Kazanskaya G M, Volkov A M, Karas'kov A M, Lomivorotov V N, Shun'kin A V
Department of Anesthesiology and, Research Institute of Circulation Pathology, Novosibirsk, 630055, Russia.
Microvasc Res. 1999 Nov;58(3):250-67. doi: 10.1006/mvre.1999.2181.
Ultrastructural changes in endothelial cells (EC) of myocardial capillaries were studied in 24 dogs which underwent hypothermia without perfusion. Biopsy specimens for electron microscopy were taken from the left ventricle of each dog in the control group, during anesthesia (prior to active cooling), and at the end of moderate (28-30 degrees ) and deep (22-24 degrees ) artificial body cooling. The following morphological types of the EC were identified both in the control group and in all test groups: those with moderately dense cytoplasm, light, dark, and irreversibly damaged cells. Dark cells showed increased numbers of plasmalemmal vesicles and appeared to be more transport-specialized as opposed to other types. In all stages of the experiment the amount of dark cells continuously increased (to 23.80, 34.62, and 47.17%, respectively). On cooling to 28-30 degrees, subcellular manifestation of reduced synthetic activity of organelles (nucleus, Golgi complex, and rough endoplasmic reticulum) was observed in all types of the EC. These changes persisted, or even increased, at the end of deep hypothermia. The transport activity of the EC changed differently in three experimental groups in all cell types. Micropinocytotic activity increased under spontaneous mild hypothermia (34-35 degrees ) during anesthesia and tended to decrease with subsequent artificial lowering of the temperature to 22-24 degrees. These ultrastructural changes seem to make up an integral part of the process of capillary endothelium adaptation to body surface cooling, and they might contribute to the development of tolerance to subsequent ischemic exposure during cardiac arrest.
对24只未进行灌注的低温犬的心肌毛细血管内皮细胞（EC）的超微结构变化进行了研究。在对照组、麻醉期间（主动降温前）以及中度（28 - 30摄氏度）和深度（22 - 24摄氏度）人工体冷却结束时，从每只犬的左心室获取用于电子显微镜检查的活检标本。在对照组和所有测试组中均鉴定出以下几种形态类型的内皮细胞：细胞质中度致密的细胞、浅色细胞、深色细胞和不可逆损伤细胞。与其他类型相比，深色细胞的质膜小泡数量增加，似乎更具运输特异性。在实验的所有阶段，深色细胞的数量持续增加（分别增至23.80%、34.62%和47.17%）。冷却至28 - 30摄氏度时，在所有类型的内皮细胞中均观察到细胞器（细胞核、高尔基体和粗面内质网）合成活性降低的亚细胞表现。这些变化在深度低温结束时持续存在甚至加剧。在所有细胞类型中，三个实验组内皮细胞的运输活性变化不同。在麻醉期间自发轻度低温（34 - 35摄氏度）下，微胞饮活性增加，随后随着温度人工降至22 - 24摄氏度，微胞饮活性趋于降低。这些超微结构变化似乎构成了毛细血管内皮适应体表冷却过程的一个组成部分，并且可能有助于在心脏骤停期间对随后缺血暴露产生耐受性。
