Abstract
To test the concept that diminished uterine blood supply might play some part in the hypertension of eclampsia 1 the carotid blood pressure was recorded in acute experiments while the aorta was partially occluded below the renal arteries.
Ten animals anesthetized with chloretone, with morphine and pen-tobarbital sodium, or by decerebration under ether were used. Six were pregnant (5 dogs, 1 cat); 4 were non-pregnant controls.
The carotid and femoral blood pressures were recorded kymo-graphically and a long-handled screw clamp was adjusted around the aorta just below the renal arteries. The incision was closed with the clamp handle protruding and the animal was left undisturbed until the blood pressure was stable. The clamp was then tightened until the femoral pressure fell to about half its previous value and the carotid pressure was followed (Table I).
In the non-pregnant control animals aortic compression was not followed by any change in carotid pressure other than the immediate adjustments discussed by Brotchner. 2 Rytand, 3 Brotchner, 2 and Goldblatt, Kahn, and Hanzal 4 have all pointed out that there is no progressive increase of arterial pressure after constriction of the aorta below the renal arteries.
In 4 of the 6 pregnant animals aortic compression was followed by a definite gradual rise of blood pressure; in the other 2 the rises were small (16 mm in 2 hours and 24 mm in one hour respectively). The rises were so gradual that one could not usually say exactly when they began. The rises under chloretone were clear-cut and amounted to 10-58 mm but no strictly hypertensive levels were reached, perhaps because of the very low initial values. In the animal under morphine and nembutal the blood pressure was more normal but the rise was small.
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