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ischemic preconditioning-induced hyperperfusion correlates with hepatoprotection after liver resection

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World Journal of Gastroenterology 2010年第15期16卷 1871-1878页

作者： Oleg Heizmann Georgios Meimarakis Andreas Volk Daniel Matz Daniel Oertli Rolf J Schauer Department of Surgery University Hospital Basel Department of Surgery Klinikum of the Ludwig-Maximilians-University-Grosshadern University of Munich Department of Surgery University Hospital of Dresden Department of Surgery Academic Hospital of the Ludwig-Maximilians-University of Munich

AIM:To characterize the impact of the Pringle ma-neuver (PM) and ischemic preconditioning (IP) on total blood supply to the liver following hepatectomies. METHODS: Sixty one consecutive patients who un-derwent hepatic resection under in flow occlusion were randomized either to receive PM alone (n = 31) or IP (10 min of ischemia followed by 10 min of reperfusion) prior to PM (n = 30). Quantification of liver perfusion was measured by Doppler probes at the hepatic artery and portal vein at various time points after reperfusion of remnant livers. RESULTS: Occlusion times of 33 ± 12 min (mean ± SD) and 34 ± 14 min and the extent of resected liver tissue (2.7 segments) were similar in both groups. In controls (PM), on reperfusion of liver remnants for 15 min, portal perfusion markedly decreased by 29% while there was a slight increase of 8% in the arterial blood flow. In contrast, following IP + PM the portal vein flow remained unchanged during reperfusion and a significantly increased arterial blood flow (+56% vs baseline) was observed. In accordance with a better postischemic blood supply of the liver, hepatocellular injury, as measured by alanine aminotransferase (ALT) levels on day 1 was considerably lower in group B compared to group A (247 ± 210 U/I vs 550 ± 650 U/I, P ischemic flow reduction of the portal vein and simultaneously increases arterial perfusion, suggesting that improved hepatic macrocirculation is a protective mechanism following hepatectomy.

关键词： ischemic preconditioning Reperfusion injury Liver Surgery Liver blood flow

ischemic preconditioning reduces ischemic brain injury by suppressing nuclear factor kappa B expression and neuronal apoptosis

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Neural Regeneration Research 2013年第7期8卷 633-638页

作者： Songsheng Shi Weizhong Yang Xiankun Tu Chunmei Chen Chunhua Wang Department of Neurosurgery Affiliated Union Hospital of Fujian Medical University Fujian Neurosurgical Institute

ischemic stroke induces a series of complex pathophysiological events including blood-brain barrier disruption, inflammatory response and neuronal apoptosis. Previous studies demonstrate that ischemic preconditioning attenuates ischemic brain damage via inhibiting blood-brain barrier disruption and the inflammatory response. Rats underwent transient （15 minutes） occlusion of the bilateral common carotid artery with 48 hours of reperfusion, and were subjected to permanent middle cerebral artey occlusion. This study explored whether ischemic preconditioning could reduce ischemic brain injury and relevant molecular mechanisms by inhibiting neuronal apoptosis. Results found that at 72 hours following cerebral ischemia, myeloperoxidase activity was enhanced, malondialdehyde levels increased, and neurological function was obviously damaged. Simultaneously, neuronal apoptosis increased, and nuclear factor-KB and cleaved caspase-3 expression was significantly increased in ischemic brain tissues. ischemic preconditioning reduced the cerebral ischemia-induced inflammatory response, lipid peroxidation, and neurological function injury. In addition, ischemic preconditioning decreased nuclear factor-KB p65 and cleaved caspase-3 expression. These results suggested that ischemic preconditioning plays a protective effect against ischemic brain injury by suppressing the inflammatory response, reducing lipid peroxidation, and neuronal apoptosis via inhibition of nuclear factor-KB and cleaved caspase-3 expression.

