肥大细胞在大鼠胰腺组织纤维化形成中的作用及其机制

目的探讨肥大细胞（MC）在大鼠胰腺组织纤维化形成中的作用和机制。方法建立经逆行胆胰管注射2％三硝基苯磺酸（TNBS）诱导大鼠慢性胰腺炎模型，将大鼠分为三组，每组40只，分别用肥大细胞膜稳定剂色甘酸钠和MC激动剂48／80化合物及生理盐水进行干预，并于第3、7、14、21和28天处死动物。H—E染色观察胰腺组织病理学改变；Van Gieson染色观察胰腺组织纤维化情况；硫堇蓝染色观察大鼠慢性胰腺炎过程中MC分布、形态和数量的改变；免疫组化染色观察大鼠慢性胰腺炎α-平滑肌肌动蛋白（α-SMA）、转化生长因子（TGF）β1的表达；逆转录-多聚酶链反应（RT—PCR）观察血管紧张素Ⅱ1型（AT1）和2型（AT2）受体蛋白的表达。结果2％TNBS胰管内注射后可于第4周引起典型大鼠胰腺组织纤维化，在胰腺纤维化区域可见大量Ⅰ型胶原沉积。在此过程中MC存在着活化及脱颗粒。胰腺组织α—SMA、TGFβ1、AT1和AT2 mRNA蛋白制模早期表达即为阳性，至第4周时最强。与对照（生理盐水）组比较，色甘酸钠组MC数量及脱颗粒现象明显减少，α-SMA、TGFβ1蛋白表达和AT1、AT2受体mRNA表达明显减少；48／80化合物组MC数量及脱颗粒现象明显增多，上述各指标的表达均有不同程度的增加。结论MC参与TNBS诱导的大鼠慢性胰腺炎的炎症和纤维化的发生及发展，其机制可能与MC促进胰腺星状细胞活化，上调血管紧张素Ⅱ受体表达等介导了胰腺纤维化的形成。     

1型血管紧张素Ⅱ受体拮抗剂对胰腺星状细胞的影响

目的探讨1型血管紧张素Ⅱ受体（AT1）拮抗剂氯沙坦对胰腺星状细胞（PSC）的影响及其可能机制。方法①从胰腺癌患者胰腺组织中分离PSC并检测其AT1的表达，用血管紧张素Ⅱ（AngⅡ）和氯沙坦干预后检测其I型胶原的表达情况。②90只雄性SD大鼠均分为正常组、对照组和治疗组。后2组胰管内注射2％三硝基苯磺酸（TNBS）制成大鼠胰腺纤维化模型。治疗组给予氯沙坦灌胃，对照组给予等容积的无菌蒸馏水。于制模后第3、7、14、21和28天分别处死大鼠，留取胰腺组织。电镜下观察胰腺组织超微结构改变；应用逆转录-聚合酶链式反应（RT-PCR）检测胰腺组织转化生长因子β1（TGFβ1）、Ⅰ型前胶原mRNA表达；应用免疫组化法检测胰腺组织α-平滑肌肌动蛋白（α—SMA）和TGFβ1蛋白表达；应用Western印迹法检测胰腺组织α—SMA动态表达水平。结果体外研究显示，AT1表达于人胰腺癌组织PSC，氯沙坦可抑制其Ⅰ型胶原的表达。体内研究表明，氯沙坦可逆转胰腺纤维化大鼠电镜下胰腺细胞异常改变；胰腺纤维化大鼠胰腺组织α-SMA、TGF61和Ⅰ型前胶原表达增加，氯沙坦可下词其表达。结论AT1拮抗剂通过阻断AT1途径抑制PSC活化及其促纤维化作用。     

