Thiopentone does not block ischemic preconditioning in the isolated rat heart

PURPOSE: Ischemic preconditioning protects the heart against subsequent prolonged ischemia by opening of adenosine triphosphate-sensitive potassium (K(ATP)) channels. Thiopentone blocks K(ATP) channels in isolated cells. Therefore, we investigated the effects of thiopentone on ischemic preconditioning. METHODS: Isolated rat hearts (n=56) were subjected to 30 min of global no-flow ischemia, followed by 60 min of reperfusion. Thirteen hearts underwent the protocol without intervention (control, CON) and in 11 hearts (preconditioning, PC), ischemic preconditioning was elicited by two five-minute periods of ischemia. In three additional groups, hearts received 1 (Thio 1, n=11), 10 (Thio 10, n=11) or 100 microg x mL(-1) (Thio 100, n=10) thiopentone for five minutes before preconditioning. Left ventricular (LV) developed pressure and creatine kinase (CK) release were measured as variables of myocardial performance and cellular injury, respectively. RESULTS: Recovery of LV developed pressure was improved by ischemic preconditioning (after 60 min of reperfusion, mean +/- SD: PC, 40 +/- 19% of baseline) compared with the control group (5 +/- 6%, P <0.01) and this improvement of myocardial function was not altered by administration of thiopentone (Thio 1, 37 +/- 15%; Thio 10, 36 +/- 16%; Thio 100, 38 +/- 16%, P=0.87-0.99 vs PC). Total CK release over 60 min of reperfusion was reduced by preconditioning (PC, 202 +/- 82 U x g(-1) dry weight) compared with controls (CON, 383 +/- 147 U x g(-1), P <0.01) and this reduction was not affected by thiopentone (Thio 1, 213 +/- 69 U x g(-1); Thio 10, 211 +/- 98 U x g(-1); Thio 100, 258 +/- 128 U x g(-1), P=0.62-1.0 vs PC). CONCLUSION: These results indicate that thiopentone does not block the cardioprotective effects of ischemic preconditioning in an isolated rat heart preparation.     

心麻液预处理的心肌保护效果

目的 研究Ｓｔ．Ｔｈｏｍａｓ晶体心麻液预处理和缺血预处理对大鼠缺血／再灌注心肌收缩功能的影响。方法 应用离体Ｌａｎｇｅｎｄｏｒｆｆ逆行灌注模型,观察晶体心麻液预处理的缺血预处理时心肌缺血及再灌注前后ＬＶＥＤＰ,ＤＰ,＋ｄｐ／ｄｔ－,ＣＦ冠脉流出液中蛋白含量和ＬＤＨ活性以及再灌注后心肌ＳＯＤ活性,ＭＤＡ和ＡＴＰ含量的变化。结果 在缺血期间,晶体心麻液预处理显著延迟了心肌缺血性挛缩的发生时间。     

Effects of ischemic preconditioning in human heart

BACKGROUND: The aim of this study is to investigate the effects of ischemic preconditioning (IP) on myocardium and the level of nitric oxide (NO) in patients undergoing aorta-coronary bypass surgery. METHODS: Twenty consecutive patients with coronary artery disease were subjected into two equal groups; the IP group and the control group. Following the onset of cardiopulmonary bypass in the study group, hearts were preconditioned with two 3-minute periods of cross-clamping separated by 2 minutes of reperfusion. In the control group, cardiopulmonary bypass was continued for 10 minutes without using cross-clamp. Arterial and coronary sinus blood samples were used to determine serum NO, malondialdehyde (MDA), creatine phosphokinase-MB (CKMB), and lactate dehydrogenase (LDH) levels. Need for defibrillation after cross-clamp removal, ECG changes, postoperative arrhythmias, ejection fraction, and fractional shortening rates were recorded as hemodynamic data. RESULTS: Serum NO level was higher in the study group 5 minutes after aortic clamp removal (199.3 +/- 92.7 vs. 112.2 +/- 35.8 micromol; p = 001). Serum MDA (2.55 +/- 0.4 vs. 4.06 +/- 0.5; etamol/ml; 5 minutes after the aortic clamp removal; p = 0.0002); CK-MB (22.8 +/- 2.5 vs. 37.4 +/- 4.1; U/L 12 hours after the operation, p < 0.0001), and LDH (501.8 +/- 46.7 vs. 611.4 +/- 128.3; IU/L 48 hours after the operation, p = 0.02) levels were significantly lower in the preconditioned group when compared with the control group. Also, need for electrical defibrillation was significantly lower in the study group; Ejection fraction (64.3 +/- 6.3 vs. 57.6 +/- 7.6; p = 0.04) and fractional shortening (31.7 +/- 3.9 vs. 26.2 +/- 4.0; p = 0.04) rates were better in the study group postoperatively. CONCLUSIONS: These data may suggest that cardioprotection by ischemic preconditioning offers higher NO production, a lower myocardial ischemia, and better functional recovery of the hearts in coronary artery surgery patients.     