关键词： neural regeneration brain injury ischemic preconditioning neural cells apoptosis nuclear factorkappa-B cleaved caspase-3 grants-supported paper photographs-containing paper neuroregeneration

ischemic preconditioning in immature hearts: mechanism and compatibility with cardioplegia

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Chinese Medical Journal 2003年第2期116卷 253-257页

作者：朱斌闵苏龙村叶铁虎 Department of Anesthesiology Peking Union Medical HospitalCAMS&PUMC Department of Anesthesiology First HospitalChongqing Medical University Anesthesiology & CPB Research Group Fuwai HospitalCAMS & PUMC

To investigate (1) whether ischemic preconditioning (IPC) could protect immature rabbit hearts against ischemia reperfusion injury and (2) the role of K ATP channel in the mechanism of myocardial protection Since cardioplegia is a t raditional and effective cardioprotective measure in clinic, our study is also d esigned to probe the compatibility between IPC and cardioplegia Methods New Zealand rabbits aged 14-21 days weighing 220-280 g were used The animals w ere anesthetized and heparinized The chest was opened and the heart was quickl y removed for connection of the aorta via Langendorff's method within 30 s after excision All hearts were perfused with Krebs Henseleit buffer balanced with gas mixture (O 2∶CO 2=95%∶5%) at 60 cm H 2O (perfusion pressure) IPC cons isted of 5 min global ischemia plus 10 min reperfusion Glibenclamide was used as the K ATP channel blocker at a concentration of 10 μmol/L before IPC Cardiac arrest was induced with 4℃ St Thomas cardioplegic solution, at which point the heart was made globally ischemic by withholding perfusion for 45 min f ollowed by 40 min reperfusion Thirty immature rabbit hearts were randomly divi ded into four groups: CON (n=9) was subjected to ischemia reperfusion only; IPC ( n=9) underwent IPC and ischemia reperfusion; Gli (n=6) was given glibenclamide and ischemia reperfusion; and Gli+IPC (n=6) underwent glibenclamide, IPC and is chemia reperfusion Coronary flow (CF), HR, left ventricle developed pressure (LVDP), and ±dp/dt max were monitored at equilibration (baseline value) an d 5, 1 0, 20, 30 and 40 min after reperfusion The values resulting from reperfusion w ere expressed as a percentage of their baseline values Arrhythmia quantificati on, myocardial enzyme in the coronary effluent and myocardial energy metaboli sm were also determined Results The recovery of CF, HR, LVDP and ±dp/dt max in preconditioned hearts was b est am ong the four groups The incidence of arrhythmia was low and less C

关键词： ischemic preconditioning immature K A TP channels ischemia cardioplegia

ischemic preconditioning enhances hepatocyte proliferation in the early phase after ischemia under hemi-hepatectomy in rats

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Hepatobiliary & Pancreatic Diseases International 2012年第5期11卷 521-526页

作者： Li-Ming Jin, Shui-Fang Jin, Yuan-Xing Liu, Lin Zhou, Hai-Yang Xie, Sheng Yan, Xiao Xu , Shu-Sen Zheng Department of General Surgery and Intensive Care Unit, First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou 310006, China Key Laboratory of Combined Multi-organ Transplantation, Ministry of Public Health, Key Laboratory of Organ Transplantation, Zhejiang Province, and Division of Hepatobiliary and Pancreatic Surgery, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China Department of General Surgery First Affiliated Hospital Zhejiang Chinese Medical University Hangzhou 310006 Hangzhou China Intensive Care Unit First Affiliated Hospital Zhejiang Chinese Medical University Hangzhou 310006 Hangzhou China Key Laboratory of Combined Multi-organ Transplantation Ministry of Public Health Key Laboratory of Organ Transplantation Zhejiang Province and Division of Hepatobiliary and Pancreatic Surgery First Affiliated Hospital Zhejiang University School of Medicine Hangzhou 310003 Hangzhou China

