Wijdicks E F, Schievink W I, Burnett J C
Department of Neurology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA.
J Neurosurg. 1997 Aug;87(2):275-80. doi: 10.3171/jns.1997.87.2.0275.
The natriuretic peptide system consists of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). The system is implicated in the control of body fluid homeostasis, causes natriuresis and diuresis (ANP and BNP), and regulates vascular tone (CNP). A reciprocal relationship between ANP and endothelin (ET) has been suggested, and earlier studies have documented a possible role of ET in cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The authors studied plasma ANP, BNP, CNP, and ET for 6 consecutive days in 13 patients with SAH by using radioimmunoassay. The median admission values for ANP were 31.5 pg/ml (range 16.8-323 pg/ml [normal 15 +/- 7 pg/ml]); for BNP, 45.3 pg/ml (range 2.2-80.2 pg/ml [normal 12 +/- 9 pg/ml]); for CNP, 7.7 pg/ml (range < 2-20 pg/ml [normal 5.2 +/- 3 pg/ml]); and for ET, 11 pg/ml (range 6.5-25.1 pg/ml [normal 7.2 +/- 4 pg/ml]). Additional increases (defined as > 100% increase on two consecutive measurements) were noted in ANP (11 patients), BNP (10 patients), and CNP (three patients), and resulted in a negative fluid balance in 10 of the 13 patients. The CNP increased in three of four patients with cerebral vasospasm and in one of nine patients without cerebral vasospasm (Fisher's exact test, p = 0.2). No major fluctuations in plasma ET were noted. In seven patients, the plasma ET level did not increase beyond 10 pg/ml during the days of measurement. In six patients, only an occasional sample showed an increase to a maximum of 25 pg/ml. Changes in BNP, ANP, and CNP were independent of each other. The authors conclude that both plasma ANP and BNP increase after SAH and often result in a negative fluid balance. Plasma ANP and BNP seem differentially regulated in the presence of SAH but not by the level of the plasma ET. The possible role of CNP as a regulatory response to cerebral vasospasm needs further exploration.
利钠肽系统由心房利钠肽（ANP）、脑利钠肽（BNP）和C型利钠肽（CNP）组成。该系统参与体液平衡的调节，可引起利钠和利尿（ANP和BNP），并调节血管张力（CNP）。已有研究提示ANP与内皮素（ET）之间存在相互关系，早期研究也已证明ET在动脉瘤性蛛网膜下腔出血（SAH）后的脑血管痉挛中可能发挥作用。作者采用放射免疫分析法，对13例SAH患者连续6天检测血浆中的ANP、BNP、CNP和ET。ANP入院时的中位数为31.5 pg/ml（范围16.8 - 323 pg/ml[正常为15±7 pg/ml]）；BNP为45.3 pg/ml（范围2.2 - 80.2 pg/ml[正常为12±9 pg/ml]）；CNP为7.7 pg/ml（范围<2 - 20 pg/ml[正常为5.2±3 pg/ml]）；ET为11 pg/ml（范围6.5 - 25.1 pg/ml[正常为7.2±4 pg/ml]）。ANP（11例患者）、BNP（10例患者）和CNP（3例患者）出现进一步升高（定义为连续两次测量升高>100%），并导致13例患者中有10例出现负水平衡。4例脑血管痉挛患者中有3例CNP升高，9例无脑血管痉挛患者中有1例升高（Fisher精确检验，p = 0.2）。未观察到血浆ET有明显波动。7例患者在测量期间血浆ET水平未超过10 pg/ml。6例患者仅偶尔有样本显示升高至最高25 pg/ml。BNP、ANP和CNP的变化相互独立。作者得出结论，SAH后血浆ANP和BNP均升高，且常导致负水平衡。在SAH情况下，血浆ANP和BNP似乎受到不同调节，但不受血浆ET水平影响。CNP作为对脑血管痉挛的调节反应的可能作用需要进一步探索。
