Induction of HELLP syndrome-like biochemical parameters by stimulation of the celiac ganglion in rats.

OBJECTIVE

An animal model of HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome was developed by means of stimulation of the celiac ganglion in rats.

METHODS

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.

RESULTS

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.

CONCLUSION

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.