人胎心不同组织心肌酶的组织化学研究

目的:探讨人心脏发育中不同组织结构中某些酶的含量及其分布规律。方法:采用组织化学方法和组织扫描光度测定法,观察胎儿和成人心脏的11种酶和化学物质。结果:心脏各种组织结构内与无氧代谢、有氧代谢和细胞增殖有关的酶及化学物质在心肌细胞内含量较高,特别是有氧代谢酶类的含量明显高于其它组织。与无氧代谢有关的酶类在血管平滑肌内含量明显高于其它组织。与神经递质代谢有关的酶、与脂类代谢有关的酶、与细胞分泌及膜活动有关的酶在神经组织中含量最高。结缔组织中各类酶含量均最低。结论:人胎心各组织结构内酶和化学物质的含量存在差别,可能与相应的结构和功能密切相关。     

Developing vasculature and stroma in engineered human myocardium

We recently developed a scaffold-free patch of human myocardium with human embryonic stem cell-derived cardiomyocytes and showed that stromal and endothelial cells form vascular networks in vitro and improve cardiomyocyte engraftment. Here, we hypothesize that stromal cells regulate the angiogenic phenotype by modulating the extracellular matrix (ECM). Human marrow stromal cells (hMSCs) support the greatest degree of endothelial cell organization, at 1.3- to 2.4-fold higher than other stromal cells tested. Stromal cells produce abundant ECM components in patches, including fibrillar collagen, hyaluronan, and versican. We identified two clonal hMSC lines that supported endothelial networks poorly and robustly. Interestingly, the pro-angiogenic hMSCs express high levels of versican, a chondroitin sulfate proteglycan that modulates angiogenesis and wound healing, whereas poorly angiogenic hMSCs produce little versican. When transplanted onto uninjured athymic rat hearts, patches with proangiogenic hMSCs develop ~ 50-fold more human vessels and form anastomoses with the host circulation, resulting in chimeric vessels containing erythrocytes. Thus, stromal cells play a key role in supporting vascularization of engineered human myocardium. Different stromal cell types vary widely in their proangiogenic ability, likely due in part to differences in ECM synthesis. Comparison of these cells defines an in vitro predictive platform for studying vascular development.     

Neurogenic lesions of the myocardium

Summary This investigation was aimed at obtaining myocardial lesions by a neurogenic route, i. e., by acting upon the myocardium with adrenalin and noradrenalin (mediators, appearing at the ends of postganglionic fibers of the cardiac sympathetic nerves after their stimulation). For this purpose very strong stimulation, either mechanical or chimical, was applied to the stellate ganglia. Myocardial lesions, of the character of cloudy swelling (swelling) of individual muscular fibers homogenization of the sarcoplasm, disappearance of the cross-striation) appear after stimulation of the stellate ganglia. These phenomena of cloudy swelling are focal in character. Later, depending upon the stage of the disease, they either resolve or, on the contrary, are enhanced, leading to the formation of small foci of necrosis in the myocardium with mildly or moderately cellular reaction. Pronounced disintegration of separate groups of muscular fibers and considerable cellular reaction were recorded in individital cases.Myocardial lesions, provoked by parenteral administration of massive doses of adrenalin, are compared to those resulting from the stimulation of the stellate ganglia, the mechanism of the action of these agents being discussed.(Presented by Active Member AMN SSSR, S. V. Anichkov) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 50, No. 12, pp. 38–43, December, 1960     

Changes in the intensity of protein synthesis in the myocardium during compensatory hyperfunction of the heart

Summary Compensatory hyperfunction of the heart in vitium cordis, hypertension and other diseases of the circulatory system connected with the cardiac overstrain of long duration represents the main factor in preservation of normal hemodynamic indices and clinical compensation. The rate of protein synthesis in the myocardium was studied under conditions of compensatory cardiac hyperfunction provoked by experimentally induced vitium cordis. As established, rapid development of hypertrophy during the first emergency stage of compensatory hyperfunction is accompanied by an intensified rate of protein synthesis (it about doubles). In the second stage of relatively stable hyperfunction the rate of protein synthesis is normal, while at the third stage — characterized by cardiosclerosis and progressive exhaustion —it is reduced 2–2.5 times. This depression of the normal renovation process of the protein myocardial structures may bring about a change in the contractile proteins of the heart, thus playing an important role in the development of cardiosclerosis and cardiac insufficiency.(Presented by V. V. Parin, Active Member of the AMN SSSR) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 50, No. 7, pp. 33–36, July, 1960     

Changes in the myocardium of the atrium in sudden death due to ischemic heart disease]

Studies of the myocardium of the right and left atria in 31 cases of sudden death due to myocardial infarction of the ventricles or in the presence of extensive-focal cardiosclerosis were carried out. Histological techniques for staining with hematoxylin-eosine, trichrome after Masson and Goldman's method were used. Microscopic investigation of the heart in 14 cases revealed fresh areas of necrosis of the myocardium atria, which the authors evaluated as infarction. The involvement of the myocardium of the atria into the pathological process influenced the course and prognosis of ischemic heart disease.     

