min及术后10周血压、心率的变化;术前及术后10周行超声心动图检查, 检测心室间隔厚度、左心室后壁厚度、左心室舒张末期内径和容积, 并计算左心室短轴缩短率和射血分数, 判断大鼠心功能的状态;术后10周取大鼠心脏标本, 行HE染色和Masson染色观察心肌肥厚和心肌纤维化程度, 判断心室重构情况。结果术后30 min, 对照组、LSG组、RSG组大鼠的心率分别为(352.4±4.3)、(320.3±4.0)和(297.9±5.9)次/min, 血压分别为(142.8±2.3)、(123.4±2.7)和(129.6±2.9)mmHg(1 mmHg=...     

白细胞介素1β对左侧星状神经节功能和活性的影响

目的探索白细胞介素1β(IL-1β)对正常犬左侧星状神经节(LSG)功能和活性的影响。方法 12只健康成年杂种犬随机分为IL-1β组(n=6)和对照组(n=6)。IL-1β组给予LSG局部微注射20μg/ml IL-1β0.1ml,而对照组给予LSG局部微注射等量0.9%生理盐水。在基础状态和LSG局部微注射30min后分别记录在高频电刺激(HFS:频率20Hz,脉宽0.1ms)LSG时的血压改变(反应LSG功能)及LSG神经活性。结果在基础状态下,HFS刺激LSG所引起的血压升高作用和LSG神经活性在IL-1β组和对照组中无显著统计学差异(P0.05)。但在注射IL-1β30min后,与对照组相比,LSG神经活性显著升高[频率:(122±6)次/分vs(56±7)次/分;振幅:(0.24±0.05)mV vs(0.09±0.02)mV,P0.05],HFS刺激LSG引起的最大血压改变明显增强[以25V电压强度刺激为例,(75.0±7.0)%vs(45.5±4.6)%,P0.05]。结论 IL-1β可显著增强LSG功能及神经活性。     

不同节段肾动脉交感神经刺激对心脏自主神经活性的影响

目的探讨高频刺激不同节段肾交感神经对右前心房自主神经节(ARGP)和右侧星状神经节(RSG)活性的影响。方法 18只成年犬随机分为肾动脉近端刺激组(n=6)、远端刺激组(n=6)和假刺激组(n=6)。在X线影像指导下,将3F刺激电极导管分别送至肾动脉的相应节段行高频电刺激或假刺激。分别在基础状态和高频刺激时测定心率、动脉血压、以及ARGP和RSG的放电频率和振幅。结果近端刺激组的犬在高频刺激时心率增加[(145±7)次/分vs(140±6)次/分,P0.05]、动脉血压升高[(128±7)/(88±8)mmHg vs(115±5)/(78±6)mmHg,P0.05],以及ARGP和RSG的放电频率[ARGP:(90±8)次/分vs(51±8)次/分;RSG:(64±13)次/分vs(31±8)次/分,P0.05]和放电振幅[ARGP:(0.80±0.09)mV vs(0.47±0.06)mV;RSG:(0.65±0.07)mV vs(0.39±0.07)mV,P0.05]也显著性增加;而远端刺激组和假刺激组的以上指标均无显著性改变(P0.05)。结论肾动脉近端的交感神经对心脏自主神经系统影响最为显著。     

内皮素-1对心脏右侧星状神经节功能和活性的影响

目的探究内皮素-1(ET-1)对正常犬心脏右侧星状神经节(RSG)功能及神经活性的影响。方法 12只成年犬随机均分为两组:ET-1组(n=6,给予RSG局部微注射0.15μmol/ml ET-1 0.1ml)和对照组(n=6,给予RSG局部微注射等量0.9%生理盐水)。两组动物均于麻醉后行右侧开胸术,暴露RSG。分别在基础状态和注射ET-1或生理盐水30min后检测RSG在高频电刺激(HFS,频率:20 Hz,脉宽:0.1 ms)下,最大窦性心率(sinusrate,SR)的变化情况,此即RSG功能。在相同时间点记录RSG的神经活性。结果在基础状态下,HFS刺激RSG引起的最大SR改变和RSG神经活性在ET-1组和对照组中无差异(P>0.05)。但在RSG局部注射ET-1 30min后,与对照组相比,RSG的功能显著增强[20V:(46.0±4.2)%vs(37.7±5.6)%,P<0.05],HFS刺激RSG引起的最大SR改变也明显增强[频率:(95±11)次/分vs(33±7)次/分;振幅:(0.20±0.04)mV vs(0.10±0.04)mV,P均<0.05]。结论 ET-1可显著增强RSG的功能及神经活性。     

