[Clinical and experimental studies on the pathogenesis in pregnancy induced hypertension].
Placental ischemia is one of the etiological factors of pregnancy induced hypertension (PIH), however, the pathogenesis of placental and renal ischemia has not been clarified. The purposes of this investigation are (1) to clarify the fetomaternal hemodynamic changes in PIH and the influence of maternal postural change on fetomaternal hemodynamics, measured by thermodilution method, impedance cardiography and pulsed doppler method during pregnancy, (2) to provide to relationship between intrauterine resting tonus and maternal hemodynamics, that is, blood pressure, placental and renal blood flow measured by electromagnetic flowmeter and thermocouple method, and renal nerve activity, and (3) to study the influence of placental ischemia on vascular sensitivity to angiotensin II measured by Magnus method in animal experiment. (1) The increase in C.O and blood volume were recognized from the beginning of pregnancy to 24 GW, and subsequently, the decreasing tendency were found from about 32 GW to the onset of labor. However this decreasing tendency were subsided in the lateral position. These circulatory changes were observed in both normotensive and PIH cases, and especially, the decrease in C.O and blood volume in late pregnancy were more remarkable in PIH than that in normotensive pregnancy. From the results of Starling curve, left ventricular work was more hyperdynamic status in PIH than that in normotensive pregnancy, these results show that there are a compensatory mechanism against high vascular resistance in PIH. A/B (S/D) ratio in uterine artery, umbilical artery and fetal aorta were lowered in II-nd and III-rd trimester and more decreased in the lateral position from the supine position, on the other hand these ratio in PIH were elevated respectively. These results show that there are the aortocaval compression by the heavy tensive uterus and subsequent sluice flow mechanism in fetoplacental circulation in the supine position in late pregnancy. (2) These vascular compression were recognized very often in PIH accompanying with increasing in uterine resting tonus. It was recognized in pregnant rabbit that an increase in uterine resting tonus in the ovarian side caused an increasing blood pressure, a decrease in renal and placental blood flow and an increase in renal sympathetic nerve activity (RSNA). After resection of the suspensory ligament of ovarii, an increase in resting tonus in the ovarian side did not only cause an increase in RSNA, but also a decrease in renal blood flow.(ABSTRACT TRUNCATED AT 400 WORDS)
Hidaka
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A
Department of Obstetrics and Gynecology, School of Medicine, Osaka City University.
D000804:Angiotensin II; D000818:Animals; D005260:Female; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D007083:Iliac Artery / Q000187:drug effects; D007511:Ischemia / Q000209:etiology; D007668:Kidney / Q000294:innervation; D008431:Maternal-Fetal Exchange; D010920:Placenta / Q000098:blood supply; D011187:Posture; D011247:Pregnancy / Q000502:physiology; D011249:Pregnancy Complications, Cardiovascular / Q000209:etiology* / Q000503:physiopathology; D011817:Rabbits; D012018:Reflex; D012039:Regional Blood Flow; D012079:Renal Circulation; D014590:Uterine Contraction / Q000187:drug effects; D014599:Uterus / Q000503:physiopathology; D014661:Vasoconstriction / Q000187:drug effects
D000804:Angiotensin II