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Clinical significance of natriuretic peptides in patients with aneurysmal subarachnoid hemorrhage

机译:钠尿肽在动脉瘤性蛛网膜下腔出血患者中的临床意义

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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.
机译:动脉瘤性蛛网膜下腔出血(SAH)后的低钠血症和血容量不足可能是由于利尿钠肽的过度分泌以及由脑血管痉挛引起的缺血性后遗症所引起的。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,在发作当天和SAH的第7天测量其血浆利钠肽(心钠素:ANP和脑利钠肽:BNP)的血浆浓度。阐明了利钠肽浓度与动脉瘤位置,SAH严重程度,低钠血症发生率和症状性血管痉挛之间的相关性。入院时和SAH后第7天,ANP的血浆浓度没有改变,而垂死SAH和A型动脉瘤破裂的患者的BNP升高。 SAH后BNP的最初增加可能归因于SAH对下丘脑的直接损害。 SAH后一周内血浆BNP浓度持续升高的患者倾向于发生低钠血症和症状性血管痉挛。尽管患者血浆BNP浓度升高,但通过输液管理进行的维持血压正常的治疗干预减少了症状性血管痉挛的发生。可以得出结论,SAH后BNP的分泌增加是由对下丘脑的直接作用引起的,而BNP的长期过度分泌会导致血钠过少,血容量不足和症状性血管痉挛过度。

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