Effects of intraparenchymal hemorrhage on extracellular cortical potassium in experimental head trauma.
Effects of intraparenchymal hemorrhage on extracellular cortical potassium in experimental head trauma.
复制标题
实验性头部创伤中实质内出血对细胞外皮质钾的影响。
DOI：
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发表时间：
1983
影响因子：
4.1
通讯作者：
D. Kornhauser
中科院分区：
文献类型：
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作者：
O. Hubschmann;D. Kornhauser
在 11 只猫身上建立了脑实质内出血模型。实质出血的发生伴随着血肿附近解剖学完整区域的大量细胞去极化和 K+ 释放。 K+ 清除速度很快，并且在大多数情况下是完全清除的。这种最初的 K+ 释放并非起源于缺血，而是细胞膜上渗出的血液的机械和化学因素的结果。相比之下，白质含水量的增加并不影响记录区域大脑皮层细胞外空间的细胞功能或K+水平。实验结果表明，K+释放发生在创伤发生时出血附近亚临界损伤的细胞区域中。细胞元素经历大量去极化，伴随着许多化学和生化变化，导致细胞肿胀。细胞去极化和 K+ 释放似乎是中枢神经系统对创伤的最初反应。这种反应的程度可能会强烈影响细胞损伤的最终程度，从而影响头部创伤患者的神经功能缺损。
A model of intraparenchymal hemorrhage was created in 11 cats. The development of the parenchymal hemorrhage was accompanied by a massive cellular depolarization and K+ release in anatomically intact areas in the vicinity of the hematoma. The K+ clearance was rapid and in most instances total. This initial K+ release was not ischemic in origin but was the result of mechanical and chemical factors of the extravasated blood on cellular membranes. In contrast, an increased water content of the white matter did not affect the cellular function or levels of K+ in the extracellular space of the cerebral cortex in the recording area. The experimental results suggest that K+ release takes place at the onset of trauma in subcritically injured cellular areas in the vicinity of a hemorrhage. The cellular elements undergo massive depolarization which is accompanied by a number of chemical and biochemical changes that lead to cellular swelling. Cellular depolarization and K+ release appear to be the initial response of the central nervous system to trauma. The extent of this response may strongly influence the final degree of cellular damage and, thus, the neurological deficit in patients with head trauma.