STUDY OF ANGIOTENSIN-II PRESSOR RESPONSE THROUGHOUT PRIMIGRAVID PREGNANCY
STUDY OF ANGIOTENSIN-II PRESSOR RESPONSE THROUGHOUT PRIMIGRAVID PREGNANCY
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DOI：
10.1172/jci107462
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发表时间：
1973-01-01
影响因子：
15.9
通讯作者：
MACDONALD, PC
中科院分区：
文献类型：
--
作者：
GANT, NF;DALEY, GL;MACDONALD, PC
本研究旨在确定年轻初移症患者在整个妊娠期间对血管紧张素II的升压反应，以确定在妊娠期间对血管紧张素II升压作用产生耐药性的时间；B)确定导致这种抗性的事件的生理顺序；c)确定在妊高征临床症状出现之前是否可以检测到输注血管紧张素II的敏感性。采用这种前瞻性方法，定义了两组不同的患者。第一组患者在整个孕期保持正常。第二组包括那些在研究初期临床血压正常，但最终发展为妊娠高血压的患者。研究了192例患者；其中，120名患者保持血压正常，72名患者发展为妊娠高血压。在两组中，早在妊娠第10周，血管对输注血管紧张素II（超过8 ng/kg/min才能引起舒张压20 mm Hg的升压反应）的抵抗就被证实。在血压保持正常的组中，最大平均血管阻力发生在妊娠18-30周，（所需的平均升压剂量为13.5至14.9 ng/kg/min）。在发生妊娠性高血压的受试者中，在妊娠第18周观察到的平均最大剂量为12.9 ng/kg/min。到第22周，两组明显分离，注定要发生高血压的受试者的平均剂量要求逐渐低于保持正常的受试者。在妊娠23 ~ 26周时，两组比较差异有统计学意义（P< 0.01）。在第28-32周期间进行一次或多次检查需要超过8 ng/kg/min的患者中，91%保持血压正常。相反，在同一时间段内，需药量低于8ng /kg/min的患者中，至少有一次，90%发生妊娠高血压。
The present study was designed to ascertain sequentially the pressor response to angiotensin II in young primigravid patients throughout pregnancy in ordera) to define when in pregnancy resistance to the pressor effects of angiotensin II develops;b) to define the physiologic sequence of events leading to this resistance; andc) to ascertain whether sensitivity to infused angiotensin II could be detected before the onset of clinical signs of pregnancy-induced hypertension.With this prospective approach, two separate groups of patients were defined. The first group of patients remained normal throughout pregnancy. The second group consisted of those patients who, while clinically normotensive during the initial phase of the study, ultimately developed hypertension of pregnancy.192 patients were studied; of these, 120 patients remained normotensive and 72 developed pregnancy-induced hypertension. In both groups, vascular resistance to infused angiotensin II (more than 8 ng/kg/min required to elicit a pressor response of 20 mm Hg in diastolic pressure) was demonstrated as early as the 10th wk of pregnancy. In the group that remained normotensive, maximum mean vascular resistance occurred at 18-30 wk of pregnancy, (mean pressor dose required being 13.5 to 14.9 ng/kg/min). In those subjects who developed pregnancy-induced hypertension, the mean maximum dose required was 12.9 ng/kg/min, which was observed at the 18th wk of pregnancy. By the 22nd wk there was a clear separation of the two groups, with the mean dose requirement of the subjects destined to develop hypertension being progressively less than that of those who remained normal. The difference between the two groups became significant (P< 0.01) by 23-26 wk of pregnancy.Among patients requiring more than 8 ng/kg/min on one or more tests done between wk 28-32, 91% remained normotensive. Conversely, during the same time period among patients requiring less than 8 ng/kg/min, on at least one occasion, 90% developed pregnancy-induced hypertension.