Poster Presentations / Pregnancy Hypertension: An International Journal of Women’s Cardiovascular Health 3 (2013) 67–99
Background/aims: Eclampsia, a leading cause of maternal mortality. Little is known about the causes of eclampsia and there is no effective treatment. Development of an animal model may help to expand our understanding and may hold great potential for the design of effective treatment. Methods: Experimental preeclampsia model was build first, rats were received a infusion of endotoxin (LPS) (1.0 lg/kg body weight) or saline solution through the tail vein during 1 h on gestational day 14, blood pressure and albuminuria were measured. On gestational day 18 all experimental rats were received electric stimulation, the seizure behaviors were observed and EEG were recorded in these rats. Terminations of pregnancy were performed on day 21 of gestation, resorptions and pups birth weights were recorded. Results: PE model rats develop many features of human PE that correlates with bad pregnancy outcomes. Both clinical behavior and EEG records documented seizure activity developed in 100% of pregnancy rats and 58.3% of non-pregnancy rats (P = 0.01). The PE model rats had a 31.25% decrease of the latency (3.3 ± 1.4 min) to evoke a full motor seizure compared with normal pregnancy rats (4.8 ± 2.2 min), and had a significant decrease contrast to non-pregnancy rats (10.6 ± 7.1 min), £¨P < 0.05). EEG recordings showed seizure activities when rats had clinically generalized tonic–clonic convulsions. Conclusion: We described a rat model of eclampsia, were the relevant predominant features of human eclampsia. doi:10.1016/j.preghy.2013.04.050
PP023. Soluble Fms-like tyrosine kinase-1 and placental growth factor expression in a rat model of pre-eclampsia Liu Lei, Liu Huishu, Brennecke Shaun, Huang Qian, Hu Bihui Background/Aims: Soluble Fms-like tyrosine kinase-1(sFlt1) and placental growth factor (PIGF) have been used clinically to predict preeclampsia (PE). This study investigated these factors in a rat model of preeclampsia induced by ultra-low-dose endotoxin. Methods: The experimental PE rat model was generated on gestational day 14. Rats were anesthetized and divided into a normal pregnancy group (NP, n = 7) (which received a normal saline infusion) and a PE model group (n = 9) (which received an infusion of lipopolysaccharide (LPS) endotoxin (1.0 lg/kg body weight). Infusions were given through the tail vein for 1 hour. Blood pressure was monitored and albuminuria, serum ALT, AST, creatinine and BUN were measured. As well, concentrations of sFlt-1 and PIGF in serum and amniotic fluid were measured by enzyme-linked immuno sorbent assay (ELISA). Results: Arterial pressure was increased (135 ± 7 versus 116 ± 3 mm Hg; P < 0.03) in the PE model rats compared with the NP rats. The concentration of sFlt-1 in the PE model group (162.7 ± 73.9 pg/ml) was significantly higher than NP group (123 ± 64 pg/ml) (P < 0.05). The serum level of PIGF in PE model group (9.7 ± 6.2 pg/ml) was significantly lower compared to the NP group (23.4 ± 12.4) (P < 0.05). The plasma sFlt-1/PIGF ratio in the PE model group (18.3 ± 5.6) was
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greater than that in the NP group (6.7 ± 2.1) (P < 0.05). Similar changes were also present in the amniotic fluid. Conclusion: sFlt-1 and PIGF levels in this rat PE model induced by ultra-low-dose endontoxin showed changes consistent with findings in preeclamptic patients, indicating that this animal model mimics human preeclampsia well in these aspects of the disorder. doi:10.1016/j.preghy.2013.04.051