Myocardial protection by ischemic preconditioning and delta-opioid receptor activation in the isolated working rat heart.

OBJECTIVE: delta-Opioid receptors are involved in the cardioprotective effect of ischemic preconditioning. This study was designed (1) to assess the protective capacities of ischemic preconditioning and the synthetic delta-opioid receptor agonist D-Ala(2)-D-Leu(5) enkephalin (DADLE) in a functionally oriented experimental model of ischemia and reperfusion and (2) to assess whether the effects of both protective measures are similarly blocked by naloxone, a nonspecific delta-opioid receptor antagonist. METHODS: Sixty-four isolated working rat hearts were subjected to 45 minutes of hypothermic ischemia at 30 degrees C followed by 25 minutes of normothermic reperfusion. Rats were pretreated with DADLE (1 mg/kg body weight intravenously), naloxone (3 mg/kg body weight intravenously), or a combination thereof within 60 minutes before onset of isolated heart perfusion. During the preischemic perfusion period, 8 hearts per group were preconditioned by one cycle of 5 minutes of normothermic global ischemia and subsequent reperfusion whereas another 8 served as nonpreconditioned controls. The postischemic functional recovery of hearts and their creatine kinase leakage were determined. RESULTS: Pretreatment with DADLE and ischemic preconditioning improved the postischemic recovery of aortic flow when compared with nonpreconditioning (57.7% +/- 4.0% and 60.8% +/- 4.3% vs 40.0% +/- 4.2% of preischemic baseline value, P <.001). Combined pretreatment with DADLE before ischemic preconditioning afforded additional aortic flow recovery compared with pretreatment with DADLE alone (68.6% +/- 3.3% vs 57.7% +/- 4.0% of preischemic baseline value; P =.038). With combined pretreatment, early postischemic creatine kinase release was lower than control in hearts without pretreatment (0.48 +/- 0.11 vs 0.80 +/- 0.12 IU/5 minutes per heart; P =.001). Naloxone abolished the beneficial functional effects of pretreatment with DADLE and ischemic preconditioning. CONCLUSIONS: Pharmacologic activation of delta-opioid receptors affords improvement of functional protection in isolated working rat hearts similar to that conferred by classic ischemic preconditioning. The combination of both pretreatments reduces ischemic cellular damage and further adds to postischemic functional recovery. These changes are reversed by naloxone, an observation providing evidence that ischemic preconditioning involves signaling through opioid receptors.     

Effect of lidocaine on ischaemic preconditioning in isolated rat heart

Background. Lidocaine is frequently used as an agent to treatventricular arrhythmias associated with acute myocardial ischaemia.Lidocaine is a potent blocker not only of sodium channels, butalso of ATP-sensitive potassium channels. The opening of thesechannels is a key mechanism of ischaemic preconditioning. Weinvestigated the hypothesis that lidocaine blocks the cardioprotectioninduced by ischaemic preconditioning. Methods. Isolated rat hearts (n=60) were subjected to 30 minof no-flow ischaemia and 60 min of reperfusion. Control hearts(CON) underwent no further intervention. Preconditioned hearts(PC) received two 5-min periods of ischaemia separated by 10min of reflow before the 30 min ischaemia. In three groups,lidocaine was infused at concentrations of 2, 10 or 20 µgml^–1 for 5 min before the preconditioning ischaemia. Leftventricular developed pressure (LVDP) and infarct size (IS)(triphenyltetrazolium choride staining) were measured as variablesof ventricular function and cellular injury, respectively. Results. PC reduced IS from 24.8 (SEM 4.1) % to 4.0 (0.7) %of the area at risk (P<0.05). Adding 2 or 10 µg ml^–1lidocaine had no effect on IS compared with PC alone (3.7 (0.7)%, 6.9 (1.8) %). Adding 20 µg ml^–1 lidocaine increasedIS to 14.1 (2.5) % compared with PC (P<0.05). Baseline LVDPwas similar in all groups (111.4 (2.1) mm Hg). Compared withCON, PC improved functional recovery (after 60 min of reperfusion;52.3 (5.9) mm Hg vs 16.0 (4.0) mm Hg, P<0.01). The improvedventricular function was not influenced by addition of 2 or10 µg ml^–1 lidocaine (47.3 (5.7) mm Hg, not significant;45.3 (7.3) mm Hg, not significant), but was blocked by the infusionof 20 µg ml^–1 lidocaine (22.5 (8.0) mm Hg, P<0.01vs PC). Conclusions. Lidocaine blocks the cardioprotection induced byischaemic preconditioning only at supratherapeutic concentrations.     