低频电磁场刺激对左侧星状神经节功能的影响

目的研究低频电磁场(LF-EMF)刺激左侧星状神经节(LSG)对其功能和神经活性的影响及其机制。方法16只健康成年家犬随机分为LF-EMF组(n=8)和对照组(n=8),电磁场刺激仪刺激探头固定至家犬左侧第二、三肋与脊柱连接的皮肤表面定位于LSG,参数设置:刺激频率:1 Hz,刺激模式:开启8s,暂停5s,刺激时间:2h。LF-EMF组接受电磁场刺激,对照组接受假刺激。在基础状态和2hLF-EMF后分别测定LSG神经活性和高频电刺激(HFS:频率20Hz,脉宽0.1ms)LSG时的血压改变,实时定量聚合酶链反应检测LSG中2型小电导钙激活钾通道分子(SK2)、早期原癌基因(c-fos)和神经生长因子(NGF)mRNA表达水平。结果基础状态时,HFS刺激LSG引起的血压升高作用和神经活性在对照组和LL-EMF组中未见统计学差异;但2hLF-EMF刺激后,相比于对照组,LF-EMF组中HFS刺激LSG引起的血压升高作用明显被抑制(32%±5%vs 43%±5%,P0.05),LSG神经活性显著降低[频率:(17±5)次/分vs(30±6)次/分;振幅:(0.08±0.02)mV vs(0.16±0.02)mV,P0.05)],同时LSG中SK2mRNA表达水平明显增高(1.64±0.12vs 1.00±0.09,P0.05),c-fos和NGF mRNA表达水平明显降低(c-fos:0.54±0.07vs 1.0±0.1,P0.05;NGF:0.67±0.08vs 1.0±0.16,P0.05)。结论 LF-EMF可通过调控神经相关蛋白表达水平抑制LSG功能及活性。     

消融Marshall韧带减少心肌梗死后室性心律失常的实验研究

目的研究射频消融Marshall韧带(LOM)远段对犬急性心肌梗死(简称心梗)后室性心律失常的影响。方法实验一:记录10只健康成年雄性犬基础状态血压、心率、心率变异性性、心室有效不应期及左侧星状神经节刺激引起血压升高的程度。测量结束后,将多极电极贴于LOM表面以记录到其电位确认消融部位后行射频消融,30min后重复测量上述指标,比较消融前后的变化。实验二:25只健康成年雄性犬随机分为对照组(不消融,n=13)、消融组(LOM远段消融,n=12),对照组仅将消融电极置于LOM远段但不给予消融能量,消融完成后结扎冠状动脉左前降支构建急性心梗模型,监测1h内室性心律失常事件。实验结束后,大体神经解剖观察LOM神经通路及走行,取正常LOM组织做苏木精-伊红(HE)和免疫组织化学染色。结果实验一:与基础状态相比,消融LOM远段可降低交感神经张力、减弱刺激LSG时血压上升幅度、延长心室有效不应期。实验二:与对照组相比,消融组心梗后室性早搏的次数、非持续性室性心动过速事件和持续时间均明显减少。大体解剖显示LSG与LOM之间有神经纤维联系,且免疫组化结果证实LOM远段富含交感神经纤维。结论 LOM远段富含交感神经,可能是LSG连接心室的交感神经解剖通路。消融LOM远段可降低心脏交感神经活性,抑制LSG功能,减少急性心梗后室性心律失常事件的发生。     

