Wijdicks E F, Ropper A H, Hunnicutt E J, Richardson G S, Nathanson J A
Department of Neurology, Massachusetts General Hospital, Boston.
Stroke. 1991 Dec;22(12):1519-24. doi: 10.1161/01.str.22.12.1519.
The causes of volume depletion and hyponatremia after subarachnoid hemorrhage are not fully understood but may be in part due to natriuresis or "cerebral salt wasting." Because previous studies using infrequent hormone sampling have given inconsistent results, we determined if elevations in atrial natriuretic factor concentrations preceded negative sodium and fluid balances.
We measured diurnal atrial natriuretic factor and vasopressin concentrations and sodium balance for 5 days in 14 consecutive patients after aneurysmal subarachnoid hemorrhage.
Plasma concentrations of atrial natriuretic factor on admission were elevated in subarachnoid hemorrhage patients (mean +/- SD 106 +/- 59 pg/ml) compared with acutely ill controls (39 +/- 30 pg/ml). In eight patients, high peak concentrations of atrial natriuretic factor, greater than 300 pg/ml or a twofold increase above baseline, were followed by natriuresis and a negative sodium balance. Three patients, two of whom became hyponatremic, developed cerebral infarcts after natriuresis. Vasopressin concentrations were slightly elevated just after hemorrhage but subsequently declined to normal values.
A markedly increased atrial natriuretic factor concentration precedes natriuresis in some patients and, with other abnormalities of water handling possibly including a relatively diminished vasopressin concentration, may cause volume depletion. Patients with natriuresis appear to be at increased risk for delayed cerebral infarction after subarachnoid hemorrhage.
蛛网膜下腔出血后容量减少和低钠血症的原因尚未完全明确，但可能部分归因于利钠作用或“脑性盐耗损”。由于既往研究采用不频繁的激素采样得出的结果不一致，我们探究了心房利钠因子浓度升高是否先于钠和液体负平衡出现。
我们对14例动脉瘤性蛛网膜下腔出血后的连续患者，测量了5天的日间心房利钠因子和血管加压素浓度以及钠平衡情况。
与急性病对照组（39±30 pg/ml）相比，蛛网膜下腔出血患者入院时血浆心房利钠因子浓度升高（均值±标准差为106±59 pg/ml）。在8例患者中，心房利钠因子出现高于300 pg/ml或高于基线两倍的高峰浓度后，随之出现利钠作用和负钠平衡。3例患者在利钠作用后发生脑梗死，其中2例出现低钠血症。出血后血管加压素浓度略有升高，但随后降至正常水平。
在一些患者中，心房利钠因子浓度显著升高先于利钠作用，并且与其他水代谢异常（可能包括血管加压素浓度相对降低）一起，可能导致容量减少。利钠作用的患者蛛网膜下腔出血后发生迟发性脑梗死的风险似乎增加。
