体外循环围术期冠状微循环的观测和意义

目的 :建立活体心脏微循环的观测方法 ,研究猪体外循环围术期冠状微循环的变化规律 ,探讨其临床意义。方法 :小型猪 12头建立体外循环 ,心脏停跳 45min ,再灌注 12 0min。以右心耳的心外膜作为微循环观测窗。分别于体外循环转流前、心脏停跳前、主动脉开放后 5、3 0、60和 12 0min六个时间点 ,用接触式显微镜连接在电视监测器屏幕上观测冠状微血管形态和微血流的动态变化 ;应用激光多普勒微循环血流计测定心肌微区灌流量。结果 :猪体外循环心肌再灌注后 5～60min ,冠状微动脉口径较缺血前显著缩小 (P <0 .0 1) ,微血管中出现搏动性颗粒状血流 ,并有血浆与血细胞分离现象 ,提示有明显的红细胞聚集与毛细血管前括约肌痉挛。再灌注 5～ 3 0min ,心肌微区灌流量亦较缺血前下降 (P <0 .0 5 )。结论 :体外循环心肌缺血 再灌注后出现了冠状微血管痉挛、微血流瘀滞和心肌微区灌流量的下降 ,冠状微循环障碍与体外循环术后心功能不全有一定的相关关系。     

心肌顿抑和冬眠的再认识

自“顿抑”和“冬眠”心肌概念的出现 ,现代心血管病学对存活心肌的评价也提出了新的更高的要求。本文就心肌顿抑和冬眠的再认识方面的一些进展情况作一综述。1　心肌顿抑的一般概念及研究进展心肌顿抑一般是指急性缺血和冠状动脉再灌注后延长的但可逆的缺血后左室收缩功能障碍的过程。心肌顿抑时节段性的功能障碍是由于缺血和再灌注两者共同造成的。Heyndrickx等 〔1〕1975年做的动物实验证实了此过程。研究者短暂闭塞了神志清醒狗的冠状动脉左前降支 ,并监测了心电图示踪和局部左室收缩功能 ,发现闭塞后 5～ 15 min冠状动脉血流迅速恢复 …     

心肌声学造影的发展及在冠心病诊治中的运用

心肌声学造影(Myocardial Contrast Echocardiography，MCE)在评价心肌微循环血流灌注，评定冠脉储备及冠脉血运重建后的疗效等方面的运用已成为一项十分重要的研究课题。MCE是指将含有微气泡的造影剂直接经冠状动脉或外周静脉注入，当微气泡通过心肌微血管床时，应用二维或多普勒超声技术使含血心肌的微气泡显像，以观察心肌血流灌注、冠脉血流储备。目前，它被认为是无创性评定心肌微循环灌注的最有潜力的工具。本文就近年来心肌声学造     

冠状静脉窦逆行灌注在双瓣置换术中的应用

目的 总结和分析二尖瓣、主动脉瓣置换手术中应用冠状静脉窦逆行灌注技术进行心肌保护.方法 30例患者分为两组:A组(顺灌联合逆灌技术)20例和B组(逆灌技术)10例.结果 术中转流平稳,血流动力学稳定,监测指标均在正常范围,无手术死亡和围手术期并发症.结论 采用冠状动脉顺行灌注联合冠状静脉窦逆行灌注或单纯采用冠状静脉窦逆行灌注心肌停搏液进行心肌保护,取得良好效果.     

冠状静脉窦逆行灌注和冠状动脉桥灌注在心脏外科手术的应用

目的 总结和分析心脏外科手术中应用冠状动脉顺行灌注联合冠状静脉窦逆行灌注和冠状动脉桥灌注技术进行心肌保护.方法 30例患者分为2组:A组(顺灌联合逆灌技术)20例和B组(顺逆灌结合桥灌技术)10例,疾病种类有:冠心病合并瓣膜病、冠心病合并室壁瘤、升主动脉病变合并主动脉瓣病变和单纯瓣膜病变.结果 术中转流平稳,血流动力学稳定,监测指标均在正常范围,无手术死亡和围手术期并发症.结论 采用冠状动脉顺行灌注联合冠状静脉窦逆行灌注或结合冠状动脉桥灌注心肌停搏液进行心肌保护,取得良好效果.     