白细胞介素17A对右侧星状神经节功能和活性的影响

目的研究白细胞介素17A(IL-17A)对右侧星状神经节(RSG)功能和神经活性的影响。方法 16只健康成年杂种犬静脉麻醉后随机分为实验组(n=8)和对照组(n=8)。分离RSG,在实验组中,向RSG中注射0.1ml IL-17A(25μg/ml),对照组注射等量的生理盐水。在基础状态和注射后30min后分别测定高频电刺激(HFS:频率20Hz,脉宽0.1ms)RSG时的心率变化以及RSG神经活性。同时实验结束后留取RSG组织用于检测早期原癌基因(c-fos)和神经生长因子(NGF)表达水平。结果实验组干预后心率加快作用明显增强(40V:57%±9%vs 40%±8%,P0.05),RSG神经活性显著增强[频率:(148±22)次/分vs(48±10)次/分;幅度:(0.09±0.01)mV vs(0.04±0.01)mV,P均0.05],同时RSG组织中c-fos和NGF表达水平明显升高(c-fos:0.58±0.08vs 0.55±0.09;NGF:0.16±0.04vs 0.11±0.03,P均0.05);而对照组以上指标无明显改变。结论 IL-17A可增强RSG功能和神经活性,增加神经相关蛋白表达水平。     

选择性去心脏交感传入神经对犬急性心肌梗死后室性心律失常的影响

目的探讨选择性去心脏交感传入神经(SCSAD)对犬急性心肌梗死(AMI)后自主神经功能、心室电生理特性和室性心律失常的影响。方法 24只成年雄性杂种犬随机分为对照组(n=8)、AMI组(n=8)和SCSAD组(n=8)。SCSAD组犬心外膜给予树胶脂毒素。对照组和AMI组犬心外膜涂抹不含树胶脂毒素的溶剂。AMI组与SCSAD组通过结扎冠状动脉(简称冠脉)左前降支建立AMI模型,对照组只分离穿线,不结扎冠脉。于结扎冠脉后15 min检测心率变异性(HRV),记录结扎后1 h室性心律失常的发生情况,对照组于相应时间点检测。ELISA法检测血清去甲肾上腺素(NE)水平。于结扎冠脉后1 h依次采用S_1S_2程控刺激测量心室有效不应期(ERP),S_1S_1 300 ms起搏测量单相动作电位(MAP)和S_1S_1动态起搏法测量动作电位时程(APD)电交替起搏周长。通过不同电压直接电刺激左侧星状神经节(LSG)后的最大收缩压变化百分比评价LSG功能。蛋白免疫印记法(Western blot)检测各组新鲜LSG组织的c-fos和神经生长因子(NGF)的表达。结果与对照组相比,AMI组HRV明显降低,SCSAD组较对照组和AMI组升高。相比对照组,AMI组和SCSAD组室性早搏发生增多,而SCSAD组较AMI组减少。与AMI组相比,SCSAD组室性心动过速发生减少,且SCSAD组与对照组相比无差异。与对照组相比,AMI组和SCSAD组血清NE水平升高,SCSAD组较AMI组低。与对照组相比,AMI组结扎后其缺血区心室ERP和MAP缩短,APD电交替起搏周长延长。SCSAD组较AMI组ERP和MAP延长,APD电交替起搏周长缩短,且SCSAD组较对照组ERP延长,MAP和APD电交替起搏周长无差异。AMI组LSG功能比对照组增强,SCSAD组较对照组和AMI组LSG功能减低。AMI组c-fos表达比对照组高,NGF表达二者无明显差异,而SCSAD组c-fos和NGF表达比AMI组低。结论 SCSAD降低AMI后心脏交感神经活性,提高心脏电生理稳定性,减少室性心律失常的发生。     

低强度神经节丛刺激对正常心室电生理性质和急性心肌缺血室性心律失常发生的影响

目的 研究低强度神经节丛(GP)刺激对正常心室电生理性质和急性心肌缺血室性心律失常发生的影响.方法 体重18～25kg的正常成年杂种犬39只随机分为正常心脏组(n=12)和急性心肌缺血组(n=27,其中对照组12只,低强度GP刺激组15只),以2根多极电生理导管记录左、右心室局部电图,以自制Ag-AgC1电极记录左、右心室单相动作电位.在正常犬,分别在6h低强度GP刺激前和刺激后测量心室各部位有效不应期(ERP)、动作电位时限(APD),APD回复性质和APD交替以及血清乙酰胆碱和去甲肾上腺素浓度;在急性心肌缺血犬,比较室性心律失常的发生情况.结果 在正常犬,6h低强度GP刺激显著延长心室各部位ERP及APD(P＜0.05),但未改变其空间离散度;6h低强度GP刺激促进APD交替发生但不改变APD回复曲线斜率及其空间离散度;6h低强度GP刺激后血清去甲肾上腺素和乙酰胆碱水平均显著增加(P＜0.05).在急性心肌缺血犬,低强度GP刺激组室性心律失常的发生率显著低于对照组(P＜0.05).结论 低强度GP刺激不增加正常心脏室性心律失常的风险且有助于抑制急性心肌缺血心脏室性心律失常的发生.     