尾加压素Ⅱ对体外高糖培养大鼠肾小球系膜细胞细胞外基质分泌的影响

目的观察尾加压素Ⅱ（UⅡ）对体外高糖培养大鼠肾小球系膜细胞（MC）细胞外基质（ECM）纤连蛋白（FN）、Ⅳ型胶原（ColⅣ）及转化生长因子（TGF）β分泌的影响。方法体外高糖培养大鼠MC,加入不同浓度UⅡ（终浓度10-7、10-8、10-9、10-10mol/L）,并设立UⅡ抑制组,37℃孵育24h,留取上清,应用ELISA法测定上清中FN、ColⅣ及TGFβ含量。结果10-8mol/LUⅡ作用下的大鼠MC培养上清中,FN、ColⅣ及TGFβ含量同对照组相比有显著升高（P〈0.05）;UⅡ10-8mol/L＋Ca2＋阻断剂尼卡地平组、UⅡ10-8mol/L＋Ca2＋螯合剂EDTA组及UⅡ10-8mol/L＋抗UⅡ抗体组同UⅡ10-8mol/L组相比较,细胞培养上清中FN、ColⅣ及TGFβ含量显著减少（P〈0.05）。结论一定浓度尾加压素Ⅱ能促进体外高糖培养的大鼠MC分泌ECMFN、ColⅣ及TGFβ。     

锌原卟啉对博莱霉素致大鼠肺纤维化模型的影响

目的观察血红素加氧酶-1（HO-1）抑制剂锌原卟啉（Znpp）对博莱霉素（BLM）致大鼠肺纤维化模型病理和病理生理改变的影响，探讨Znpp在BLM诱导肺纤维化发病中的作用。方法健康sD大鼠60只随机分三组：生理盐水（Ns）组、BLM组、Znpp组。气管内注入BLM制作肺纤维化模型。分别在第7天、第14天、第21天和第28天，每组处死5只大鼠，取肺组织HE染色，观察其病理改变；检测支气管肺泡灌洗液（BALF）中细胞计数及中性粒细胞百分比、转化生长因子-β（TGF—β）和总胆红素含量；检测肺组织中还原型谷胱甘肽（GSH）和羟脯氨酸（HYP）含量。结果病理显示BLM组和Znpp组肺组织在早期炎症阶段两者之间炎症程度无明显差异，但后期肺纤维化阶段时，BLM组纤维化程度显著高于Znpp组。用Znpp干预后没有抑制炎症细胞浸润肺组织，但有效抑制了TGF—β、总胆红素和HYP水平，减少了GSH耗竭。结论应用Znpp可以显著减轻BLM致大鼠肺纤维化，但其作用机制并不通过抑制早期炎症反应，而是通过其抗损伤、抗氧化、抗纤维化机制发挥治疗作用。     

拮抗血管紧张素Ⅱ对5/6肾切除大鼠肾小管间质血小板反应蛋白1表达的影响

目的：观察血小板反应蛋白1（TSP1）在大鼠纤维化肾组织中的表达，以及血管紧张素Ⅱ（AngⅡ）对肾小管上皮细胞表达TSP1的影响。方法：建立5／6肾切除SD大鼠模型，设假手术组，手术组，氨氯地平组。缬沙坦组，雷米普利组。术后定时检测血压，分别于成模后0、4、12周取材，检测血肌酐、尿素氮、24h尿蛋白定量并计算Ccr。采用Masson染色观察肾小管间质纤维化（TIF）的程度；通过免疫组化观察TSP1、转化生长因子1（TGF-β1）、纤维连接蛋白（fibronectin，FN）在各组大鼠肾组织中表达及分布；采用免疫荧光共染技术观察TSP1／TGF-β1两者共区域表达随病变进展的变化；抽提肾皮质组织总RNA，RT—PCR法检测TSP1、TGF-β1和FN mRNA转录水平的表达。体外实验，以1 μM AngⅡ刺激人肾小管上皮细胞（HK-2）24h，10μM氯沙坦（Losartan）进行干预，分别采用RT-PCR、免疫荧光和Western blot检测TSP1、TGF-β1、FN mRNA转录水平和蛋白表达的改变，ELISA法检测培养基中活性和总TGF-β1的含量。结果：①正常大鼠肾小管间质基本无TSP1分布；而在5／6肾次全切大鼠的肾小管间质区内，小管上皮细胞、肌成纤维细胞和浸润的单核／巨噬细胞均能表达TSP1，12周手术组TSP1蛋白表达水平较假手术组上调近5倍：且较之0周和4周手术组亦明显增加（均P〈0．01），12周手术组TSP1mRNA和蛋白表达水平较假手术组分别上调1．94倍和5倍（均P〈0．05）；②TSP1表达增加与Ccr减退呈负相关（r=-0．472，P〈0．01）；12周手术组大鼠肾组织TIF程度以及TGF-β1、FN的表达较假手术组均明显上调（均P〈0．05），并与TSP1表达增加呈正相关；③缬沙坦／雷米普利处理组TSP1表达也上调，但程度明显低于手术组和氨氯地平组（均P〈0．05），而二组之间无差别；④AngⅡ能明显上调HK-2细胞TSP1、TGF—β1和FN mRNA转录水平和蛋白表达，而氯沙坦能抑制TSP1和TGF—β1的mRNA转录和蛋白合成，下调培养上清液中活性和总TGF-β1的含量。结论：肾小管间质病变的进展过程中，AngⅡ能使TSP1表达上调，其改变程度与肾功能损害密切相关；血管紧张素转换酶抑制剂／血管紧张素Ⅱ受体拮抗剂能减少TSPl和TGF—β1在纤维化肾组织中的表达，从而进一步对细胞外基质的沉积进行调节。     

