Tsubokawa Tamiji, Kurita Hiroki, Kaneko Nobuyuki, Iino Naoko, Shiokawa Yoshiaki
Department of Neurosurgery, Kyorin University School of Medicine, 6-20-2 Shinkawa, Mitaka-shi, Tokyo 181-8611, Japan.
No To Shinkei. 2003 Nov;55(11):953-60.
Hyponatremia and hypovolemia following aneurysmal subarachnoid hemorrhage (SAH) might be speculated by exaggerated secretion of natriuretic peptides and resulted ischemic sequela caused by cerebral vasospasm. We measured serum concentration of natriuretic peptides and investigated their influence on post-SAH hyponatremia. Among 49 patients of SAH, their plasma concentration of the natriuretic peptides (atrial natriuretic peptide: ANP and brain natriuretic peptide: BNP) were measured at the day of ictus and 7th day of SAH. The correlation between concentration of natriuretic peptides and location of aneurysm, severity of SAH, incidence of hyponatremia and symptomatic vasospasm were elucidated. The plasma concentration of ANP did not alter on admission and 7th day post SAH, whereas that of BNP increased in the patients with moribund SAH and those with ruptured A-com aneurysm. The initial increase of BNP following SAH could be attributed to direct damage of SAH on the hypothalamus. Hyponatremia and symptomatic vasospasm tended to occur in the patients who had persistent increase of plasma BNP concentration during one week post SAH. Therapeutic intervention to maintain normonatremia by fluid-management decreased occurrence of symptomatic vasospasm, even though patients with increased plasma BNP concentration. It might be concluded that increased secretion of BNP following SAH is caused by direct effect to the hypothalamus and prolonged hyper secretion of BNP resulted hyponatremia, hypovolemia and exaggerated symptomatic vasospasm.
动脉瘤性蛛网膜下腔出血(SAH)后出现的低钠血症和血容量不足,可能是由于利钠肽分泌过多以及脑血管痉挛导致的缺血性后遗症所致。我们测量了利钠肽的血清浓度,并研究了它们对SAH后低钠血症的影响。在49例SAH患者中,于发病当日及SAH后第7天测量了他们血浆中的利钠肽(心房利钠肽:ANP和脑利钠肽:BNP)浓度。阐明了利钠肽浓度与动脉瘤位置、SAH严重程度、低钠血症发生率及症状性血管痉挛之间的相关性。SAH患者入院时及SAH后第7天,ANP的血浆浓度未发生改变,而在病情严重的SAH患者及前交通动脉瘤破裂患者中,BNP的血浆浓度升高。SAH后BNP的初始升高可能归因于SAH对下丘脑的直接损害。SAH后1周内血浆BNP浓度持续升高的患者往往会出现低钠血症和症状性血管痉挛。通过液体管理维持正常血钠水平的治疗干预可降低症状性血管痉挛的发生率,即使是血浆BNP浓度升高的患者。可以得出结论,SAH后BNP分泌增加是由对下丘脑的直接作用引起的,而BNP的长期过度分泌导致了低钠血症、血容量不足和症状性血管痉挛加剧。