This paper is to present the various concepts and techniques of the experiments to test the relationship of acute and chronic uterine and/or placental ischemia to development of arterial hypertension during pregnancy. For many years attempts have been made with varying success to produce pre-eclampsia experimentally by reducing uterine blood supply.
Experimentally, Bastiaanse and Mastboomn in 19 49 have produced acute hypertension by compressing the aorta below the level of the renal arteries in pregnant rabbits under general anesthesia. The same procedure in non-pregnant animals was of no consequence. However, these authors as well as Kumar2) in 1962 came to similar conclusion that the rise in blood pressure was somewhat temporary in nature. Since the collateral circulations develop rapidly in most of the experimental animals, Kumar had to perform partial clamping of uterine arteries in pregnant dogs three times to maintain uterine :ischemia. Hodari et al. a,4) have reported in 1967 that placing constrictive teflon bands about the uterine arteries in the dog before pregnancy leads predictably to a reversible syndrome of hypertension and proteinuria during pregnancy. Acute; experimental ischemia of the uterus and/or placenta is based upon the work of Goldblatt. Bastiaanse and Mastboomu and Page5) have noted that hypertension followed partial clamping of the abdominal aorta in the pregnant dog. Berger and Cavanagh° in 1963 acutely produced experimental arterial hypertension in pregnant rabbits by digital compression of one uterine horn as well as by retroplacental insertion of "z" sutures. They concluded that placental ischemia was essential for the experimental production of hypertension and that a humoral factor, probably of placental origin, was produced.
This paper is also to confirm these several important observations and to prove pressor substance, probably some kind of renin-like Immoral factor produced by uterine and/or placental ischemia. Authors, using rabbits pregnant and non-pregnant, observed the changes of arterial blood pressure as well as proteinuria and body weight after compromising uterine blood supply during pregnancy. The results obtained could be summarized briefly as below.
1. Chronic experimental ischemia produced by either partial ligation of both uterine arteries with both ovarian arteries blocked or partial ligation of aorta was responsible fore arterial hypertension and proteinuria during pregnancy which developed as a gradual process during entire pregnancy. Acute experimental ischemia also gave similar result as far as arterial hypertension is concerned even though there could be possible experimental artifact with acute operative trauma. Partial ligatin of aorta as in chronic experiment and "z" fashion suture of Berger and Cavanaghs´ were used to reduce,uterine and/or placental blood flow.
2. The existence of pressor, substance in the circulating blood of such an experimentally induced hypertensive pregnant rabbits that is possibly originated from uterus-placenta-fetus complex rather than kidney could be reasonably explained.
3. Circulating blood of these hypertensive pregnant rabbits when transfused to a non-pregnant rabbit a demonstrable hypertensive effect was noticed. But at least three to four hours after transfusion the arterial blood pressure returned to normal value to explain that the so-called pressor substance is destroyed or inactivated in relatively short period of time.
|