ABSTRACT
Objective To determine the significance of renin angiotensin system (RAS) expressed on placenta in pregnancy induced hypertension (PIH). Methods The expression of placental angiotensin Ⅱtype 1 receptor (AT 1R) and angiotensinogen (AGT) in patients with PIH ( n =20) were investigated and compared with controls ( n =15) using immunohistochemistry and semi quantitative reverse transcription polymerase chain reaction (RT PCR). Results AT 1R was mainly found in the syncytiotrophoblasts, cytotrophoblasts,the vascular endothelial cells and smooth muscle cells. The expression of AT 1R in PIH group (112.43?11.75) was higher than that of control group (170.47? 10.59) ( P
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Objective To evaluate the effects and possibility of nitroglycerin on Pregnancy induced hypertension (PIH) treatment Methods In comparision with the third trimester normal pregnant women (Normal group) (n=11), 34 moderate/severe PIH cases were divided into three groups: PIH treated only with magnesium sulfate (Mg group) (n=11); PIH treated only with nitroglycerin (Ng group) (n=11); and PIH treated with Mg+ Ng (Combination group) (n=12). The endothelial nitric oxide synthase (eNOS) in placenta was investigatd immunohistochemiscally and quantitatively. Data such as platelet aggregation (PAg), umbilcal artery of S/D ratio and resistance index (RI) with color Doppler and the effect of decrement of blood pressure on PHI groups were evaluated. Results In comparision with Normal group, (1) the quantity of eNOS of PIH cases was signaficently lower (P
ABSTRACT
Objective To investigate whether insulin resistance is a cause of pregnancy induced hypertension (PIH). Methods All patients who had abnormal 50g glucose screening test accepted 75g oral glucose tolerance test (OGTT) and insulin sensitive index (ISI) was calculated. These patients were followed up and divided into two groups (PIH group and normal pregnancy group) at third trimester of pregnancy. The difference of ISI between the PIH group and normal pregnancy group was compared. Results Fast blood glucose, fast blood insulin and ISI were (4.2?0.7)mmol/L vs. (3.8?0.7)mmol/L, (107.8?48.8)pmol/L vs. (50.4?40.5)pmol/L, and -3.25?0.27 vs. -2.58?0.66 in PIH group and normal group, respectively ( P 0.05). Conclusions Insulin resistance during second trimester of pregnancy may be one of the causes of pregnancy induced hypertension.