BACKGROUND: Ischemia/reperfusion (I/R) injury is an important barrier to liver surgery and transplantation because it impairs remnant liver/reduced-size-graft regeneration. ischemic preconditioning (IPC), as an effective measure to overcome I/R injury, has been shown to enhance the regenerative capacity of hepatocytes. However, investigations have always focused on regeneration in the late phase after reperfusion. This study aimed to investigate whether IPC enhances hepatocyte proliferation in the early phase after reperfusion and possible underlying mechanisms. METHODS: A total of 90 rats were divided into three groups: hemi-hepatectomy alone (PHx group), 60 minutes of ischemia plus hemi-hepatectomy (I/R group), and a cycle of 10 minutes of alternating I/R prior to 60 minutes of ischemia plus hemi-hepatectomy (IPC group). Each group was divided into five subgroups sacrificed after 0.5, 2, 6, 12 or 24 hours (n=6/ subgroup). Subsequently, serum concentrations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) were measured; caspase-3 and proliferating cell nuclear antigen (PCNA) proteins were also determined by Western blotting. Furthermore, PCNA was detected by immunohistochemistry to identify the expression site.RESULTS: Serum ALT and AST levels after 2-24 hours of reperfusion in the PHx and IPC groups were remarkably decreased compared to the I/R group, and the serum TNF-α was relatively lower. A significant increase of serum IL-6 levels was found in the PHx and IPC groups compared with the I/R group at each time point. Furthermore, PCNA expression was remarkably increased in the IPC group after 6-12 hours of reperfusion, and in the earlier 0.5 and 6 hours time points after reperfusion have shown the massive PCNA-positive hepatocytes. At the same time, the expression of liver p-JNK was higher in the IPC group in the early phase after reperfusion than that of the I/R group and its expression was consistent with the PCNA. CONCLUSION:

关键词： reperfusion injury ischemic preconditioning hepatocytes proliferation hemi-hepatectomy

ischemic preconditioning Inhibits Over-expression of Arginyl-tRNA Synthetase Gene Rars in Ischemia-injured Neurons

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2016年第4期36卷 554-557页

作者：沈寅赵洪洋王海均王文良张立志符荣 Department of Neurosurgery Union Hospital Tongji Medical College Huazhong University of Science and Technology

The expression changes of Rars gene in ischemia-injured neurons were investigated by detecting its translational product arginyl-t RNA synthetase（Arg RS）, and the inhibitory effects of ischemic preconditioning（IPC） on Rars gene were explored. Both IPC model and prolonged ischemia（PI） model were established by using the classic oxygen glucose deprivation（OGD） method. The primary cultured neurons were assigned into the following groups： the experimental group（IPC＋PI group）, undergoing PI after a short period of IPC; the conditional control group（PI control group）, subjected to PI without IPC; blank control group, the normally cultured neurons. The Rars transcriptional activities and Arg RS expression levels were measured at different time points after re-oxygenation（3 h/6 h/12 h/24 h）. Data were collected and statistically analyzed. Compared to the blank control group, the Rars activities and Arg RS levels were significantly increased in PI control group, peaking at the time point of 6 h after re-oxygenation. Rars activities and Arg RS levels were significantly lower in the experimental group than in the PI control group at different time points after re-oxygenation. PI insult can induce an escalating activity of Rars and lead to Arg RS over-expression in primary cultured neurons. IPC can inhibit the increased Rars activity and down-regulate Arg RS expression of ischemia-insulted neurons. This mechanism may confer ischemic tolerance on neurons.

关键词： ischemic preconditioning arginyl-tRNA synthetase Rars oxygen glucose deprivation

ischemic preconditioning partially suppresses and postpones integrin α_Vβ_3 mRNA expression following transient global cerebral ischemia in C57BL/6 mice

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Neural Regeneration Research 2010年第23期5卷 1782-1786页

作者： Mei Liu Xiaomeng Ma Xiaohong Chen Ying Jiang Aimin Wu Fuhua Peng Yingying Liu Rongbiao Pi Department of Neurology the Third Affiliated Hospital of Sun Yat-sen University Guangzhou 510630 Guangdong Province China Department of Pharmacology and Toxicology School of Pharmaceutical Sciences Sun Yat-sen University Guangzhou 510020 Guangdong Province China

Previous studies of integrin αvβ3 have focused on ischemic brain damage, although the role of integrin αvβ3 in ischemic preconditioning （IP） has rarely been reported. The present study analyzed the effects of IP on integrin αvβ3 mRNA expression following cerebral ischemia through the use of hematoxylin-eosin staining and real-time quantitative polymerase chain reaction techniques. Integrin avid3 mRNA expression in the ischemia group peaked at 24 hours after ischemia-reperfusion. In the IP ＋ ischemia group, integrin αvβ3 mRNA expression increased after 24 hours, but remained significantly less than the ischemia group, and expression continued to increase until 7 days after ischemiaJreperfusion. These results demonstrate that IP effectively attenuated upregulation of integrin αvβ3 mRNA expression at 24 hours after ischemia.