芪丹通脉片对缺血/再灌注犬心肌微血管功能的影响

目的评价中药复方芪丹通脉片对急性缺血再灌注致心肌微血管功能的影响。方法应用12只健康犬,随机分为对照组(control)和芪丹通脉片治疗组(QDTMT treatment group),对照组经十二指肠给予生理盐水(1.5ml/kg),给药后30min分离冠状动脉左前降支,放置电磁流量计探头测定血流量,在其下缘左前降支1/2处结扎90min,松开后再灌注180min观察,分别于灌胃前、缺血90min和再灌注180min静脉快速均匀推入微泡声学造影剂SONOVUE,FLASH模式进行静脉声学造影,实时连续记录心肌声学造影前后的图像采用,采用Echopac图象工作站软件包进行分析心肌声学造影的图像视频密度,根据时间-视频密度曲线计算曲线下面积(area under curve,AUC)以评价心肌微血管的血流灌注状态,根据图像分析缺血心肌范围的影响。芪丹通脉片组则经十二指肠给予芪丹通脉片浸膏混悬液(1g/ml,1.5ml/kg),其余实验过程同对照组。并在不同时间点从冠状静脉窦采血,检测血清中NO和血浆中ET-1的含量。结果在基础状态、缺血前和缺血90min,对照组和芪丹通脉片干预组的时间-视频密度曲线计算曲线下面积(AUC)以及缺血后出现的灌注缺损所占左心室的百分比没有显著差异。然而再灌注180min两组的AUC存在显著差异(14.09±2.31 vs 11.47±1.55,P<0.05),左心室心肌灌流均没有完全恢复,但芪丹通脉片能够显著促进再灌注后心肌微循环灌流的恢复(92.10±2.2)%,与对照组(87.49±4.12)%比较,存在显著差异(P<0.05)。在缺血90min和再灌注180min,芪丹通脉片处理组血清中NO和血浆中ET-1分别为(68.98±10.01)μmol/L、(67.55±9.81)μmol/L和(114.73±11.89)μg/L,(139.97±12.36)μg/L,与对照组存在显著差异(56.38±8.27)μmol/L,(53.55±6.03)μmol/L和(137.40±13.48)μg/L,(161.90±19.14)μg/L,(P<0.05)。结论芪丹通脉片能够促进心肌缺血/再灌注后微循环血流的恢复,调节循环血中的NO和ET含量,改善微循环功能,抑制缺血/再灌注所致的心肌损伤。     

纳洛酮对缺血/再灌注损伤家兔心肌前列腺素代谢产物及再灌注血流的影响

目的 观察纳洛酮对缺氧心肌组织再灌注血流及前列腺素代谢产物生成的影响。方法 30只新西兰大白兔随机分为：再灌注组10只，结扎冠状动脉左前降支1h再开放4．5h；纳洛酮组10只，手术过程同前，同时静注纳洛酮；假手术组10只，手术过程同前，不结扎前降支动脉。用激光多谱勒血流测定仪测定再灌注组及纳洛酮组结扎前、后及稃灌注4．5h后缺血区心肌再灌注血流量：放射免疫法测定各组再灌注4．5h后的血浆6-酮-前列腺素F1α血栓素B，含量。结果 （1）结扎前，再灌注组及纳洛酮组局部心肌组织血流无差别；再灌注后，两组血流均较前下降，再灌注组的缺血区血流量明显低于纳洛酮组（P〈0．01）。（2）再灌注后，再灌注组、纳洛酮组血浆血栓素B1含量及血栓素B2／6-酮-前列腺素F1α比值显著高于假手术组，再灌注组又高于纳洛酮组，各组间血浆6．酮．前列腺素F1α含量无显著性差异。结论 纳洛酮可以抑制缺血／再灌注后家兔心肌血栓素B2的生成。改善再灌注部位血流。     

冠心病患者心肌声学造影定量分析的初步研究

拟探讨MCE定量分析在缺血性心脏病上的诊断价值。对10例临床诊断冠心病的患者行MCE,从时间-强度曲线中获得造影剂再灌注强度峰值(SIpeak),再灌注时间(Rt),再灌注率(b)和心肌血流量(SI×b)。同一检查对象不同心肌节段的4个参数(SIpeak、Rt、b和SI×b)均有统计学上的差异(P<0.05),对照组和观察组SIpeak具有统计学上的差异,SIpeak预测缺血性心脏病的ROC曲线下面积(AUC)为0.782,最佳临界值为64.4,以SIpeak≤64.4来预测缺血性心脏病,敏感性83.3%,特异性69.0%。利用超声造影匹配成像技术能够较满意地显示心肌灌注状态,初步研究表明通过MCE及Qontrast多参数定量分析软件可以评价心肌梗死区和缺血区的血流灌注缺损。SIpeak是预测缺血性心脏病的敏感指标。     

