Morphologic changes in tubular cells from in situ kidneys following experimental hypothermia and rewarming
Morphologic changes in tubular cells from in situ kidneys following experimental hypothermia and rewarming
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实验性低温和复温后原位肾脏肾小管细胞的形态变化
DOI：
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发表时间：
2005
期刊：
影响因子：
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通讯作者：
Sigurd Lindal
中科院分区：
文献类型：
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作者：
T. Tveita;Katja Salomon Johansen;A. H. Lien;Reidar Myklebust;Sigurd Lindal
尽管意外深低温复温后可能会发生肾功能衰竭，但在实验低温和临床病例报道中，这一课题很少受到关注。为了探索低温和低温后肾脏形态的完整性，我们使用了意外低温的实验动物模型，在降温和复温过程中，心脏支持循环，而不伴随心脏停搏或缺血。本文研究了3组戊巴比妥钠麻醉大鼠肾小管上皮细胞超微结构的变化：1)对照组(n=6)在37 °C下维持4 h；2)低温大鼠(n=6)核心冷却后在15~13 °C下维持4 h；低温肾脏的电子显微镜(EM)显示线粒体变圆，失去对比度。虽然不是所有的活组织检查都观察到了这些变化，但在所有肾脏中都发现了这些变化。其中三个肾脏的大部分EM上均可见局灶性肾小管坏死区。复温肾脏的电子显微镜显示线粒体超微结构的变化与低温后的相似，但总体上这种变化更为显著。显微镜下可见10个肾中有7个可见细胞外水肿、细胞内水肿、线粒体肿胀、染色质边集、单个肾小管细胞坏死、坏死物碎屑进入管腔。从实验性低温复温，没有发生缺血或缺氧，从而导致肾小管细胞的超微结构变化，类似于急性肾小管坏死时观察到的变化，与肾功能衰竭有关。
Although renal failure may occur following rewarming from deep accidental hypothermia, this subject has received little attention in experimental hypothermia and clinical case reports. In order to explore the integrity of hypothermic and posthypothermic renal morphology we used an experimental animal model of accidental hypothermia where the heart supports the circulation throughout cooling and rewarming without accompanying cardioplegia or ischemia. Ultrastructural changes in renal tubular cells from three groups of pentobarbital anesthetized Wistar rats: 1) controls (n=6) maintained at 37 °C for 4 h, 2) hypothermic rats (n=6) core‐cooled and maintained at 15–13 °C for 4 h, and 3) rewarmed rats (n=10), were studied as a sensitive indicator of renal damage. Electron micrographs (EM) from hypothermic kidneys showed rounded up mitochondria with loss of contrast. These changes were observed in several though not all of the biopsies, but they were found in all kidneys. Areas exhibiting focal tubular necrosis were seen on most EM from three of these kidneys. EM from rewarmed kidneys showed alterations of mitochondrial ultrastructure with similarities to those observed after hypothermia, but in general the changes were more prominent. Extracellular edema, intracellular edema, swelling of mitochondria, margination of chromatin, necrosis of single tubular cells, and disrupting necrotic debris into tubular lumen could be found in micrographs from 7 of the 10 kidneys examined. Rewarming from experimental hypothermia, without episodes of ischemia or hypoxia, thus induces ultrastructural changes in renal tubular cells similar to changes observed in acute tubular necrosis, associated with renal failure.