转化生长因子β1和核心蛋白聚糖在胰腺星状细胞中的表达

背景：胰腺星状细胞(PSCs)在胰腺纤维化的进程中具有重要作用，因此有必要对影响该细胞活化的细胞因子进行研究。目的：建立一种从大鼠中分离、培养PSCs的成熟方法，研究原代培养2～3代的传代PSCs中转化生长因子(TGF)-β。及其拮抗剂核心蛋白聚糖的mRNA(转录水平)和蛋白(翻译水平)的表达和分布。方法：取大鼠胰腺组织进行酶消化和不连续密度梯度离心以获得原代PSCs。采用免疫细胞化学染色检测PSCs中α-平滑肌肌动蛋白(SMA)、结蛋白(desmin)和纤维连接蛋白(FN)的表达；采用免疫细胞化学染色和原位杂交方法检测传代PSCs中TGF-β1和核心蛋白聚糖的蛋白和mRNA的表达。结果：体外成功分离并培养PSCs后，免疫细胞化学染色结果显示该细胞可活化，细胞质中出现α-SMA、desmin和FN阳性表达。在传代PSCs中，TGF-β1 mRNA在细胞核和细胞质内均有表达，其蛋白则主要在细胞质内表达；核心蛋白聚糖则无论mRNA或蛋白均主要在细胞核内表达。结论：大鼠PSCs可成功地在体外分离并培养。在培养过程中，该细胞可自发活化并向成纤维样细胞分化。PSCs可自分泌TGF-β1和核心蛋白聚糖，并可能在基因转录水平进行自身调控，从而对胰腺纤维化的形成产生一定影响。     

持续抑制超氧歧化酶活性诱导大鼠慢性胰腺炎模型

目的 观察大鼠腹膜内注射超氧歧化酶(SOD)抑制剂二乙基二硫代氨基甲酸盐(DETC)后胰腺的病理改变,并与大鼠胰管内注射三硝基苯磺酸(TNBS)所制备的慢性胰腺炎(CP)模型相比较.方法 将大鼠按随机表法分为DETC组、DETC对照组、TNBS组、TNBS对照组、正常对照组.DETC组大鼠腹膜内注射DETC 750 mg/kg体重,每周2次,DETC对照组在腹腔内注射等容积生理盐水.TNBS组大鼠胰管内注入含2％TNBS的乙醇磷酸盐缓冲液,TNBS对照组注入等容积乙醇磷酸盐缓冲液.正常对照组不做任何处理.术后2、4、6、8周分批处死大鼠,取血检测淀粉酶活性,取胰腺组织行病理及超微结构检查,检测组织内SOD、谷胱甘肽过氧化物酶(GSH-PX)活性和丙二醛(MDA)含量,免疫组化法检测组织α-平滑肌肌动蛋白(α-SMA),结蛋白(Desmin),胶原Ⅰ、Ⅲ,TGF-β1,纤维连接蛋白(FN)的表达,RT-PCR法检测组织TGF-β1 mRNA表达.结果 DETC组大鼠无死亡,TNBS组大鼠死亡率为15％.2组大鼠血淀粉酶活性差异无统计学意义.4周时DETC组大鼠胰腺纤维化评分为(3.4±1.1)分,显著高于TNBS组的(3.0±1.3)分(t=3.462,P＜0.05);6周时胰腺组织腺体破坏评分为(9.1±1.8)分,显著高于TNBS组的(8.4±1.8)分(t=2.943,P＜0.05);细胞空泡样变、脂肪浸润评分较TNBS组高,但差异均无统计学意义.DETC组和TNBS组在制模2周后即可见胰腺超微结构改变,4周后可见大量新生或已趋成熟的胶原纤维.2周时DETC组SOD活性较TNBS组显著下降(t=5.468,P＜0.05),GSH-PX活性在2、6周时较TNBS组显著下降,(t值分别为6.497,10.125,P＜0.05),而MDA活性在6、8周时较TNBS组均显著升高(t值分别为3.350,5.407,P值＜0.05).DETC组和TNBS组大鼠胰腺组织α-SMA,Desmin,胶原Ⅰ、Ⅲ,TGF-β1和FN表达及TGF-β1 mRNA表达水平差异均无统计学意义.结论 应用DETC持续抑制SOD活性可成功诱导CP.DETC组大鼠的胰腺脂肪浸润和纤维化程度较TNBS组出现得更早、更严重.采用该法制模操作简单,大鼠死亡率低,是一种较理想的制备CP模型的方法.     