用ESR检测兔心肌顿抑时一氧化氮的动态变化

目的：用顺磁共振技术（ESR）测定兔在心肌缺血再灌注过程中心肌顿抑时，血液中一氧化氮（NO）动态变化。方法：结扎前降支制成心肌缺血-再灌注模型，经颈动脉左心室插管，多导生理仪记录左心室最大上升速率（dp/dt_max）、心室舒张末压力、动脉血压、心率等血液动力学指标。分别于缺血前、缺血5 min、10 min，再灌注5 min、10 min、30 min、60 min、90 min、120 min各时点取静脉血1 mL，在电子自旋共振仪记录NO波谱，测定NO水平。结果：在再灌注5 min、120 min时，NO浓度明显高于缺血前[(23.4±4.8) mm vs (12.0±0.5) mm，(21.4±1.8) mm vs (12.0±0.5) mm，P<0.01]。心肌收缩功能在缺血5 min时已经开始受损[(4965±295.6) mmHg/s vs (3967±315.3) mmHg/s，与缺血前比较P<0.01]，但是在再灌注5 min时明显低于缺血5 min时[(3327±120.4) mmHg/s vs(3967±315.3) mmHg/s，P<0.05]。结论：再灌注早期NO升高而心肌收缩力下降，提示NO对早期缺血再灌时心肌顿抑有加重作用。     

一种新的基于MCE的心肌微循环定量分析系统的研制

基于心肌声学造影(MCE)的心肌微循环定量分析系统,对实时MCE图像进行处理,通过非线性回归分析方法计算出心肌供血区内心肌血容量、血流速度、血流量以及三者的心内、外膜层跨壁梯度等冠脉微循环临床诊断指标,能有效满足临床需求,实现了实时MCE的定量分析.     

Regional contractile blockade at the onset of reperfusion reduces infarct size in the dog heart

An important mechanism of lethal myocardial reperfusion injury is the development of cellular hypercontracture at the onset of reperfusion. Hypercontracture can lead to cytolysis by mutual mechanical disruption of myocardial cells. 2,3-Butanedione monoxime (BDM) inhibits myofibrillar cross-bridge cycling and may therefore reduce infarct size in ischaemic reperfused myocardium. This study investigated whether a temporary presence of BDM protects against myocardial reperfusion injury in an intact-animal preparation. Anaesthetized open-chest dogs (n=10) underwent 1 h of left anterior descendent artery (LAD) occlusion and received intracoronary BDM (25 mM, n=5) or vehicle (n=5) for 65 min starting with an anoxic local infusion 5 min before reperfusion. Infarct size was assessed by triphenyltetrazolium staining after 6 h reperfusion. The infusion of BDM was accompanied by a transient reduction of left ventricular systolic pressure from 84.3±11.2 mm Hg during occlusion to 66.4±9.9 mm Hg at 30 min reperfusion (mean±SD, P<0.01 vs. control). LAD-flow and regional wall motion in the area at risk showed no difference between groups. Infarct size (% of area at risk) was reduced from 24.4±8.7 (control) to 6.6±2.0% (BDM) (P<0.01). The results demonstrate that development of necrosis in reperfused myocardium can be greatly reduced by temporary presence of the contractile inhibitor BDM at the onset of reperfusion.     

