Seidl D C, Hughes H C, Bertolet R, Lang C M
Lab Anim Sci. 1979 Aug;29(4):472-8.
In this study, normal nonpregnant, normal full-term pregnant, fasting ketotic and spontaneous pregnancy toxemic guinea pigs were compared to define the mechanism of this disease. In addition to conventional clinical, laboratory and pathologic studies, arterial blood pressure (thoracic and abdominal aortic) measurements and angiography were used. The results showed that in spontaneous cases of pregnancy toxemia, there is an aortic compression just caudal to the renal arteries. This compression reduced the aortic diameter by 22% of prerenal level as compared to 10% for fasting ketotic and normal pregnant guinea pigs. The aortic compression also resulted in a 30% postcompression reduction in blood pressure. No pressure differences were seen in the other groups. The postulated etiology for true toxemia of pregnancy in guinea pigs is, therefore, similar to that of man where aortic compression produces uterine ischemia and the resultant syndrome.
在本研究中,对正常未怀孕、正常足月怀孕、禁食性酮症和自发性妊娠毒血症豚鼠进行比较,以确定该疾病的发病机制。除了常规的临床、实验室和病理学研究外,还进行了动脉血压(胸主动脉和腹主动脉)测量及血管造影。结果显示,在自发性妊娠毒血症病例中,肾动脉尾侧存在主动脉受压情况。与禁食性酮症和正常怀孕豚鼠的10%相比,这种压迫使主动脉直径较肾动脉水平前缩小了22%。主动脉受压还导致压迫后血压降低30%。其他组未观察到血压差异。因此,豚鼠真性妊娠毒血症的推测病因与人类相似,即主动脉受压导致子宫缺血及由此产生的综合征。