Effect of the stellate ganglion on atrial fibrillation and atrial electrophysiological properties and its left-right asymmetry in a canine model

OBJECTIVE:

To investigate the effect of the stellate ganglion (SG) and its left-right asymmetry on atrial fibrillation (AF) inducibility, AF duration and atrial electrophysiological properties.

METHODS:

Sixteen adult mongrel dogs were randomly assigned to three groups. The control group (n=4) underwent 6 h rapid atrial pacing (RAP) only; the right SG (RSG) group (n=6) underwent 6 h RSG stimulation plus RAP; and the left SG (LSG) group (n=6) underwent 6 h LSG stimulation plus RAP. AF induction rate, AF duration, effective refractory period (ERP) and dispersion of ERP (dERP) were measured.

RESULTS:

In the RSG group, the induction rate of AF was significantly increased in sites in the right atrium (RA) compared with baseline (P<0.05). In the LSG group, the induction rate of AF was significantly increased (P<0.05) compared with baseline in the left atrium (LA), left superior pulmonary vein and left inferior pulmonary vein, respectively. Compared with RSG stimulation, right stellate ganglionectomy markedly decreased the AF induction rate of the RA (P<0.05). Compared with LSG stimulation, left stellate ganglionectomy markedly decreased the AF induction rate of the LA, the left superior pulmonary vein and the left inferior pulmonary vein (P<0.05). In the RSG group, the ERP was significantly shortened (P<0.05) and the dERP was significantly increased (P<0.05) in RA sites (P<0.05). The ERP was significantly shortened in the LSG group (P<0.05). The dERP was significantly increased (P<0.05) in LA and pulmonary vein sites (P<0.05).

CONCLUSIONS:

Unilateral electrical stimulation of the SG in combination with RAP can successfully establish a canine model of acute AF mediated by excessive sympathetic activity. SG stimulation facilitates AF induction and aggravates electrical remodelling in sites in the atrium and pulmonary vein. Inhibiting sympathetic nerve activation through unilateral stellate ganglionectomy can reduce AF initiation.     

Modulation of QT interval by cardiac sympathetic nerve sprouting and the mechanisms of ventricular arrhythmia in a canine model of sudden cardiac death

INTRODUCTION: We previously reported that there is a high incidence of sudden cardiac death (SCD) in dogs with myocardial infarction (MI), complete AV block (CAVB), and nerve growth factor (NGF) infusion to the left stellate ganglion (LSG). Whether or not QT interval prolongation underlines the mechanism of SCD was unclear. METHODS AND RESULTS: We analyzed QT intervals in three groups of dogs. All dogs had CAVB and MI. The LSG group (n = 9) and right stellate ganglion (RSG) group (n = 6) received NGF infusion via the osmotic pumps over a 5-week period to LSG and RSG, respectively. The control group (n = 6) received no NGF. The dogs either died suddenly or were sacrificed within 2 to 3 months after MI. Heart rhythm and QT and RR intervals were monitored using implantable cardioverter defibrillator ECG recordings. There was a time-dependent increase of QTc intervals in the LSG group and a time-dependent decrease of QTc intervals in the RSG group. At the end of NGF infusion, QTc intervals in the LSG group (408 +/- 41 msec) were significantly longer than those in the control (350 +/- 41 msec; P < 0.05) and RSG groups (294 +/- 23 msec; P < 0.01). In the LSG group, 4 of 9 dogs died of SCD. There was no SCD in either the RSG or control group. Immunocytochemical staining showed NGF infusion to LSG and RSG resulted in left and right ventricular sympathetic nerve sprouting and hyperinnervation, respectively. CONCLUSION: NGF infusion to the LSG in dogs with MI and CAVB resulted in increased QT interval and incidence of ventricular tachycardia, ventricular fibrillation, and SCD, whereas NGF infusion to the RSG shortened QT interval and reduced the incidence of ventricular tachycardia. These findings indicate that QT interval prolongation is causally related to the occurrence of ventricular arrhythmia in dogs with nerve sprouting, MI, and CAVB.     