Changes in Passive But Not Active Mechanical Properties Predict Recovery of Function of Stunned Myocardium

The time course of alterations in active and passive mechanical properties of stunned myocardium during ischemia and throughout reperfusion has not been thoroughly quantified. This investigation tested the hypothesis that the amount of injury as well as the rate and extent of recovery of contractile function in postischemic, reperfused myocardium are directly correlated to changes in regional active and passive elastance and viscosity. A modified viscoelastic Voigt model was employed to quantify myocardial mechanical properties. Left ventricular pressure and segment length (in both ischemic and normal regions) were fit to the model consisting of an active elastic spring in parallel with a viscous damper and a passive elastic spring. The mechanical properties of myocardium from dogs which recovered (50%) baseline regional contractile function as determined by percent segment shortening (n=7) were compared to those from dogs that did not recover function (n=7). Both groups displayed decreased active elastance in the ischemic region during coronary artery occlusion, and this decrease was maintained in the nonrecovery group. Increases in viscosity of ischemic myocardium were observed in both groups during coronary occlusion but returned to control only in the recovery group. The nonrecovery group demonstrated increased passive elastance in the ischemic region during coronary occlusion and throughout the reperfusion period whereas the recovery group remained unchanged. We conclude that functional recovery of stunned myocardium is directly related to alterations in mechanical properties caused by ischemia and that changes in passive elastance during occlusion may predict the ability of ischemic myocardium to recover contractile function. © 1999 Biomedical Engineering Society. PAC99: 8719Rr, 8719Uv, 8710+e     

The protective effect of iloprost, a PGL2 analogue, on ultratructure of ischemic and reperfused myocardial myocytes.

Iloprost was used in experiments with dogs to investigate its ultrastructure-preserving effects on the myocardium during ischemia and reperfusion, focussed especially on the mitochondria. Ischemia was performed by ligation of the left anterior descending coronary artery (LAD) for 90 min followed by reperfusion of 180 min. Samples were taken from the ischemic and non-ischemic area before ligation of LAD, immediately after ischemia and reperfusion. Iloprost was applicated into the left femoral vein after the end of LAD ligation. Ultrastructural-morphometric analysis revealed that iloprost was able to diminish damages of the mitochondria after ischemia and reperfusion as well. Mitochondrial oedema and intramitochondrial structure degenerations (destruction of cristae and matrix) were minimized in contrast to results of unprotected animals, which had to undergo the same procedure as indicated by volume, volume densities of mitochondria, and of the intramitochondrial compartments, confirmed by independent secondary morphometric parameters. There were no remarkable differences between the corresponding parameters of mitochondria in the ischemic and non-ischemic area.     

Ca2+ sensitivity of stunned myocardium after skinning using retrograde infusion of detergent

Myofilament Ca2+ desensitization contributes to the contractile dysfunction of ischemic/reperfused ("stunned") myocardium. We examined the presence of reduced Ca2+ sensitivity of isometric force in chemically skinned fibers obtained from stunned myocardium using different modes of applying the detergent Triton X-100. Langendorff-perfused rat hearts underwent 20 min ischemia/20 min reperfusion, which caused a 35 +/- 3% decrease in left ventricular developed pressure, compared to continuously perfused control hearts. Stunned and control hearts were randomly allocated to two different permeabilization protocols: In group A, trabeculae were dissected and immersed in skinning solution containing 1% Triton X-100 for 20 min. Group B hearts remained fixed to the aortic cannula and skinning solution was infused retrogradely for 6 min prior to dissection of trabeculae. Extraction of cytosolic marker proteins was more complete in group-B than in group-A preparations. Group-A preparations from stunned hearts exhibited significant Ca2+ desensitization (pCa50 = 5.07 and 5.15 in stunned and control myocardium, respectively). In group B no such difference was observed, all preparations showing higher Ca2+ sensitivity and maximum force than group-A preparations (pCa50 = 5.32 in stunned versus 5.33 in control hearts). Prolonging group-A skinning to 150 min also abolished the difference in Ca2+ sensitivity between stunned and control myocardium. In conclusion, compared to a conventional protocol, skinning by perfusion results in more complete permeabilization and better preservation of myocardial contractile function. Ischemia/reperfusion at this moderate degree of contractile dysfunction induces Ca2+ desensitization at least partially by factors that can be extracted by thorough skinning.     

低浓度11,12-EET预干预对大鼠心肌缺血/再灌注损伤的影响

目的:观察外源性低浓度 11,12-EET预干预对大鼠在体心肌缺血/再灌注损伤的影响。方法:雄性Wistar大鼠,开胸,结扎和松开冠状动脉左前降支,复制心肌缺血/再灌注模型;采用缺血 5min/再灌注 5min两次造成缺血预处置。实验分 3组:对照组;缺血预处置组;外源性 11,12-EET预干预组。每组再分为A、B 2小组:A组动物心肌缺血 10min/再灌注 10min,主要观察缺血/再灌注各时程之心律失常;B组动物缺血 6 0min/再灌注 30min,主要观察缺血期心律失常、心功能的变化及再灌注后心肌梗死范围。结果:缺血预处置和 11,12-EET(6 2 4× 10^-8mol/L)预干预均可减轻缺血/再灌注心律失常及心功能的变化,降低心肌梗死范围。结论:11,12-EET预干预具有类缺血预处置样的心肌保护作用.     