缺血后处理对大鼠离体心脏缺血再灌注损伤的作用

目的探讨缺血后处理对大鼠离体心脏缺血再灌注损伤的作用。方法24只Wistar大鼠,随机分为3组(n=8):正常对照组(C组)、缺血再灌注组(I/R组)、缺血后处理组(IPC组)。采用大鼠离体心脏Langendorff灌流模型,C组用K-H液灌注160min;I/R组全心缺血40 min,再灌注120 min; IPC组全心缺血40 min后,再灌注10 s,缺血10 s,反复6次,然后持续再灌注118 min。测定再灌注15、30、120 min时冠脉流量(CF)及冠脉流出液心肌肌钙蛋白I(cTnI)浓度,再灌注120 min时,取心肌组织,测定丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性,电镜下观察心肌细胞超微结构。结果缺血再灌注可导致CF降低,冠脉流出液cTnI浓度升高,心肌SOD活性下降,MDA含量升高,心肌细胞超微结构产生病理学改变,缺血后处理可减弱上述改变。结论缺血后处理减轻脂质过氧化反应,对大鼠离体缺血再灌注心脏产生保护作用。     

缺血预处理对兔离体心脏长期保存的心肌保护作用

目的　观察缺血预处理对离体心脏长期保存的心肌保护作用。方法　将 2 4只家兔随机分为 4组 ,每组 6只 ,分成空白对照组、预处理组、保存组和预处理后保存组。离体兔心脏用Langendorff装置灌注稳定后 ,分别给予缺血预处理后再灌注、心脏保存 1 8h后再灌注及缺血预处理后再经 1 8h保存后再灌注 60min ,观察左室收缩功能的恢复率、冠脉回流液中碱性磷酸激酶(CK)、乳酸脱氢酶 (LDH)的浓度以及心肌形态结构改变。结果　预处理组同空白对照组相比 ,各项指标差异无显著性 (P >0 .0 5)。单纯保存组同对照组相比 ,左室收缩功能明显减弱 ,冠脉回流液中心肌酶的漏出明显增加 ,光镜及电镜观察心肌损伤严重。而经预处理后再保存组 ,左室收缩功能的恢复率较单纯保存组有明显提高 [(51 .9± 7.5) %比 (36 .6± 4 .9) % ,P <0 .0 5] ,心肌酶漏出明显减少 [CK :(31 2± 52 )IU/L比 (642± 1 0 8)IU/L ;LDH :(2 9± 9)IU/L比 (76± 1 0 )IU/L ,P <0 .0 5] ,光镜及电镜观察 ,心肌损伤程度明显减轻。结论　缺血预处理过程本身对心肌细胞无明显损伤 ,是比较安全的 ;缺血预处理对离体心脏长期保存有明显的保护作用     

缺血预处理对大鼠离体心脏心肌线粒体功能的影响

目的研究缺血预处理（IPC）对大鼠离体心脏心肌线粒体功能的影响。方法SD大鼠72只，随机分为4组（n=18）：对照组（CON组）、缺血再灌注组（IR组）、缺血预处理组（IPC组）和5-羟葵酸（5-HD）拮抗IPC组（5-HD＋IPC组）。采用Langendorff装置建立大鼠离体心脏缺血再灌注模型，IPC组在全心停灌前，给予2次缺血预处理，每次缺血5min，间隔5min；5-HD＋IPC组预处理前灌注5-HD 10min。各组于平衡末、缺血前、再灌注30min各取6个心脏，分离心肌线粒体并测定线粒体呼吸控制率（RCR）、磷氧比（ADP／O2）、NADH氧化酶（NADH-OX）、琥珀酸氧化酶（SUC-OX）、细胞色素C氧化酶（CYTC-OX）的活性。结果与CON组比较，IR组、IPC组和5-HD＋IPC组再灌注30min RCR、ADP／O2、NADH-OX、SUC-OX和CYTC＋OX的活性降低（P〈0．05）；与IR组比较，IPC组和5-HD＋IPC组再灌注30min上述各指标升高（P〈0．05）；与IPC组比较，5-HD＋IPC组再灌注30min上述各指标降低（P〈0．05）。结论缺血预处理可改善大鼠离体心脏缺血再灌注时心肌线粒体的功能，其机制与mitoKATP的激活有关。     

