Okuchi K, Fujioka M, Fujikawa A, Nishimura A, Konobu T, Miyamoto S, Sakaki T
Department of Neurosurgery, Nara Medical University, Kashihara, Japan.
Acta Neurochir (Wien). 1996;138(8):951-6; discussion 956-7. doi: 10.1007/BF01411284.
To prevent symptomatic cerebral vasospasm, we have used hypervolaemia (HV) or volume expansion in patients with aneurysmal subarachnoid haemorrhage (SAH) in recent years. In these patients we could not perform effective fluid and sodium (Na) replacement because of rapid and overwhelming water and Na loss. Although this phenomenon is characteristic under hypervolaemic states, we regard it important to elucidate the mechanism underlying initiation of vasospasm after aneurysmal SAH. Patients with aneurysmal SAH, operated on within 24 hours of onset, were analysed prospectively. We selected 17 patients in good pre-operative condition. Intravascular volume expansion was accomplished with plasma fractionate or albumin and crystalloid solutions in all patients. We divided the 17 patients into two groups; symptomatic spasm group (S-group) consisting of 4 cases developing transient ischaemic symptoms and non-symptomatic spasm group (NS-group) consisting of 13 cases. In S-group, rapid and marked natriuresis developed characteristically before the onset of ischaemic symptoms. The differences in daily Na balance between the two groups were significant on the 3rd and 5th days (p < 0.05). The mean cumulative Na balance in S-group during the 10 days of the study (-375 +/- 159 mEg) was higher than that of NS-group (-24.4 +/- 225 mEq) (p < 0.05). Rapid natriuresis preceded the development of ischaemic symptoms, and was important as a trigger for symptomatic vasospasm after SAH. We considered that hormonal disorders were implicated in this phenomenon, and atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), renin, and aldosterone were each measured three times during the period, with no significant differences, found between the two groups. It was speculated that another potent natriuretic factor, similar to ANP, induced a rapid selective natriuresis resulting in symptomatic vasospasm.
近年来，为预防有症状的脑血管痉挛，我们对动脉瘤性蛛网膜下腔出血（SAH）患者采用了高血容量疗法（HV）或扩容疗法。在这些患者中，由于水分和钠的快速大量丢失，我们无法进行有效的液体和钠（Na）补充。尽管这种现象在高血容量状态下具有特征性，但我们认为阐明动脉瘤性SAH后血管痉挛起始的潜在机制很重要。对发病后24小时内接受手术的动脉瘤性SAH患者进行了前瞻性分析。我们选择了17例术前状况良好的患者。所有患者均通过血浆成分或白蛋白及晶体溶液进行血管内容量扩充。我们将这17例患者分为两组；有症状痉挛组（S组）由4例出现短暂缺血症状的患者组成，无症状痉挛组（NS组）由13例患者组成。在S组中，缺血症状发作前典型地出现了快速且显著的利钠现象。两组在第3天和第5天的每日钠平衡差异有统计学意义（p < 0.05）。研究10天期间S组的平均累积钠平衡（-375 +/- 159 mEq）高于NS组（-24.4 +/- 225 mEq）（p < 0.05）。快速利钠先于缺血症状出现，并且是SAH后有症状血管痉挛的重要触发因素。我们认为激素紊乱与这一现象有关，在此期间对心房利钠肽（ANP）、抗利尿激素（ADH）、肾素和醛固酮各进行了三次测量，两组之间未发现显著差异。据推测，另一种类似于ANP的强效利钠因子诱导了快速选择性利钠，导致有症状的血管痉挛。