A new electrocardiographic marker for sympathetic nerve stimulation: modulation of repolarization by stimulation of stellate ganglia

Activation of cardiac sympathetic nerves alters ventricular repolarization; however, these changes remain poorly characterized. The goal of this study was to examine effects of sympathetic stimulation on repolarization to identify electrocardiographic markers of sympathetic activation. Pigs underwent median sternotomy and bilateral thoracotomy to expose the stellate ganglia. Changes in T-wave duration, amplitude, repolarization vector, and time from peak to end (Tp-Te) were continuously monitored. Within 15 seconds of unilateral left or right stellate ganglion (LSG/RSG) stimulation, T-wave amplitude increased 6- and 4.5-fold, respectively, in lead aVF. T-wave duration and Tp-Te both increased 200% during LSG stimulation but only 50% and 30%, respectively, with RSG stimulation. During LSG stimulation, frontal and horizontal T-wave vectors, respectively, changed from 1.9° ± 22.8° and 333.8° ± 9.7° at baseline to 83.4° ± 3.9° (inferiorly) and 306.7° ± 1.8° (posteriorly). During RSG stimulation, frontal and horizontal T-wave vectors changed from 348.2° ± 21.6° and 333.8° ± 10.3° before stimulation to 280.7° ± 4.6° (superiorly) and 118.1° ± 5.6° (anteriorly). During stellate stimulation, T-wave vectors are displaced to angles specific for LSG activation (posteroinferiorly) or RSG activation (anterosuperiorly); T-wave amplitude, duration, and Tp-Te increase; and ST-duration decreases. Displaced repolarization vector and changes in T-wave morphometrics provide a novel marker of unilateral sympathetic nerve stimulation.     

Differential β-adrenoceptor expression induced by nerve growth factor infusion into the canine right and left stellate ganglia

BACKGROUND: Nerve growth factor (NGF) infusion into the right stellate ganglion (RSG) is antiarrhythmic, while NGF infusion into the left stellate ganglion (LSG) is proarrhythmic in dogs with myocardial infarction (MI) and complete atrioventricular block (CAVB). This functional asymmetry suggests differential neural remodeling. OBJECTIVES: To test the hypothesis that NGF infusion into the RSG and the LSG can lead to differential beta-adrenoceptor (beta-AR) expression in dogs with MI and CAVB. METHODS AND RESULTS: We performed immunostaining to quantify beta(1)-AR and beta(3)-AR immunoreactivity in six dogs with MI and CAVB, nine dogs with MI, CAVB, and NGF infusion to the LSG, six dogs with MI, CAVB, and NGF infusion to the RSG, and six normal dogs. There was significantly increased beta(3)-AR immunoreactivity in dogs with NGF infusion into the LSG and significantly decreased beta(3)-AR immunoreactivity in dogs with NGF infusion into the RSG compared with controls and with the MI and CAVB group. There were no significant differences in beta(1)-AR immunoreactivity among these four groups. To determine protein and mRNA expression of beta-ARs, we created MI and CAVB and infused NGF into the LSG in six additional dogs. The noninfarcted left ventricle free wall was harvested 1 week later. The protein level and receptor density of beta(3)-AR (but not beta(1)- or beta(2)-AR) significantly increased in these six dogs compared with normal controls. CONCLUSIONS: We conclude that NGF infusion into the RSG and the LSG in dogs with MI and CAVB induced differential beta(3)-AR expression in the left ventricular myocardium.     