Effects of ischemia and omeprazole preconditioning on functional recovery of isolated rat heart

Objective

The aim of this study was to compare protective effects of ischemic and potential protective effects of pharmacological preconditioning with omeprazole on isolated rat heart subjected to ischemia/reperfusion.

Methods

The hearts of male Wistar albino rats were excised and perfused on a Langendorff apparatus. In control group (CG) after stabilization period, hearts were subjected to global ischemia (perfusion was totally stopped) for 20 minutes and 30 minutes of reperfusion. Hearts of group II (IPC) were submitted to ischemic preconditioning lasting 5 minutes before 20 minutes of ischemia and 30 minutes of reperfusion. In third group (OPC) hearts first underwent preconditioning lasting 5 minutes with 100μM omeprazole, and then submitted 20 minutes of ischemia and 30 minutes of reperfusion.

Results

Administration of omeprazole before ischemia induction had protective effect on myocardium function recovery especially regarding to values of systolic left ventricular pressure and dp/dt max. Also our findings are that values of coronary flow did not change between OPC and IPC groups in last point of reperfusion.

Conclusion

Based on our results it seems that ischemic preconditioning could be used as first window of protection after ischemic injury especially because all investigated parameters showed continuous trend of recovery of myocardial function. On the other hand, preconditioning with omeprazole induced sudden trend of recovery with positive myocardium protection, although less effective than results obtained with ischemic preconditioning not withstand, we must consider that omeprazole may be used in many clinical circumstances where direct coronary clamping for ischemic preconditioning is not possible.     

Remifentanil preconditioning protects against ischemic injury in the intact rat heart

BACKGROUND: Opioid receptors mediate cardiac ischemic preconditioning. Remifentanil is a new, potent ultra-short-acting phenylpiperidine opioid used in high doses for anesthesia. The authors hypothesize that pretreatment with this drug confers cardioprotection. METHODS: Male Sprague-Dawley rats were anesthetized and the chest was opened. All animals were subjected to 30 min of occlusion of the left coronary artery and 2 h of reperfusion. Before the 30-min occlusion, rats received either preconditioning by ischemia (ischemic preconditioning, 5-min occlusion, 5-min reperfusion x 3) or pretreatment with remifentanil, performed with the same regime (3 x 5-min infusions) using 0.2, 0.6, 2, 6, or 20 microg.kg.min intravenously. The experiment was repeated with naltrindole (a selective Delta-opioid receptor antagonist, 5 mg/kg), norbinaltorphimine (a selective kappa-OR antagonist, 5 mg/kg), or CTOP (a selective mu-opioid receptor antagonist, 1 mg/kg) administered before remifentanil-induced preconditioning or ischemic preconditioning, respectively. Infarct size, as a percentage of the area at risk, was determined by 2,3,5-triphenyltetrazolium staining. RESULTS: There was a dose-related reduction in infarct size/area at risk after treatment with remifentanil that was similar to that seen with ischemic preconditioning. This effect was prevented or significantly attenuated by coadministration of a mu, kappa, or Delta-opioid antagonist. The infarct-sparing effect of ischemic preconditioning was abolished by blockade of kappa-opioid receptors or Delta-opioid receptors but not by mu-opioid receptors. CONCLUSION: Remifentanil mimics cardioprotection via all three opioid receptors. This differs from ischemic preconditioning, which confers cardioprotection via kappa- and Delta-, but not mu-opioid receptors. Part of the protective effect of remifentanil may be produced by mu-agonist activity outside the heart.     

Landiolol does not enhance the effect of ischemic preconditioning in isolated rat hearts

Purpose  

To determine the effect of landiolol on ischemic preconditioned rat hearts.     