内洋地黄素拮抗剂上调缺血再灌注损伤大鼠心肌细胞膜钠泵亚基的表达

目的： 观察内洋地黄素特异性拮抗剂地高辛抗血清对心肌缺血再灌注（MIR）损伤大鼠心肌组织内洋地黄素水平、钠泵活性、线粒体总钙浓度以及钠泵各亚基基因表达的影响，探讨内洋地黄素在心肌缺血再灌注损伤中的作用及其机制。方法: 将56只雄性SD大鼠随机分成7组，每组8只。假手术对照组（sham）：丝线穿过左冠状动脉前降支，但不结扎；缺血再灌注组（MIR）：结扎左冠状动脉前降支30 min，再灌注45 min；生理盐水组（NS）、维拉帕米组（Ver）、小剂量、中剂量、大剂量地高辛抗血清组（ADA）：于再灌注前5 min经股静脉分别注射生理盐水、维拉帕米5 mg·kg^-1、地高辛抗血清8.6 mg·kg^-1、 17.3 mg·kg^-1、34.5 mg·kg^-1，容积均为5 mL·kg^-1，5 min内注射完毕，其余同MIR模型组。再灌注结束后，立即取缺血区左室心肌检测心肌匀浆内洋地黄素水平、心肌细胞膜Na+ K+_ATP酶和Ca2+_Mg2+_ATP酶活性、线粒体总钙浓度；分别采用RT-PCR及Western blotting方法和免疫组化方法检测心肌钠泵α₁、α₂、α₃和β₁亚基mRNA及蛋白水平基因表达的改变。结果: 心肌缺血再灌注损伤时，心肌组织内洋地黄素水平明显升高，心肌细胞膜钠泵和Ca2+_Mg2+_ATP酶活性显著下降，线粒体总钙浓度升高，钠泵α₁、α₂、α₃和β₁亚基在mRNA及蛋白水平基因表达均明显下降；维拉帕米除具有降低线粒体总钙浓度外，对其它各项指标无明显影响。地高辛抗血清呈剂量依赖性地显著降低心肌组织内洋地黄素水平，恢复细胞膜钠泵和Ca2+_Mg2+_ATP酶活性，降低线粒体总钙浓度，上调钠泵α₁、α₂、α₃和β₁亚基mRNA及蛋白水平的基因表达。结论: 心肌缺血再灌注促进机体内洋地黄素分泌增加，后者通过下调心肌细胞膜上的钠泵α₁、α₂、α₃和β₁亚基基因表达抑制钠泵活性，进而抑制Ca2+_Mg2+_ATP酶活性，导致线粒体内钙超载，介导心肌缺血再灌注损伤。内洋地黄素特异性拮抗剂地高辛抗血清通过阻断内洋地黄素的生物学作用，上调钠泵各亚基的基因表达，发挥其抗心肌缺血再灌注损伤的作用。     

Early Changes in Myocardial Microcirculation in Asymptomatic Hypercholesterolemic Subjects: As Detected by Perfusion CT

Intramyocardial microvessels show functional changes in early stages of atherosclerosis prior to epicardial coronary artery stenosis. However, clinical CT does not have adequate spatial resolution to resolve the microvessels. To clinically detect changes in the function of the intramyocardial microcirculation, the spatial heterogeneity of the distribution of myocardial perfusion (F) and intramyocardial microcirculatory blood volume (Bv) was determined by perfusion CT. Two human subject groups were studied: (i) a “Control” group (24) with no risk factors nor evidence of coronary artery disease (CAD), and (ii) an “At-Risk” group (24) with hypercholesterolemia, but no evidence of CAD. In the perfusion CT image, a region of interest (ROI) covering the left ventricular myocardium was subdivided into multiple nested ROI (nROI) of equal size and used to compute F and Bv for each nROI. No significant differences between the groups were demonstrable in overall myocardial F, or Bv. The nROI data showed significantly increased spatial heterogeneity in the “At Risk” group when compared to “Control” subjects. This study demonstrates that subresolution distribution at the microcirculatory level can be quantified with myocardial perfusion CT and significant changes in these parameters occur in hypercholesterolemic subjects before they have developed significant changes in conventional perfusion parameters.     