内皮素-1和整合素α5β1在慢性胰腺炎纤维化中的表达及临床意义

通过胆胰管内注射三硝基苯磺酸（TNBS）制备大鼠慢性胰腺炎纤维化模型，采用RT-PCR和Westernblot技术检测1、2、3、4、5、6及7周内皮素-1（ET-1）和整合素α5β1mRNA和蛋白在大鼠胰腺组织中的表达。结果显示，ET-1和整合素仪，α5β1在慢性胰腺炎纤维化过程中有过度表达，与对照组比较，有统计学差异。认为ET-1和整合素的过表达在慢性胰腺炎纤维化的发生、发展中起重要作用。     

三硝基苯磺酸（TNBS）诱导大鼠胰腺纤维化的病理学演变

目的：观察三硝基苯磺酸(TNBS)胰管内注射诱导大鼠慢性胰腺炎胰腺纤维化过程中的病理演变规律，进一步从病理学角度揭示其发生机制。方法：通过胰管内注射含2%TNBS的乙醇磷酸盐缓冲液诱导大鼠慢性胰腺炎模型，对照组仅注射等体积乙醇磷酸盐缓冲液，并于术后72h、3周、4周、5周、6周、7周处死大鼠。应用光镜、电镜观察不同时间点胰腺组织的病理学变化。结果：2%TNBS胰管注射后早期主要以胰腺组织炎症、水肿，腺泡细胞坏死等改变为主；3周后则以纤维化为主，主要表现为胰腺星状细胞活化和成纤维细胞增生，腺泡萎缩及间质内大量纤维沉积。结论：胰管内注射TNBS引起的慢性胰腺炎的病理改变是基于胰腺实质急性损伤而发生的胰腺组织再生与修复，最终形成胰腺纤维化。     

调肝理脾方对酒精性大鼠肝纤维化的抑制作用及其方证探讨

目的：探讨调肝理脾方对酒精性大鼠肝纤维化的抑制作用。方法：Wistar雄性大鼠以“酒精-吡唑-玉米油”混合液灌胃16周，制备酒精性肝纤维化大鼠模型，将存活动物随机分成3组：模型对照组、调肝理脾方治疗组、西药对照（安珐特）治疗组，另设正常对照组。4周后检测大鼠血清中肝纤维化指标，观测肝组织病理学及肝组织中TGF—β1蛋白表达变化。结果：16周末模型大鼠肝功能显著异常，肝纤维化明显；经4周治疗，与模型组比较，治疗组及对照组大鼠血清中HA含量均有显著下降趋势（P〈0．01），且调肝理脾方能显著下调大鼠肝组织中TGF—β1蛋白含量，其效果优于西药对照组。结论：调肝理脾方能有效阻止和逆转酒精性肝纤维化的进程，疗效优于西药对照组，方证相关有其病理学基础。     