糖尿病阻碍二氮嗪预适应对大鼠缺血再灌注心肌的保护作用

LVDP、+do/dtmax、-dp/dtmax恢复率明显增加(P<0.05).而糖尿病大鼠两组比较无明显差异(P>0.05).结论 糖尿病阻碍DPC对大鼠缺血再灌注心肌的保护作用,这一现象可能与心肌急性胰岛素抵抗有关.     

Effects of various protocols of ischemic preconditioning on rat tram flaps

We used rat transverse rectus abdominis musculocutaneous (TRAM) flaps to investigate whether the ischemic cycle duration and number of cycles influenced the effectiveness of ischemic preconditioning (IPC). First, the animals were divided into one control group and four treatment groups. Controls received no preconditioning; flaps with IPC were treated by two cycles of pedicel clamping and reperfusion for either 5 or 10 min. Then the best of IPC protocols in first part was selected, and flaps were subjected to one or three cycles of IPC before 4 h of normothermic ischemia. The preconditioned flap survival area had improved 2.5-3 times over that of the control area by postoperative day 7. Serum creatine phosphokinase (CPK), water content, and malondialdehyde (MDA) in muscle were significantly decreased in the preconditioned groups after 4 h of reperfusion. Especially, 2 and 3 cycles of the 10/5-min combination were more effective than other protocols of IPC.     

比较缺血后处理和缺血预适应对大鼠离体心的保护作用

目的比较缺血后处理和缺血预适应对离体大鼠心脏缺血再灌注损伤的保护作用并探讨其机制。方法大鼠随机分为4组：停灌／再灌组（I／R）；预适应组（IPC）；后处理组（Post-con）；预适应加后处理组（IPC＋Post-con），行Langendorff心脏灌流。观测血流动力学，心肌梗死面积，CK、LDH、SOD、MDA，超微结构，细胞凋亡，bcl-2和bax的表达。结果与I／R比较，IPC、Post-con和IPC＋Post-con均能显著减小梗死面积（分别为：46．34±2．80，24．20±2．31、24．40±2．39、25．58±3．15，P〈0．01），减少凋亡指数（分别为：1．84±0．44，1．02±0．41、1、10±0、37、0．96±0．27，P〈0．05），且3组之间指标差异无统计学意义（P〉0．05）。结论IPC和Post-con均能改善心脏缺血再灌注后的梗死面积，抗凋亡，但两者联合应用并不能产生更好的保护效果。     

Effects of hydrogen sulphide on ischaemia–reperfusion injury and ischaemic preconditioning in the isolated, perfused rat heart

OBJECTIVE: Hydrogen sulphide (H(2)S) protects the heart against ischaemia-reperfusion injury caused by low flow or local ischaemia. We hypothesised that: (1) H(2)S protects against global ischaemia-reperfusion injury of the heart, (2) H(2)S plays a mechanistic role in ischaemic preconditioning, and (3) H(2)S acts by phosphorylation of protein kinases. METHODS: Isolated, perfused rat hearts were used in two series. Series 1: group 1.1 (n=10), 40 min of ischaemia and 120 min of reperfusion, group 1.2 (n=7), like 1.1 except that 40 microM NaHS was added to the perfusate during stabilisation and throughout the experiment. Group 1.3 (n=10), like 1.1, but endogenously produced H(2)S was blocked by D,L-propargylglycine. Series 2: group 2.1 (n=10) control, 30 min of ischaemia followed by 120 min of reperfusion. Group 2.2 (n=10) ischaemic preconditioning before sustained ischaemia and 120 min of reperfusion. Group 2.3 (n=10) like 2.2 except of D,L-propargylglycine treatment like in group 1.3. Mitogen activated protein kinases including extracellular signal-regulated kinases (ERK 1/2), the stress-activated/c-Jun NH2 terminal kinases (JNK), P38, as well as protein kinase B/AKT (AKT), adenosine monophosphate dependent protein kinase (AMPK) and the inducible heat shock protein 72 were measured by Western blotting. Adenine nucleotides (ATP, ADP, and AMP) were measured by high-pressure liquid chromatography and energy charge was calculated. RESULTS: Infarct size was increased by D,L-propargylglycine (40+/-6 vs 27+/-10% in controls, p=0.03, Bonferroni post hoc test). There was a non-significant decrease in infarct size in the NaHS group (to 20+/-13%). Western blot analysis indicated an upregulation of heat shock protein 72 in the NaHS treated group and a reduced phosphorylation of AKT in the D,L-propargylglycine group. D,L-propargylglycine had no effect on ischaemic preconditioning or on phosphorylation of protein kinases (ERK, AKT, P38, JNK and AMPK) in preconditioned hearts. No difference in energy charge was found between groups, although ADP was increased in the NaHS-treated group. CONCLUSION: Endogenous H(2)S production protects against global ischaemia, and H(2)S may be a part of the endogenous cell defence. However, endogenous H(2)S did not appear to be important in ischaemic preconditioning, and protein kinases were not important for the effect of H(2)S. Exogenous H(2)S may provide myocardial protection, possibly acting by expression of heat shock protein 72.     

