title: Experimental preeclampsia produced by chronic constriction of the lower aorta: validation with longitudinal blood pressure measurements in conscious rhesus monkeys.
abstract: OBJECTIVE
  Our goals were (1) to determine whether hypertension, proteinuria, and glomerular endotheliosis can be produced by chronic reduction of lower aortic pressure in pregnant rhesus monkeys and (2) to study the time course of the development of hypertension by means of longitudinal arterial blood pressure measurements in conscious, unrestrained pregnant rhesus monkeys.
  
  
  METHODS
  Indwelling arterial catheters were placed at 103 +/- 4 days of gestation (term 160 days) for measurement of arterial pressure before and after reduction of lower aortic pressure. At 116 +/- 7 days lower aortic pressure was reduced by 24 +/- 11 mm Hg in 11 monkeys (experimental group) by a stricture on the aorta just below the renal arteries; six monkeys (controls) underwent a sham operation. Resting on the aorta just below the renal arteries; six monkeys (controls) underwent a sham operation. Resting pressures were measured three to five times per week by a tether-and-swivel system.
  
  
  RESULTS
  Baseline arterial pressure averaged 81 +/- 6 mm Hg. In the experimental group four monkeys had adverse outcomes (one maternal death with severe hypertension, one abruptio placentae with stillbirth, and two spontaneous preterm deliveries with hypertension). There was one preterm delivery in the control group. Of the seven monkeys with aortic stricture who continued to term, four developed sustained hypertension (mean pressure 18 +/- 6 mm Hg above baseline), proteinuria, and moderate-to-severe glomerular endotheliosis. None of the controls had hypertension or proteinuria, but two had endotheliosis.
  
  
  CONCLUSIONS
  These observations confirm that a syndrome resembling preeclampsia can be produced by a reduction of lower aortic pressure, and they demonstrate that the associated hypertension is not an artifact of anesthesia. This model may prove useful in studying the pathophysiologic mechanisms of preeclampsia.
authors.affiliation: Department of Obstetrics, Gynecology, and Reproductive Sciences, University of California, San Francisco.
authors.forename: C A
authors.initials: CA
authors.lastname: Combs
authors.forename: M A
authors.initials: MA
authors.lastname: Katz
authors.forename: J L
authors.initials: JL
authors.lastname: Kitzmiller
authors.forename: R J
authors.initials: RJ
authors.lastname: Brescia
mesh_terms: D000818:Animals; D001011:Aorta / Q000502:physiology*; D001794:Blood Pressure; D003250:Constriction; D004195:Disease Models, Animal; D004727:Endothelium / Q000473:pathology; D005260:Female; D006973:Hypertension; D007678:Kidney Glomerulus / Q000473:pathology; D008253:Macaca mulatta; D008854:Microscopy, Electron; D010976:Platelet Count; D011225:Pre-Eclampsia / Q000473:pathology / Q000503:physiopathology*; D011247:Pregnancy; D011507:Proteinuria