右侧星状神经阻滞对大鼠体外循环微循环的影响

目的：研究右侧星状神经节阻滞（ SGB）对大鼠体外循环（ CPB）转流期间微循环变化的影响。方法选用20只SD大鼠随机分为体外循环组（C组）10只,右侧行星状神经节阻滞＋体外循环组（RC组）10只。两组转体循环后转流1 h。在转流前,定于动脉静脉置管成功后为T0;体外循环转流开始后30 min为T1;体外循环后1 h为T2。3个时间点观察两组大鼠的血压、心率、血气及乳酸含量,计算动静脉血氧分压差（ Pa-vO2）。结果两组大鼠乳酸、Pa-vO2和血压不同时间点差异有统计学意义（ P＜0.05）;两组心率、乳酸和Pa-vO2的组间和分组间有交互作用（P＜0.05）;两组心率和乳酸的组间差异有统计学意义（P＜0.05）。结论SGB能改善大鼠体外循环后的灌注,可提高机体的摄氧能力,改善机体的微循环。     

Effects of thoracic spinal cord stimulation on cardiac autonomic regulation of the sinus and atrioventricular nodes

INTRODUCTION: Thoracic spinal cord stimulation (SCS) has been used to treat angina pectoris and to produce cardiac autonomic control. We studied the effect of thoracic SCS on sinus node and AV nodal function to test the hypothesis that SCS modulated autonomic regulation of the electrophysiology of these structures. METHODS AND RESULTS: The effects of thoracic SCS on sinus cycle length and AH interval were studied in 47 dogs in five experimental groups: group 1: intact autonomic nerves; group 2: bilateral ansae subclaviae transection and efferent stellate stimulation; group 3: ansae transection, bilateral vagi transection, and efferent stellate stimulation; group 4: bilateral vagi transection and efferent vagal stimulation; and group 5: bilateral vagal stimulation and bilateral ansae subclaviae transection. Under fluoroscopic guidance, the spinal stimulator electrode was advanced to the T1-T2 position and threshold determined by adjusting the output to produce muscle contraction. Parameters were measured at baseline prior to SCS and during SCS, at 90% threshold. Ansae subclaviae and vagi nerves were isolated using standard approaches. Stellate and vagal stimulation were each performed using a constant current stimulator and at three different frequencies. Sinus cycle length and AH intervals (the latter at constant right atrial pacing of 400 msec) were measured with and without SCS at baseline and at each level of nerve stimulation. Nitric oxide was measured using the coronary sinus overflow method, from a luminal balloon catheter placed deep in the coronary sinus. SCS resulted in an increase in sinus cycle length from 507 +/- 23 msec to 544 +/- 22 msec (P = 0.02) and AH interval from 71 +/- 4 msec to 74 +/- 4 msec (P = 0.03). Ansae subclaviae transection had no effect on this increase, while vagal transection eliminated the increase in sinus cycle length and AH with SCS. The increase in these parameters with SCS was maintained during both stellate stimulation (group 2) and vagal stimulation (group 5) across all three levels of neural stimulation. CONCLUSION: SCS appears to enhance parasympathetic activity, mediated via the vagus. This may have implications for use of thoracic SCS to treat chronic angina and perhaps prevent sudden cardiac death.     

左侧神经节阻滞用于19例冠心病冠脉搭桥术患者效果观察

目的探讨左侧星状神经节阻滞（SGB）对冠心病冠脉搭桥术患者术中血浆内皮素、皮质醇、去甲肾上腺素的影响。方法将38例拟行冠状动脉搭桥术患者随机分为星状神经节阻滞组（SGB组）和对照组,分别用1％利多卡因和生理盐水10ml行左侧SGB,患者入室后局麻下放入Swan-Ganz导管,分别于入室后（T0）,SGB后5min（T1）、10min（T2）、15min（T3）,麻醉诱导气管插管即刻（T4）,切皮即刻（T5）和劈胸骨即刻（T6）各时间点抽静脉血分离血浆,放免法测血浆内皮素（ET）、去甲肾上腺素（NE）、皮质醇（COR）水平。结果SGB组SGB后10、15min血浆ET、NE显著降低（P〈0．05）;COR亦有下降趋势,但麻醉前后比较和两组间比较无统计学差异。结论单次左侧SGB对冠心病患者血浆ET、NE、COR改变有明显调节作用。     