Three layer functional model and energy exchange concept of aging process

Relying on a certain degree of abstraction, we can propose that no particular distinction exists between animate or living matter and inanimate matter. While focusing attention on some specifics, the dividing line between the two can be drawn. The most apparent distinction is in the level of structural and functional organization with the dissimilar streams of ‘energy flow’ between the observed entity and the surrounding environment. In essence, living matter is created from inanimate matter which is organized to contain internal intense energy processes and maintain lower intensity energy exchange processes with the environment. Taking internal and external energy processes into account, we contend in this paper that living matter can be referred to as matter of dissipative structure, with this structure assumed to be a common quality of all living creatures and living matter in general. Interruption of internal energy conversion processes and terminating the controlled energy exchange with the environment leads to degeneration of dissipative structure and reduction of the same to inanimate matter, (gas, liquid and/or solid inanimate substances), and ultimately what can be called ‘death.’ This concept of what we call dissipative nature can be extended from living organisms to social groups of animals, to mankind. An analogy based on the organization of matter provides a basis for a functional model of living entities. The models relies on the parallels among the three central structures of any cell (nucleus, cytoplasm and outer membrane) and the human body (central organs, body fluids along with the connective tissues, and external skin integument). This three-part structural organization may be observed almost universally in nature. It can be observed from the atomic structure to the planetary and intergalactic organizations. This similarity is corroborated by the membrane theory applied to living organisms. According to the energy nature of living matter and the proposed functional model, the decreased integrity of a human body's external envelope membrane is a first cause of the structural degradation and aging of the entire organism. The aging process than progresses externally to internally, as in single cell organisms, suggesting that much of the efforts towards the restoration and maintenance of the mechanisms responsible for structural development should be focused accordingly, on the membrane, i.e., the skin. Numerous reports indicate that all parts of the human body, like: bones, blood with blood vessels, muscles, skin, and so on, have some ability for restoration. Therefore, actual revival of not only aging tissue of the human body's membrane, but the entire human body enclosed within, with all internal organs, might be expected. We assess several aging theories within the context of our model and provide suggestions on how to activate the body's own anti-aging mechanisms and increase longevity. This paper presents some analogies and some distinctions that exist between the living dissipative structure matter and inanimate matter, discusses the aging process and proposes certain aging reversal solutions.     

Unusual responses of nocturnal pineal melatonin synthesis and secretion to swimming: Attempts to define mechanisms

Abstract: The effect of swimming at night on rat pineal melatonin synthesis was compared with that of light exposure at night. Rats were forced to swim at 0030 hr (lights out at 2000 hr) and sacrificed by decapitation 15 and 30 min later, immediately after swimming. Other groups of animals were exposed to white light (650μW/cm²) for 15 and 30 min at same time. Swimming caused a rapid and highly significant drop in the melatonin content in the pineal gland; however, the activity of N-acetyltransferase (NAT), the supposed rate limiting enzyme in the melatonin production, was not changed. Despite the drop in pineal melatonin levels, serum concentrations of the indole remained elevated in the rats that swam. In contrast, melatonin levels in the pineal and serum of light exposed rats fell precipitously, accompanied by a significant suppression of NAT activity. Since we anticipated that the strenuous exercise associated with swimming may induce release of artrial natriuretic peptide (ANP) from the heart, which in turn could cause the release of pineal melatonin, in a second study we injected physiological saline intravenously to stretch the cardiac muscle and release ANP. Three milliliters of normal saline was injected during the day into the jugular vein of anesthetized rats that were pretreated with isoproterenol to stimulate pineal melatonin production. Animals were killed 15 min after the saline injection, and pineal NAT activity and pineal melatonin levels were measured. The saline injections caused no alteration in the elevated levels of either NAT or melatonin. These data suggest that the disparity in pineal NAT activity (which was high) and pineal melatonin (which was low), in animals swum at night, may not be caused by ANP which is released during strenuous exercise such as swimming.     

The immunoneuroendocrine role of melatonin

Abstract: A tight, physiological link between the pineal gland and the immune system is emerging from a series of experimental studies. This link might reflect the evolutionary connection between self-recognition and reproduction. Pinealectomy or other experimental methods which inhibit melatonin synthesis and secretion induce a state of immunodepression which is counteracted by melatonin. In general, melatonin seems to have an immunoenhancing effect that is particularly apparent in immunodepressive states. The negative effect of acute stress or immunosuppressive pharmacological treatments on various immune parameters are counteracted by melatonin. It seems important to note that one of the main targets of melatonin is the thymus, i.e., the central organ of the immune system. The clinical use of melatonin as an immunotherapeutic agent seems promising in primary and secondary immunodeficiencies as well as in cancer immunotherapy. The immunoenhancing action of melatonin seems to be mediated by T-helper cell-derived opioid peptides as well as by lymphokines and, perhaps, by pituitary hormones. Melatonin-induced-immuno-opioids (MHO) and lymphokines imply the presence of specific binding sites or melatonin receptors on cells of the immune system. On the other hand, lymphokines such as -γ-interferon and interleukin-2 as well as thymic hormones can modulate the synthesis of melatonin in the pineal gland. The pineal gland might thus be viewed as the crux of a sophisticated immunoneuroendocrine network which functions as an unconscious, diffuse sensory organ.     