Quantitative relations between parenchyma and stroma of the myocardium in rabbits with atherosclerotic cardiosclerosis

The relative volume of the muscle fibers, connective-tissue cells, capillaries, and ground substance and the surface area of the muscle fibers and capillaries per unit volume of tissue were measured in the myocardium of animals with diffuse cardiosclerosis accompanying experimental atherosclerosis. A significant decrease was found in the relative volume of the ground substance of the stroma.Laboratory of Pathological Anatomy, Institute of Clinical and Experimental Medicine, Siberian Division, Academy of Medical Sciences of the USSR, Novosibirsk. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Kraevskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 84, No. 8, pp. 247–250, August, 1977.     

Histology of experimental stress ulcer: the effect of cimetidine on adrenaline-induced gastric lesions in the rabbit.

The gastric mucosal injury produced by i.p. instillation of adrenaline in the rabbit was examined and assessed histologically. Mucosal lesions were classified by microscopy into two types bearing distinct histological features. In Type A oedema only was seen and in Type B erosion and/or haemorrhage were added. Statistical analysis revealed that mucosal lesions were related to adrenaline dose. Cimetidine was ineffective in protecting against the stress-related gastric lesion in the present rabbit model. Biochemical studies demonstrated that severe lesions were associated with depleted mucosal histamine.     

慢性心力衰竭时心肌组织中CGRP的含量变化及mRNA表达

目的探讨心肌组织降钙素基因相关肽(CGRP)含量变化及mRNA的表达与慢性心力衰竭(CHF)发生、发展的关系。方法以阿霉素(ADR)制备慢性心衰模型,采用放射免疫学方法和逆转录聚合酶链反应进行检测。结果CHF时,心肌组织中CGRP含量为34.82±3.01,高于正常心肌组织中CGRP的含量24.77±3.84,差异具有统计学意义;而CGRP的mRNA表达降低。结论心肌组织中CGRP含量变化及其mRNA的表达调控,与CHF的发生、发展密切相关。     

Invasion in breast lesions: the role of the epithelial–stroma barrier

Despite the significant biological, behavioural and management differences between ductal carcinoma in situ (DCIS) and invasive carcinoma of the breast, they share many morphological and molecular similarities. Differentiation of these two different lesions in breast pathological diagnosis is based typically on the presence of an intact barrier between the malignant epithelial cells and stroma; namely, the myoepithelial cell (MEC) layer and surrounding basement membrane (BM). Despite being robust diagnostic criteria, the identification of MECs and BM to differentiate in‐situ from invasive carcinoma is not always straightforward. The MEC layer around DCIS may be interrupted and/or show an altered immunoprofile. MECs may be absent in some benign locally infiltrative lesions such as microglandular adenosis and infiltrating epitheliosis, and occasionally in non‐infiltrative conditions such as apocrine lesions, and in these contexts this does not denote malignancy or invasive disease with metastatic potential. MECs may also be absent around some malignant lesions such as some forms of papillary carcinoma, yet these behave in an indolent fashion akin to some DCIS. In Paget's disease, malignant mammary epithelial cells extend anteriorly from the ducts to infiltrate the epidermis of the nipple but do not typically infiltrate through the BM into the dermis. Conversely, BM‐like material can be seen around invasive carcinoma cells and around metastatic tumour cell deposits. Here, we review the role of MECs and BM in breast pathology and highlight potential clinical implications. We advise caution in interpretation of MEC features in breast pathology and mindfulness of the substantive evidence base in the literature associated with behaviour and clinical outcome of lesions classified as benign on conventional morphological examination before changing classification to an invasive lesion on the sole basis of MEC characteristics.     

Polyploidy in the myocardium and compensatory reserve of the heart

The mammalian heart is a polyploid organ. Cardiac myocytes undergo polyploidization in the early postnatal ontogeny, and the degree of their polyploid depends on the conditions of heart growth. The myocardium of healthy persons is characterized by considerable individual variability of polyploidy. The principal mechanism by which normal and compensatory growth of the heart occurs in adult mammals is through increases of cytoplasmic mass in postmitotic myocytes. In the normal myocardium, the protein mass of myocytes does not correspond to the gene dosage, while their protein mass in a hypertrophic myocardium becomes a multiple of their ploidy. The capacity of polyploid myocytes to grow so as to double their mass constitutes the reserve of cardiac growth. This reserve, which is laid down in the early ontogeny, materializes in response to functional overloading of the heart in adult life. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 119, N ^o 5, pp. 454–459, May, 1995 Presented by D. S. Sarkisov, Member of the Russian Academy of Medical Sciences