关键词： integrin αvβ3 ischemic preconditioning ischemic tolerance global cerebral ischemia blood-brain barrier： mice

Extracellular ascorbic acid fluctuation during the protective process of ischemic preconditioning in rabbit renal ischemia-reperfusion model measured

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Chinese Medical Journal 2010年第11期123卷 1441-1446页

作者： LIU Lei LIN Yu-qing YAN Long-tao HONG Kai HOU Xiao-fei MAO Lan-qun MA Lu-lin Department of Urology Peking University Third Hospital Beijing100191 China Institute of Cllemistry Chinese Academy of Sciences Beijing100190 China

Background Ascorbic acid has important antioxidant ischemic preconditioning on later ischemia-reperfusion ascorbic acid in ischemic preconditioning in the kidney. properties, and may play a role in the protective effects of Herein, we examined the role of endogenous extracellular Methods We developed a solitary rabbit kidney model where animals received ischemia-reperfusion only （ischemia-reperfusion group, n=-15） or ischemic preconditioning followed by ischemia-reperfusion （ischemic preconditioning group, n=15）. Ischemia-reperfusion was induced by occluding and loosening of the renal pedicle. The process of ischemic preconditioning included 15-minute brief ischemia and 10-minute reperfusion. In vivo microdialysis coupled with online electrochemical detection was used to determine levels of endogenous extracellular ascorbic acid in both groups. The extent of tissue damage was determined in kidney sections stained with hematoxylin and eosin. Serum creatinine and urea nitrogen were also detected to assess renal function. Results During ischemia-reperfusion, the extracellular ascorbic acid concentration during ischemia increased rapidly to the peak level （（130.01±9.98）%）, and then decreased slowly to near basal levels. Similar changes were observed during reperfusion （peak level, （126.78±18.24）%）. In the ischemic preconditioning group there was a similar pattern of extracellular ascorbic acid concentration during ischemic preconditioning. However, the ascorbic acid level was significantly lower during the ischemia and early reperfusion stage compared to the ischemia-reperfusion group. Additionally, the extent of glomerular ischemic collapse, tubular dilation, tubular denudation, and loss of brush border were markedly attenuated in the ischemic preconditioning group. Levels of serum creatinine and urea nitrogen were also decreased significantly in the ischemic preconditioning group. Conclusions ischemic preconditioning may protect renal tissue against ischemia-reperfusion injury via use of extracellular ascorbic acid

关键词： in vivo microdialysis online electrochemical detection, ascorbic acid, renal ischemia-reperfusion ischemic preconditioning

ADAMTS-1 expression in rat myocardium after ischemic preconditioning： age-associated differences

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Chinese Medical Journal 2011年第1期124卷 95-99页

作者： WANG Yong HUANG Cong-xin ZHOU Yi-feng CHENG Jin-song WANG Hui WU Wen-jing LIAO Wen-qiang WEN Jian-yan KE Yuan-nan ZHENG Jin-gang Department of Cariology Renmin Hospital of Wuhan University Wuhan Hubei 430060 China Department of Cardiology China-Japan Friendship Hospital Beijing 100029 China

