Salerno F, Badalamenti S, Moser P, Lorenzano E, Incerti P, Dioguardi N
Istituto di Medicina Interna, Universitá degli Studi di Milano, Milan, Italy.
Gastroenterology. 1990 Apr;98(4):1063-70. doi: 10.1016/0016-5085(90)90034-x.
The plasma levels of atrial natriuretic factor in liver cirrhosis can be affected by various factors, such as ascites, renal function, use of diuretics drugs and dietary sodium intake. Moreover, the influence of high intra-abdominal pressure on cardiac atrial natriuretic factor release in patients with tense ascites has not been investigated. The aim of the present study was to evaluate the circulating levels of atrial natriuretic factor and their relationships to plasma renin activity, aldosterone concentration, and urinary sodium excretion in 45 cirrhotic patients divided into 4 groups: (a) cirrhotics without ascites; (b) nonazotemic cirrhotics with ascites; (c) cirrhotics with ascites and functional renal failure; and (d) cirrhotics with ascites taking diuretics. In some patients with tense ascites, atrial natriuretic factor was also measured after rapid abdominal relaxation by large volume paracentesis. Plasma levels of atrial natriuretic factor obtained in 13 healthy control subjects after 5 days on a 40-50 mEq sodium daily intake were 22.8 +/- 3.3 pg/ml. Mean plasma atrial natriuretic factor levels were normal in patients without ascites (35.1 +/- 11.4 pg/ml) and in those with ascites taking diuretics (27 +/- 9.2 pg/ml), but elevated in patients with ascites not taking diuretics (59.6 +/- 12 pg/ml) and in those with ascites and functional renal failure (58.5 +/- 16.6 pg/ml). These data show that plasma atrial natriuretic factor levels are elevated only in cirrhotic patients who are ascitic and not taking diuretics. In these patients atrial natriuretic factor levels were directly correlated with urinary sodium excretion, even though sodium balance was positive. This could be the consequence of the contrasting effects of antinatriuretic factors, as suggested by the inverse relationships between atrial natriuretic factor and urinary sodium on the one hand and plasma renin activity and plasma aldosterone concentration on the other. Twenty-six patients with tense ascites (12 taking diuretics and 14 not) were treated with rapid large-volume paracentesis (6500 +/- 330 ml of ascitic fluid removed in 168 +/- 16 min). At the end of the procedure, plasma atrial natriuretic factor levels had increased in all patients (from 45.5 +/- 10.1 to 100 +/- 17 pg/ml), whereas plasma renin activity and plasma aldosterone concentration had decreased (from 10.3 +/- 1.6 to 7 +/- 1.3 ng/ml/h, and 1160 +/- 197 to 781 +/- 155 pg/ml, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)
肝硬化患者血浆心房利钠因子水平会受到多种因素影响,如腹水、肾功能、利尿剂使用及饮食钠摄入等。此外,对于张力性腹水患者,高腹内压对心脏心房利钠因子释放的影响尚未得到研究。本研究旨在评估45例肝硬化患者分为4组后的循环心房利钠因子水平及其与血浆肾素活性、醛固酮浓度和尿钠排泄的关系:(a)无腹水的肝硬化患者;(b)非氮质血症性有腹水的肝硬化患者;(c)有腹水且伴有功能性肾衰竭的肝硬化患者;(d)有腹水且服用利尿剂的肝硬化患者。在一些张力性腹水患者中,还通过大量腹腔穿刺快速放腹水使腹部松弛后测量了心房利钠因子。13名健康对照者在每日摄入40 - 50 mEq钠5天后测得的血浆心房利钠因子水平为22.8±3.3 pg/ml。无腹水患者(35.1±11.4 pg/ml)和服用利尿剂的腹水患者(27±9.2 pg/ml)的血浆心房利钠因子平均水平正常,但未服用利尿剂的腹水患者(59.6±12 pg/ml)和有腹水且伴有功能性肾衰竭的患者(58.5±16.6 pg/ml)的该水平升高。这些数据表明,仅在有腹水且未服用利尿剂的肝硬化患者中血浆心房利钠因子水平升高。在这些患者中,尽管钠平衡为正,但心房利钠因子水平与尿钠排泄直接相关。这可能是利钠因子与抗利钠因子作用相反的结果,一方面心房利钠因子与尿钠呈负相关,另一方面与血浆肾素活性和血浆醛固酮浓度呈负相关。26例张力性腹水患者(12例服用利尿剂,14例未服用)接受了快速大量腹腔穿刺治疗(在168±16分钟内抽出6500±330 ml腹水)。治疗结束时,所有患者的血浆心房利钠因子水平均升高(从45.5±10.1升至100±17 pg/ml),而血浆肾素活性和血浆醛固酮浓度降低(分别从10.3±1.6降至7±1.3 ng/ml/h和从1160±197降至781±155 pg/ml)。(摘要截取自400字)