金属硫蛋白对供心的保护作用

目的探讨金属硫蛋白(MT)对离体心脏的保护作用。方法16只Wistar大鼠,随机分为2组,对照组腹腔注射蒸馏水0.5ml,24h后取离体心脏行离体灌注(Langendorff模型),测定心功能,然后灌注HTK心脏保护液,4℃下保存3h,再行Langendorff灌注,10min后转为工作心模型15min;实验组腹腔注射36g/LZnSO4(1.5ml/kg),24h后取离体心脏,随后的处理同对照组。测定心肌组织中MT、ATP、丙二醛(MDA)及Ca2 的含量以及超氧化物歧化酶(SOD)的活性,测定心功能指标、心肌含水量(MWC)、心肌肌酸激酶(CK)和乳酸脱氢酶(LDH)漏出率;测定心肌细胞线粒体内Ca2 ATPase活性、Ca2 含量及其合成ATP能力;观察心肌超微结构。结果实验组MT的含量明显高于对照组(P<0.01);实验组心功能指标、心肌组织中ATP含量及SOD活性均优于对照组(P<0.05,P<0.01),实验组MWC、MDA和Ca2 的含量以及CK、LDH漏出率均低于对照组(P<0.05,P<0.01);实验组心肌细胞线粒体内Ca2 ATPase活性及合成ATP能力均优于对照组(P<0.01),Ca2 含量低于对照组(P<0.01);实验组心肌细胞超微结构的损伤较对照组明显减轻。结论MT对鼠离体心脏具有保护作用。     

Effects of ischemic liver preconditioning on hepatic ischemia/reperfusion injury in the rat

To minimize bleeding during major liver resections or liver transplantation, surgical measures have been adopted that induce ischemia-reperfusion injury (I/R) which may significantly contribute to morbidity and mortality of partial liver resections. Several methods have sought to minimize I/R hepatic lesions. The present project assessed the protective role of ischemic preconditioning (IPC) in rat livers. The IPC was accomplished by clamping the hepatic pedicle for 5 minutes, followed by a 5-minute reperfusion (R) period before a 2-hour ischemia. Thereafter, reperfusions of 1, 3, and 24 hours were compared among IPC and control groups without IPC. Liver biopsy and blood samples were measured for mitochondrial respiratory control ratio (RCR), serum aspartate aminotransferase (AST), and alanine aminotransferase (ALT). IPC protected liver mitochondrial function. Serum aminotransferase levels were significantly lower among animals undergoing IPC compared with groups without IPC. Thus, we verified the effects of IPC for hepatocellular protection against I/R lesions.     

阿霉素预处理替代缺血预处理提供鼠肝缺血耐受力的实验研究

目的 探讨缺血预处理（IPC）延迟保护作用的发生机制以及应用阿霉素预处理（DPC）是否可以模拟IPC的延迟保护作用。方法 建立大鼠部分肝脏热缺血再灌注模型。IPC组采用肝脏缺血10min，再灌注10in，DPC组经静脉注射阿霉素（1mg/kg体重），对照组等量生理盐水注射。肝组织HSP70和HO－1蛋白和血清TNF－α、IL－10浓度分别采用Western blot法和ELISA法测定。结果 IPC后HO－1和HSP70含量分别于12h和24h达到高峰；IPC和DPC后24h诱导HSP70、HO－1的量无显著差异（P＞0.05）。对照组缺血再灌注后3h血清中TNF－α、AST、ALT、LDH及W／D（湿重／干重）的水平明显升高，而IL－10的含量降低，和假手术组相比差异显著（P＜0.01）；IPC或DPC后降低了TNF－α的释放和AST、ALT、LDH及W／D的水平，提高了IL－10的含量，和对照组相比差异显著（P＜0.01）。结论 IPC的延迟保护作用与HSP70和HO－1的诱导生成有关，DPC可以模拟IPC的延尺性保护作用，诱导HSP70和HO－1的产生。