PP024. Effects of intravenous magnesium sulfate on the characteristics of eclamptic seizures induced by electrical stimuli in a rat preeclampsia/eclampsia model Liu Lei, Liu Huishu, Huang Qian, Brennecke Shaun, Hu Bihui Background/Aims: Eclampsia is a serious complication of pregnancy and remains a leading cause of maternal mortality worldwide. Magnesium sulfate is commonly used in the prophylaxis and treatment of eclampsia. However, uncertainty remain regarding its anticonvulsant mechanism(s) of action. This study examined the effects of intravenous magnesium sulfate on the characteristics of eclamptic seizures in a rat preeclampsia/eclampsia model. Methods: All rats were implanted with stainless nickelcadmium alloy bipolar electrodes one week before fertilization. Next, an experimental rat preeclampsia (PE) model was induced on gestational day 14 by anaesthetising rats and infusing over 1 hour into their tail veins lipopolysaccharide (LPS) (1.0 lg/kg body weight) (with control rats receiving normal saline). The rats were then divided into three groups: a normal pregnancy (NP) group (n = 6) which received a continuous infusion of saline; a control PE model group (n = 7) (which had previously received the LPS treatment) which also received a continuous infusion of saline; and a treated PE model group (n = 8) (which had previously received the LPS treatment) which received a continuous infusion of magnesium sulfate (60 mg/kg/day). The continuous infusions in all three groups were delivered by implanted osmotic minipumps. Measurements were made of blood pressure, albuminuria, serum ALT, AST, and creatinine, BUN and serum magnesium concentrations. On gestational day 18, all experimental rats received a standardized electrical stimulus. Seizure activity was assessed using electroencephalogram (EEG) recordings. Terminations of pregnancy were performed on gestational day 21. Resorptions and pup birth weights were recorded. Results: The pregnant LPS treated rats developed many features of human PE (e.g. hypertension, proteinuria, liver and kidney dysfunctions). The mean concentration of Mg2+ in the magnesium sulfate therapy group (0.86 ± 0.24 mmol/L) was significantly higher (p < 0.05) than in both the control PE model group (0.61 ± 0.12 mmol/L) and the NP group (0.62 ± 0.09 mmol/L). The magnesium sulfate therapy group had a significantly (p < 0.05) increased latency period (21.7 ± 8.9 min) to evoke a full motor seizure compared to both the NP group (4.8 ± 2.2 min)and the control PE model group (3.3 ± 1.4 min), there being no significant difference (p > 0.05) between the latency periods of the NP group and the control PE model group. Overall, the
Background/aims: Eclampsia, a leading cause of maternal mortality. Little is known about the causes of eclampsia and there is no effective treatment. Development of an animal model may help to expand our understanding and may hold great potential for the design of effective treatment. Methods: Experimental preeclampsia model was build first, rats were received a infusion of endotoxin (LPS) (1.0 lg/kg body weight) or saline solution through the tail vein during 1 h on gestational day 14, blood pressure and albuminuria were measured. On gestational day 18 all experimental rats were received electric stimulation, the seizure behaviors were observed and EEG were recorded in these rats. Terminations of pregnancy were performed on day 21 of gestation, resorptions and pups birth weights were recorded. Results: PE model rats develop many features of human PE that correlates with bad pregnancy outcomes. Both clinical behavior and EEG records documented seizure activity developed in 100% of pregnancy rats and 58.3% of non-pregnancy rats (P = 0.01). The PE model rats had a 31.25% decrease of the latency (3.3 ± 1.4 min) to evoke a full motor seizure compared with normal pregnancy rats (4.8 ± 2.2 min), and had a significant decrease contrast to non-pregnancy rats (10.6 ± 7.1 min), £¨P < 0.05). EEG recordings showed seizure activities when rats had clinically generalized tonic–clonic convulsions. Conclusion: We described a rat model of eclampsia, were the relevant predominant features of human eclampsia. doi:10.1016/j.preghy.2013.04.050
