Effect of hypoxia on the cerebral adaptation to acute hyponatremia in experimental animals.
Effect of hypoxia on the cerebral adaptation to acute hyponatremia in experimental animals.
复制标题
缺氧对实验动物脑适应急性低钠血症的影响。
DOI：
10.1007/s00467-006-0309-x
复制
发表时间：
2007
期刊：
影响因子：
--
通讯作者：
Trachtman,Howard
中科院分区：
文献类型：
--
作者：
Trachtman,Howard
Anyone who has been reading the literature about hyponatremia in steady doses over the past 20 years could become exasperated and conclude that the endless stream of articles addressing the pathogenesis, epidemiology, manifestations, diagnosis, and proper management of this electrolyte disorder are nothing more than intellectual squabbling. It would be easy to lose hope of shedding new light or reaching a consensus on this contentious issue. However, in actuality, there is much that nephrologists actually agree about on this topic. First, it is widely recognized that hyponatremia is the most common electrolyte disturbance in hospitalized patients [1]. In addition, an abnormally low serum sodium concentration can occur in the context of a low, normal, or expanded extracellular fluid volume [2, 3]. The syndrome of inappropriate anti-diuretic hormone (ADH) release probably accounts for a large percentage of cases, and it reflects abnormal vasopressin release that can be triggered by either osmotic or nonosmotic stimuli [4]. Finally, the primary target organ in patients with hyponatremia is the brain, and they are susceptible to developing acute cerebral edema due to the movement of water down its gradient from the extracellular to the intracellular compartments [2, 3]. It is at this point that the going gets tougher. The debate begins to heat up noticeably when people start to ask what is the timeframe during which hyponatremia is a life-threatening problem? What is acute and what is chronic? The argument intensifies even further when the pathogenesis of the neuropathological lesions in the brain in patients with hyponatremia is addressed. Is it the consequence of the electrolyte disturbance per se, or the treatment used to correct the low serum sodium concentration? Is the damage solely due to osmolal injury or are other factors such as elevated arginine vasopressin (AVP) levels or reduced cerebral perfusion involved in the process? Needless to say, things are almost out of control when prognosis and liability are raised in the context of the management of a patient with hyponatremia.Allan Arieff and his colleagues have been studying hyponatremia for over three decades and have published numerous reports about the changing profile of the entity and the impact of therapy on patient outcomes. Because of the logistical constraints involved in systematically evaluating different treatment regimens in the acute setting, they have tried to systematically translate lessons learned from experimental animals to the bedside. For example, they have shown that the risk of developing clinical symptoms as a consequence of hyponatremia is not the same in all patients. Juvenile animals and menstruating female animals manifest increased cerebral edema in response to acute hyponatremia compared to male counterparts and postmenopausal females. This is reflected by increased brain sodium content and reduced activity of the Na-K ATPase, which may be inhibited by circulating estrogens [5]. Interestingly, these findings are paralleled by data in patients which suggest that the young children and