再灌注对于实验性心肌梗塞家兔心功能的影响

开胸、全麻家兔在冠状动脉左室支结扎后随机分为两组:组Ⅰ,连续观察4小时不给与任何处理(n=9),组Ⅱ,冠脉结扎1小时后去除结扎线并继续观察3小时(n=10)。冠脉结扎前。后及再灌注后,同步、连续记录心电图、平均动脉压、左心室内压及心室内压变化速率。观察结束后处死动物测定心肌梗塞范围并取电镜标本。结果表明,冠脉结扎1小时引起上述各项指标显著抑制,与结扎前数值相比均具有显著性差异。再灌注后,组Ⅱ动物的心脏功能进一步下降,与组Ⅰ对应数据相比均具有显著性差异,且该组动物均伴有心肌内出血。比较两组动物的梗塞范围无统计学差异。再灌注的损害作用可能不仅仅是由于细胞水肿、出血等因素限制了冠脉血流的恢复;另外,毛细血管内及细胞中胞饮空泡的部分恢复可能促进了一些有害的大分子代谢产物的转运。     

钙敏感受体在大鼠心肌缺血/再灌注损伤的表达变化及与心肌损伤关系

目的： 观察钙敏感受体（CaSR）在大鼠心肌缺血/再灌注时的表达变化，揭示其与心肌缺血/再灌注损伤的关系。方法： Wistar大鼠随机分为5组：假手术组（sham组）、缺血再灌注1、2、4和6 h组（I/R 1 h、2 h、4 h、6 h组）。采用冠状动脉结扎和松结的方法，复制大鼠在体心肌缺血/再灌注损伤模型，记录左室收缩压（LVSP）和左室内压最大变化速率（±dp/dtmax），测定血清LDH、SOD活性和MDA含量，透射电镜观察心肌超微结构变化， RT-PCR法检测心肌组织中CaSR mRNA的表达变化。结果：LVSP、左室内压±dp/dtmax及SOD活性随再灌注时间延长而减低，LDH活性和MDA含量在再灌注2 h时最高；心肌超微结构损伤在再灌注1 h、2 h较重，随再灌注时间延长而减轻；大鼠心肌缺血/再灌注1 h、2 h心肌组织CaSR的mRNA表达升高，再灌注4 h、6 h后降低。结论： CaSR mRNA表达多时心肌损伤较重，CaSR可能参与了心肌缺血/再灌注损伤。     

参麦注射液对大鼠心肌缺血再灌注损伤的保护效应及其与热休克蛋白的关系

目的 :研究参麦注射液对大鼠心肌缺血再灌注损伤的保护效应以及与热休克蛋白 (HSP70 )的关系。方法 :用在体左冠状动脉前降支穿线结扎法制备心肌缺血再灌注模型。 60只SD大鼠分为三组 ,假手术组n =10只 ,缺血再灌注组n =2 5只 ,参麦注射液干预组n =2 5只。缺血 3 0min ,再灌注 12 0min。观察心肌梗死范围和心肌细胞超微结构变化 ,采用S P免疫组化法 ,检测HSP70 的表达。结果 :参麦注射液干预组与缺血再灌注组相比 ,缺血面积 ( % ) ( 3 8.3 6± 2 .62vs 42 .3 2±2 .2 8,P <0 .0 1) ;梗死面积 ( % ) ( 59.3 6± 2 .44vs 65.63± 1.68,P <0 .0 1)。HSP70 表达 ( 0 .13 8± 0 .0 2 2vs 0 .12 2± 0 .0 18,P <0 .0 1)。电镜下 ,缺血再灌注组 ,肌纤维挛缩 ,核固缩 ,线粒体嵴疏松 ,空泡形成。参麦注射液干预后 ,肌节清晰 ,线粒体嵴较密集 ,无明显空泡形成。结论 :参麦注射液能保护心肌超微结构 ,缩小缺血、梗死范围 ,其机制可能与HSP70 的表达增加有关