PP023. Soluble Fms-like tyrosine kinase-1 and placental growth factor expression in a rat model of pre-eclampsia Liu Lei, Liu Huishu, Brennecke Shaun, Huang Qian, Hu Bihui Background/Aims: Soluble Fms-like tyrosine kinase-1(sFlt1) and placental growth factor (PIGF) have been used clinically to predict preeclampsia (PE). This study investigated these factors in a rat model of preeclampsia induced by ultra-low-dose endotoxin. Methods: The experimental PE rat model was generated on gestational day 14. Rats were anesthetized and divided into a normal pregnancy group (NP, n = 7) (which received a normal saline infusion) and a PE model group (n = 9) (which received an infusion of lipopolysaccharide (LPS) endotoxin (1.0 lg/kg body weight). Infusions were given through the tail vein for 1 hour. Blood pressure was monitored and albuminuria, serum ALT, AST, creatinine and BUN were measured. As well, concentrations of sFlt-1 and PIGF in serum and amniotic fluid were measured by enzyme-linked immuno sorbent assay (ELISA). Results: Arterial pressure was increased (135 ± 7 versus 116 ± 3 mm Hg; P < 0.03) in the PE model rats compared with the NP rats. The concentration of sFlt-1 in the PE model group (162.7 ± 73.9 pg/ml) was significantly higher than NP group (123 ± 64 pg/ml) (P < 0.05). The serum level of PIGF in PE model group (9.7 ± 6.2 pg/ml) was significantly lower compared to the NP group (23.4 ± 12.4) (P < 0.05). The plasma sFlt-1/PIGF ratio in the PE model group (18.3 ± 5.6) was
75
greater than that in the NP group (6.7 ± 2.1) (P < 0.05). Similar changes were also present in the amniotic fluid. Conclusion: sFlt-1 and PIGF levels in this rat PE model induced by ultra-low-dose endontoxin showed changes consistent with findings in preeclamptic patients, indicating that this animal model mimics human preeclampsia well in these aspects of the disorder. doi:10.1016/j.preghy.2013.04.051
PP024. Effects of intravenous magnesium sulfate on the characteristics of eclamptic seizures induced by electrical stimuli in a rat preeclampsia/eclampsia model Liu Lei, Liu Huishu, Huang Qian, Brennecke Shaun, Hu Bihui Background/Aims: Eclampsia is a serious complication of pregnancy and remains a leading cause of maternal mortality worldwide. Magnesium sulfate is commonly used in the prophylaxis and treatment of eclampsia. However, uncertainty remain regarding its anticonvulsant mechanism(s) of action. This study examined the effects of intravenous magnesium sulfate on the characteristics of eclamptic seizures in a rat preeclampsia/eclampsia model. Methods: All rats were implanted with stainless nickelcadmium alloy bipolar electrodes one week before fertilization. Next, an experimental rat preeclampsia (PE) model was induced on gestational day 14 by anaesthetising rats and infusing over 1 hour into their tail veins lipopolysaccharide (LPS) (1.0 lg/kg body weight) (with control rats receiving normal saline). The rats were then divided into three groups: a normal pregnancy (NP) group (n = 6) which received a continuous infusion of saline; a control PE model group (n = 7) (which had previously received the LPS treatment) which also received a continuous infusion of saline; and a treated PE model group (n = 8) (which had previously received the LPS treatment) which received a continuous infusion of magnesium sulfate (60 mg/kg/day). The continuous infusions in all three groups were delivered by implanted osmotic minipumps. Measurements were made of blood pressure, albuminuria, serum ALT, AST, and creatinine, BUN and serum magnesium concentrations. On gestational day 18, all experimental rats received a standardized electrical stimulus. Seizure activity was assessed using electroencephalogram (EEG) recordings. Terminations of pregnancy were performed on gestational day 21. Resorptions and pup birth weights were recorded. Results: The pregnant LPS treated rats developed many features of human PE (e.g. hypertension, proteinuria, liver and kidney dysfunctions). The mean concentration of Mg2+ in the magnesium sulfate therapy group (0.86 ± 0.24 mmol/L) was significantly higher (p < 0.05) than in both the control PE model group (0.61 ± 0.12 mmol/L) and the NP group (0.62 ± 0.09 mmol/L). The magnesium sulfate therapy group had a significantly (p < 0.05) increased latency period (21.7 ± 8.9 min) to evoke a full motor seizure compared to both the NP group (4.8 ± 2.2 min)and the control PE model group (3.3 ± 1.4 min), there being no significant difference (p > 0.05) between the latency periods of the NP group and the control PE model group. Overall, the