零平衡超滤对老年冠状动脉搭桥围术期心肺功能的影响

目的评估体外循环（ECC）中采用零平衡超滤对老年冠状动脉搭桥围术期心肺功能的影响。方法选取拟行冠状动脉搭桥术患者20例，随机分为两组，超滤组和对照组。分别在术前0．5h（T1）、主动脉阻断后30min（T2）、ECC结束后1h（T3）、8h（T4）、24h（T5）、48h（T6）抽取静脉血，测定血浆肌酸肌酶同工酶（CK-MB）、心肌肌钙蛋白I（cTnI）、肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）的水平．监测并记录T1～T6各时间的肺泡-动脉血氧分压差P（A-a）O2，并记录患者心脏自动复跳率及术后恢复情况。结果超滤组患者心脏自动复跳率明显高于对照组；超滤组术后机械通气时间及ICU停留时间显著短于对照组（P〈0．05）；两组患者ECC后CK-MB、cTnI、TNF-α、IL-6血浆浓度均有不同程度升高，但超滤组患者血浆CK—MB、IL-6浓度在T2～T6均低于对照组（P〈0．01或P〈0．05）．超滤组cTnI浓度在T2～T5、TNF-α浓度在T3～T5低于对照组（P〈0.05）；超滤组肺泡-动脉血氧分压差在T3低于对照组（P〈0．05）。结论ECC中采用零平衡超滤对老年冠状动脉粥样硬化性心脏病患者的心肺功能有一定程度的保护作用。     

Spontaneous stellate ganglion nerve activity and ventricular arrhythmia in a canine model of sudden death.

BACKGROUND: Little information is available on the temporal relationship between instantaneous sympathetic nerve activity and ventricular arrhythmia in ambulatory animals. OBJECTIVE: The purpose of this study was to determine if increased sympathetic nerve activity precedes the onset of ventricular arrhythmia. METHODS: Simultaneous continuous long-term recording of left stellate ganglion (LSG) nerve activity and electrocardiography was performed in eight dogs with nerve growth factor infusion to the LSG, atrioventricular block, and myocardial infarction (experimental group) and in six normal dogs (control group). RESULTS: LSG nerve activity included low-amplitude burst discharge activity (LABDA) and high-amplitude spike discharge activity (HASDA). Both LABDA and HASDA accelerated heart rate. In the experimental group, most ventricular tachycardia (86.3%) and sudden cardiac death were preceded within 15 seconds by either LABDA or HASDA. The closer to onset of ventricular tachycardia, the higher the nerve activity. The majority of HASDA was followed immediately by either ventricular arrhythmia (21%) or QRS morphology changes (65%). HASDA occurred in a circadian pattern. HASDA occurred twice as often in the experimental group than in the control group. Electrical stimulation of LSG increased transmural heterogeneity of repolarization (Tpeak-end intervals) and induced either ventricular tachycardia or fibrillation in the experimental group but not in the control group. Immunohistochemical studies revealed increased synaptogenesis and nerve sprouting in the LSG in the experimental group. CONCLUSION: Two distinct types of LSG nerve activity (HASDA and LABDA) are present in the LSG of ambulatory dogs. The majority of malignant ventricular arrhythmias are preceded by either HASDA or LABDA, with HASDA particularly arrhythmogenic.     

罗格列酮对哮喘大鼠引哮喘发作潜伏期的影响

目的 观察过氧化物酶体增殖物活化受体γ(PPARγ)配体罗格列酮(RSG)对支气管哮喘(哮喘)大鼠气道哮喘发作潜伏期的影响.方法 SD大鼠75只,分为正常对照组(A组)、哮喘组(B组)、RSG治疗组(C组),每组25只.制备各组大鼠体外去上皮气管环,比较在0.05 mmol·L-1、0.5 mmol·L-1、5.0 mmol·L-1浓度梯度乙酰胆碱(ACh)激发下,各组大鼠体外气管环收缩张力大小.观察三种浓度0.01 mmol·L-1、0.1 mmol·L-1、1.0 mmol·L-1RSG对A、B两组大鼠体外气管环的ACh量效曲线的影响,比较各组大鼠引喘潜伏期差异.结果 三组大鼠引喘潜伏期分别为A组(121.50±17.44)s,B组(61.50±17.68)s,C组(94.40±21.17)s,差异有统计学意义(P＜0.05,n=20).三组大鼠气管环对三种浓度ACh的反应率,B＞C＞A组,差异有统计学意义(P＜0.05,n=20).RSG可引起A、B两组大鼠体外气管环ACh量效曲线右移.结论 RSG可延长哮喘发作潜伏期,降低气道收缩张力,可能具有减轻气道高反应性、减少哮喘发作的作用.