Melatonin and photoperiodic time measurement: Seasonal breeding in the sheep

Abstract: Well-established circadian physiology supports the view that photoperiodic time measurement utilizes the coincidence between the presence of light and a photosensitive phase of a 'biological clock' to alter reproductive status—the so-called external coincidence model of seasonal breeding. In this review, we examine the mechanism whereby photoperiod interacts with presumed suprachiasmatic nuclei activity to allow endogenous melatonin to normally synchronize reproductive activity to the optimal time of year. The Romney Marsh sheep is particularly explored as an experimental model. It is suggested that the on/off activity of seasonal reproduction may be a robust mechanism able to be predictably manipulated by the judicious use of the light/dark cycle and exogenous melatonin, but firmly based on circadian principles.     

Response of rat pineal melatonin to calcium, magnesium, and lithium is circadian stage dependent

Abstract: Herein we documented the response of pineal melatonin production to electrolytes known to be effective on pineal function in view of a possible circadian stage dependence. We studied the release of melatonin by perifused rat pineal glands at 2 different circadian stages corresponding to the middle of the light and dark periods, i.e., respectively, 7 and 19 HALO (Hours After Light Onset, L:D = 12:12). The initial efflux rates were, as expected, much higher in the perifusates of glands removed from rats sacrificed during the dark phase than of those removed during the light phase. After 3 hr of perifusion, melatonin release reached similar levels which were found constant up to the 8th hr of perifusion, whatever the circadian stage. Perifusion of the glands with physiological concentrations for the rat of calcium (5.2 mmol/1) and magnesium (1.34 mmol/1) resulted in a stimulatory effect on the pineal glands removed from rats sacrificed in the middle of the dark period (19 HALO), whereas no effects were observed on the pineal glands removed from rats sacrificed during the light (7 HALO). Lithium (0.28 and 0.55 mmol/1) was ineffective on melatonin release in pineal glands removed 7 and 19 HALO. Our results show differences in the initial efflux rates of melatonin and in the response of perifused pineal glands to calcium and magnesium according to the circadian stage.     

Conservative management of perforated duodenal diverticulum： A case report and review of the literature

Duodenal diverticula are a relatively common condition. They are asymptomatic, unless they become complicated, with perforation being the rarest but most severe complication. Surgical treatment is the most frequently performed approach. We report the case of a patient with a perforated duodenal diverticulum, which was diagnosed early and treated conservatively with antibiotics and percutaneous drainage of secondary retroperitoneal abscesses. We suggest this method could be an acceptable option for the management of similar cases, provided that the patient is in good general condition and without septic signs.     

Changes in connexin43, the gap junction protein of astrocytes, during development of the rat pineal gland

Abstract: The abundance of gap junctions between rat pineal astrocytes formed by connexin43 (Cx43) was studied during development. Levels and distribution of Cx43 were measured by immunoblotting and indirect immunofluorescence, respectively. The amount of Cx43 in cells located within the gland was low until about the 7th postnatal day and increased to adult values between the 14th and 21st days postpartum. Although astrocytes, recognized by their vimentin immunoreactivity, were scarce before birth, they were abundant by the 7th postnatal day suggesting that the low levels of Cx43 found at this age corresponded to a low expression of this protein. Localization of the immunoreactivity to Cx43 and vimentin showed a close correlation, indicating that mature or immature pineal astrocytes form gap junctions made of Cx43. Since Cx43 levels attained their adult values at about the time the innervation and the functional state of the gland reached maturity (2–3 weeks after birth), it is proposed that astrocyte gap junctions are involved in the function of the adult rat pineal gland.     

Language of CTO interventions – Focus on hardware

The knowledge of variety of chronic total occlusion (CTO) hardware and the ability to use them represents the key to success of any CTO interventions. However, the multiplicity of CTO hardware and their physical character and the terminology used by experts create confusion in the mind of an average interventional cardiologist, particularly a beginner in this field. This knowledge is available but is scattered. We aim to classify and compare the currently used devices based on their properties focusing on how physical character of each device can be utilized in a specific situation, thus clarifying and simplifying the technical discourse.