Angiotensin IIに対する血管反応性の基礎と臨床 : 妊娠中毒症の病態に基づく発症予知・予防法について (<シンポジウム>妊娠中毒症 : その病態論的アプローチ)

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This paper shows the basic and clinical evaluations of pressor responsiveness to angiotensin II (A II) using A II sensitivity test (AST) in normotensive and hypertensive pregnant women. The results are as follows: I. Basic findings of A II pressor responsiveness 1. AST was performed sequentially from as early in gestation as possible throughout the remainder of pregnancy. At clinic visit the patients received A II infusions sufficient to raise baseline diastolic blood pressure by 20mmHg. The dose (ng/kg/min) of A II required to elevate 20mmHg of diastolic blood pressure was recorded as the EPD. Increased EPD indicates the dullness of refractoriness to A II. The EPD in normotensive women (non-PIH) increased as early as midpregnancy, but EPD in women destined to develop pregnancy-induced-hypertension (PIH) decreased significantly after the 20th week of gestation. 2. Plasma angiotensin level in non-PIH increased significantly compared to that of PIH. There exists a detinite correlation between EPD in pregnant women and plasma angiotensin level. 3. The plasma TxB_2/6-keto-PGF_<1α> ratio increased significantly in PIH compared with that of non-PIH because of the increase in the amount of TxB_2. In the 2nd trimester, the ratio in women destined to developed PIH showed a significantly higher value than that of the non-PIH. 4. In healthy men and castrated rats the EPD significantly increased after the administration of progesterone. At 20 and 30 weeks' gestation, the plasma progesterone/estrogen ratio in women destined to develop PIH decreased significantly compared to that of the non-PIH. These findings suggest that increased EPD during normal pregnancy results from the increased plasma angiotensin level, the imbalance of TxB_2/6-keto-PGF_<1α>, and progesterone or progesterone metabolites which increases during pregnancy. The impairment of these physiological changes during normal pregnancy may cause the loss of refractoriness to A II in PIH. II. Clinical evaluations of AST 1. In high risk pregnant women, AST was serially performed every other week between 26 and 32 of gestation. If the EPD of 12ng/kg/min at 30 weeks' gestation was used as the critical criterion for PIH, AST had 91% sensitivity and 89% specificity in the detection of onset of PIH. The negative predictive value was 99%. 2. In healthy men and female rabbits the EPD could be increased by short-term treatment with eicosapentaenoic acid without change of the systolic blood pressure. 3. In pregnant women and pregnant rats the EPD was significantly increased after oral calcium supplementation. No side effects of the calcium administration were observed. III. Clinical adaptation of AST and calcium supplementation According to protocol which was designed to predict onset of PIH by AST and to prevent it by calcium supplementation, pregnant women who had high risk factor of PIH were managed. The incidence of PIH in the group on the protocol was significantly lower than that of control patients who were not managed with protocol. In conclusion, normal pregnancy is associated with a dull of pressor response to A II. Women who are destined to develop PIH reveal an increased vascular sensitivity to infused A II several weeks before the onset of the first clinical symptoms. The increased vascular sensitivity to A II can be detected by AST, and calcium supplementation to pregnant women who revealed an increased vascular response to A II can help to prevent the onset of PIH clinically.
社団法人日本産科婦人科学会の論文
1988-08-01

Angiotensin IIに対する血管反応性の基礎と臨床 : 妊娠中毒症の病態に基づく発症予知・予防法について (<シンポジウム>妊娠中毒症 : その病態論的アプローチ)

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