Kanayama N, She L, Maehara K, Kajiwara Y, Terao T
Department of Obstetrics and Gynecology, Hamamatsu University School of Medicine, Japan.
J Hypertens. 1996 Apr;14(4):453-9.
An animal model of HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome was developed by means of stimulation of the celiac ganglion in rats.
The celiac ganglion in pregnant or non-pregnant rats was exposed to endotoxin (lipopolysaccharide, LPS) (500 micrograms/50 microliters), potassium chloride (0.2 mol/l/50 microliters), or saline solution (50 microliters). In another group of rats the bifurcation of the abdominal aorta was exposed to LPS (500 micrograms/50 microliters). Blood pressure, platelet count, hematocrit, serum aspartate transaminase (AST), alanine transaminase (ALT), lactate dehydrogenase (LDH), and plasma norepinephrine and epinephrine were measured for 6 h after treatment. Histopathologic studies were also performed in these rats.
A significant increase in blood pressure, AST, ALT, LDH, norepinephrine, and epinephrine was found in the endotoxin-treated pregnant rats compared with control rats treated with the saline solution. A significant decrease in platelet count was found in endotoxin-treated pregnant rats compared with the control rats. A significant increase in blood pressure, AST, norepinephrine, and epinephrine was found in the potassium chloride-treated pregnant rats compared with control rats. Blood pressure and biochemical parameters remained unchanged in the pregnant rats treated with LPS at the bifurcation of the abdominal aorta, as in those treated with saline at the celiac ganglion. Histologic examination of liver tissues treated with LPS or potassium chloride showed varying degrees of ischemic necrosis of hepatocytes similar to that observed in the human HELLP syndrome. Blood pressure, biochemical parameters, and histologic findings in non-pregnant rats were almost the same as those in pregnant rats.
This study suggests that exogenous stimulation of the celiac ganglion causes an increase in the blood pressure and liver ischemia, resulting in HELLP syndrome-like disease in pregnant and non-pregnant rats.
通过刺激大鼠腹腔神经节建立溶血、肝酶升高、血小板减少（HELLP）综合征的动物模型。
将内毒素（脂多糖，LPS）（500微克/50微升）、氯化钾（0.2摩尔/升/50微升）或盐溶液（50微升）作用于怀孕或未怀孕大鼠的腹腔神经节。另一组大鼠的腹主动脉分叉处接受LPS（500微克/50微升）。治疗后6小时测量血压、血小板计数、血细胞比容、血清天冬氨酸转氨酶（AST）、丙氨酸转氨酶（ALT）、乳酸脱氢酶（LDH）以及血浆去甲肾上腺素和肾上腺素。还对这些大鼠进行了组织病理学研究。
与用盐溶液处理的对照大鼠相比，经内毒素处理的怀孕大鼠的血压、AST、ALT、LDH、去甲肾上腺素和肾上腺素显著升高。与对照大鼠相比，经内毒素处理的怀孕大鼠的血小板计数显著降低。与对照大鼠相比，经氯化钾处理的怀孕大鼠的血压、AST、去甲肾上腺素和肾上腺素显著升高。腹主动脉分叉处接受LPS治疗的怀孕大鼠的血压和生化参数保持不变，与腹腔神经节接受盐溶液治疗的大鼠相同。用LPS或氯化钾处理的肝组织的组织学检查显示肝细胞有不同程度的缺血坏死，类似于人类HELLP综合征中观察到的情况。未怀孕大鼠的血压、生化参数和组织学结果与怀孕大鼠几乎相同。
本研究表明，对腹腔神经节的外源性刺激会导致血压升高和肝脏缺血，从而在怀孕和未怀孕大鼠中引发类似HELLP综合征的疾病。
