Relationship between Calcium Accumulation and Recovery of Cat Brain after Prolonged Cerebral Ischemia
Relationship between Calcium Accumulation and Recovery of Cat Brain after Prolonged Cerebral Ischemia
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猫脑长期缺血后钙积累与恢复的关系
DOI：
10.1038/jcbfm.1983.50
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发表时间：
1983
影响因子：
6.3
通讯作者：
L. Csiba
中科院分区：
文献类型：
--
作者：
K. Hossmann;W. Paschen;L. Csiba
对18只成年常温猫脑组织钙含量与缺血后电生理和代谢恢复的关系进行了研究，其中12只猫全脑缺血1h，再灌流3h。6只动物作为对照。通过记录皮层脑电(ECoG)和诱发电位来评估功能恢复，通过对完整脑切片的ATP、葡萄糖和pH进行局部评估来评估生化恢复。一组动物接受钙拮抗剂氟桂利嗪(0.1 mg/kg静脉注射，然后在再循环阶段持续静脉滴注0.1 mg/kg/h)；另一组不接受这种治疗。所有6只未经治疗的动物的诱发电位(以及4只动物的自发皮层脑电活动)在缺血后恢复。在有ECoG活动的动物中，生化恢复是均匀的，表现为局部组织ATP和葡萄糖含量恢复到正常。在一只没有ECoG活动的动物中，出现了几个能量代谢受损的小区域。在生化恢复区，脑组织钙离子显著增加∼35%(对照组，0.330±0.045；缺血区，0.447±0.194μg/mg蛋白；均值±SD)。伴随这些变化的是钠(对照组，7.72±1.92；缺血组，10.50±2.47μg/mg蛋白)、钾(对照组，29.52±0.85，缺血组，27.66±2.30μg/mg蛋白)和组织pH升高(对照组，7.10±0.096；缺血组，7.307±0.083)。未恢复区pH降至6.288±0.157，钙含量为0.602±0.235，钠含量为11.70±4.6，钾含量为23.00±3.91μg/mg蛋白质。钙拮抗剂氟桂利嗪的治疗并没有减少组织中的钙含量，也没有改善缺血后的功能或代谢恢复：6只接受治疗的动物中，3只显示了皮层脑电活动，1只只显示了诱发电位，2只完全没有恢复。结论：钙拮抗剂氟桂利嗪不能阻止脑缺血后钙蓄积。然而，观察到的钙升高并没有干扰缺血后早期的电生理和生化恢复。因此，它的病理生理学重要性可能与更多延迟的缺血后障碍有关。
The relationship between brain tissue calcium content and postischemic electrophysiological and metabolic recovery was investigated in 18 adult normothermic cats, 12 of which were submitted to 1 h of complete ischemia and 3 h of recirculation. Six animals served as controls. Functional recovery was estimated by recording the electrocorticogram (ECoG) and evoked potentials, and biochemical recovery by regional evaluation of ATP, glucose, and pH in intact brain sections. One group of animals was treated with the calcium antagonist flunarizine (0.1 mg/kg i. v., followed by continuous i. v. infusion of 0.1 mg/kg/h during the recirculation phase); another group did not receive this treatment. Evoked potentials in all six untreated animals (and in four also, spontaneous ECoG activity) returned after ischemia. In the animals with ECoG activity, biochemical recovery was homogeneous, as indicated by a return toward normal of regional tissue ATP and glucose content. In one animal without ECoG activity, several small regions were present in which energy metabolism was impaired. In regions with biochemical recovery, brain tissue calcium significantly increased by ∼35% (controls, 0.330 ± 0.045; ischemia, 0.447 ± 0.194 μg/mg protein; means ± SD). Changes were accompanied by a parallel increase in sodium (controls, 7.72 ± 1.92; ischemia, 10.50 ± 2.47 μg/mg protein), a slight decrease of potassium (controls, 29.52 ± 0.85; ischemia, 27.66 ± 2.30 μg/mg protein), and an increase of tissue pH (controls, 7.10 ± 0.096; ischemia, 7.307 ± 0.083). In regions without biochemical recovery, pH fell to 6.288 ± 0.157, and calcium content was 0.602 ± 0.235, sodium content 11.70 ± 4.60, and potassium content 23.00 ± 3.91 μg/mg protein. Treatment with the calcium antagonist flunarizine did not reduce tissue calcium content, nor did it improve functional or metabolic recovery after ischemia: three of six treated animals exhibited ECoG activity, one showed only evoked potentials, and two showed no recovery at all. It is concluded that postischemic accumulation of calcium in brain tissue cannot be prevented by the calcium antagonist flunarizine. However, the observed increase of calcium did not interfere with the early postischemic electrophysiological and biochemical recovery. Its pathophysiological importance, therefore, may be associated with more delayed postischemic disturbances.
DOI：
--
发表时间：
1982-05
期刊：
Pathologie-biologie
影响因子：
--
作者：
T. Wieloch;B. Siesjö
通讯作者：
T. Wieloch;B. Siesjö
脑缺血中的离子转移。
影响因子：
6.1
作者：
Yanagihara,T;McCall,JT
通讯作者：
McCall,JT