Background It has been found that cardiac protection afforded by ischemic preconditioning （IPC） is significantly reduced in the senescent myocardium. ADAMTS-1 （a disintesrin and metalloprotease with thrombospondin type 1 motifs） has been shown to inhibit angiogenesis in a variety of in vitro and in vivo assays. The aim of this study was to investigate the age-associated differences in ADAMTS-1 protein expression in rat myocardium after ischemic preconditioning. Methods Sixty-four young （4 months） and old （24 months） male Sprague-Dawley rats were randomly assigned to an IPC group （40 rats） or a sham group （rats）. A model of delayed IPC was induced and rats were sacrificed and myocardial samples were harvested from the ischemic-reperfused region for immunohistochemical detection of ADAMTS-1 at serial time points after IPC. A model of myocardial infarction was produced by ligation of the left anterior descending coronary artery in additional sets of young and old rats after sham or IPC procedures, then age-associated myocardial infarction survival after IPC was calculated. Results ADAMTS-1 expression increased significantly in old rats compared to young rats （P 〈0.05）. The mean densities of ADAMTS-1 protein at 0, 6, 12, and 24 hours in young-IPC group after IPC were 0.05＋0.01, 0.13±0.03, 0.16±0.04, and 0.12±0.03 vs. 0.07±0.03, 0.20±0.03, 0.24±0.05, and 0.21±0.04 in old-IPC group. IPC resulted in diminished survival rates （5/35 vs. 6/14, old-IPC group vs shortening （（13.9±2.8）% vs. （18.3±2.3）%, P 〈0.05） and old-sham group, P 〈0.05）, reduced left ventricular fractiona increased the myocardial infarction size （（37.9±3.2）% vs （32.8±5.1）%, P 〈0.05） in the older rats. Conclusions Cardioprotection with IPC is attenuated in the older heart. ADAMTS-1 expression induced by IPC is greater in old rats. Over-expression of anti-angiogenic factors might be a potential mechanism behind reduced protection after IPC associated with aging.

关键词： ADAMTS-1 protein ischemic preconditioning age immunohistochemistry myocardial infarction

Role of nitric oxide during early phase myocardial ischemic preconditioning in rats

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Chinese Medical Journal 2008年第13期121卷 1210-1214页

作者： HAN Hong-guang WANG Zeng-wei ZHANG Nan-bin ZHU Hong-yu Department of Cardiovascular Surgery Xijing Hospital of Fourth Military Medical University Xi'an Shaanxi 710032 China Department of Cardiovascular Surgery General Hospital of Shenyang Military Command Shenyang Liaoning 110016 China

Background To date, there have been no reports on altered nitric oxide （NO） content in ischemia/reperfusion with regard to in vivo preconditioning procedures. These studies are important for understanding the mechanisms of NO during early myocardial ischemic preconditioning. The aim of the present study was to investigate the mechanisms of NO during early myocardial ischemic preconditioning by measuring levels of NO and cyclic guanosine monophosphate （cGMP）, as well as activity of nitric oxide synthase （NOS） in ischemia/reperfusion with respect to preconditioning in rats. Methods Sixty-six female Sprague-Dawley rats were randomly divided into four groups： ischemic preconditioning group （IP）, ischemia/reperfusion group （I/R）, control group （CON）, and preconditioning procedure group （PC）. In the PC group, rats were further divided into PC1-, PC1＋, PC2-, PC2＋, PC3-, and PC3＋ subgroups. Rats underwent left coronary artery occlusion and reperfusion, and subsequently, NOS activity and levels were assessed with spectrophotometric analysis. cGMP contents were measured with radioimmunoassay. Results The level of NO and cGMP, as well as the activity of NOS, were significantly higher in the IP group compared to the I/R and CON groups （P 〈0.05）. During preconditioning prior to prolonged ischemia, NO and cGMP levels varied markedly with ischemia and reperfusion. The levels of NO repeatedly increased when the heart was exposed to three episodes of 5-minute ischemia, and were almost completely reversed during each reperfusion period. NO and cGMP levels were significantly different between the 5-minute period of ischemia and the same period of reperfusion during preconditioning. Conclusions NO plays an important role during early phase myocardial ischemic preconditioning in rats. NO and cGMP could be triggers and mediators of early phase myocardial ischemic preconditioning. Altered NOS activity following ischemic stress could be the primary inducer of higher NO levels detected. NO and cGMP fluctuations might be the trigger

关键词： ischemic preconditioning nitric oxide nitric oxide synthase cyclic guanosine monophosphate rats