PURPOSE: Plasma levels of renin, angiotensin II and aldosterone are increased during normal pregnancy. However, these values in preeclampsia are decreased to nearly that of a nonpregnant subject, and vascular sensitivity to angiotensin II is increased. In preeclampsia, aldosterone is decreased less than rennin. Therefore current studies were undertaken to determine the relationship between aldosterone to renin ratio (ARR) and uterine artery perfusion via RI value. MATERIALS AND METHODS: In this study, the relationship between plasma aldosterone and renin concentration was determined in 27 preeclamptic women and 50 normal pregnant women, whose gestational weeks were matched. The aldosterone to renin ratio was calculated and compared between the two groups. Doppler velocimetry of the uterine artery, which was used to calculate resistance index (RI), was performed on all subjects. The relationship between ARR and RI value was reviewed. RESULTS: In the preeclampsia group, RI value of the uterine artery was significantly higher than that of normal pregnant women. Both plasma renin and aldosterone concentrations were lower in the preeclampsia group. However, the ratio of these two parameters was significantly higher (38.3 vs. 16.1, p < 0.001); the greater ARR, the higher the RI of the uterine artery (r(2)=0.053, p=0.048). CONCLUSION: This study demonstrates that a high aldosterone to renin ratio may have a negative effect on perfusion of the uterine artery and play an important role in the pathophysiology of preeclampsia.
Adult ; Aldosterone/*blood ; Arteries/metabolism ; Case-Control Studies ; Female ; Gestational Age ; Health ; Humans ; Pre-Eclampsia/*blood ; Pregnancy ; Renin/*blood ; Uterus/*blood supply/*metabolism

Animals ; Blotting, Western ; Epidermal Growth Factor ; analysis ; Female ; Ischemia ; physiopathology ; Kidney ; embryology ; metabolism ; Models, Animal ; Pregnancy ; Rats ; Rats, Wistar ; Receptor, Epidermal Growth Factor ; analysis ; Uterus ; blood supply

OBJECTIVENeonatal asphyxia is one of the main causes for the acute respiratory distress syndrome (ARDS) in full-term newborns. Now it is believed that the reduced amount and abnormal function of pulmonary surfactant due to various causes is a major factor leading to acute lung injury. This study aimed at using an intrauterine acute ischemic-hypoxia rat model and investigating the effect of intrauterine acute ischemic-hypoxia on the expression of surfactant protein A (SP-A) and surfactant protein B (SP-B) in neonatal rat lungs.

METHODSThe rat model of acute intrauterine ischemic-hypoxia was established by ligating the unilateral uterine horn vessels of Wistar rats at the 21st gestational day. While the rat pups from the other side of the uterus, of which the uterine horn vessel was not ligated, were the sham-operation group. Rat pups were delivered by cesarean section at the 20, 30 and 40 min following the ischemic-hypoxia insult. The rat pups delivered by cesarean section from the gestation of 21 days were the normal control group. There were 42 rat pups and 6 pups in each group in this study. The distribution of SP-B protein in the neonatal rat lungs of different period of ischemia was examined by using SABC method. The average gray value of SP-B staining in type II alveolar epithelial cells were measured by Universal Imaging Porporation with Meta Morph software. The reverse transcription polymerase chain reaction (RT-PCR) was performed to quantitate the expression of SP-A and SP-B mRNA.

RESULTSFollowing the intrauterine acute ischemic-hypoxia, the numbers of type II alveolar epithelial cells with the positive SP-B staining were markedly declined. The average gray values at the 20, 30 and 40 min after the ischemia were 78.89 +/- 1.08, 79.69 +/- 0.13 and 80.00 +/- 0.63, respectively, which increased significantly compared with the normal control group (76.13 +/- 0.43, P < 0.01). The expression of SP-A and SP-B mRNA was weak following the ischemic-hypoxia insult. The relative amounts of SP-A (1.16 +/- 0.06, 1.14 +/- 0.01 and 1.13 +/- 0.04, respectively) and SP-B (0.81 +/- 0.02, 0.78 +/- 0.02 and 0.79 +/- 0.04, respectively) at the 20, 30 and 40 min after the ischemia were reduced significantly compared with controls (1.27 +/- 0.09 and 0.89 +/- 0.06, respectively, P < 0.05 and < 0.01) and reduced gradually following the prolongation of the insult. There were no significant differences (P > 0.05) between the normal and sham operation control groups on the expressions of SP-B protein as well as the SP-A and SP-B mRNA.

CONCLUSIONThe reduced synthesis of SP-B protein and the reduced expression of SP-A and SP-B mRNA might be caused by intrauterine acute ischemic-hypoxia, which may support theoretically the early application of pulmonary surfactant including SP-A and SP-B for treating the lung injuries of asphyxia in newborns.

Animals ; Animals, Newborn ; Female ; Gene Expression ; Hypoxia ; physiopathology ; Ischemia ; physiopathology ; Lung ; metabolism ; Pregnancy ; Pulmonary Surfactant-Associated Protein A ; genetics ; Pulmonary Surfactant-Associated Protein B ; genetics ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; Uterus ; blood supply

OBJECTIVETo observe the effect of Taohong Siwu decoction (THSWD) on micro-vascular density (MVD) in rat uterus, the content of angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) in serum, and the expression of tyrosine kinasa receptor (Tie-2) in uterus.

METHODEarly pregnancy rats were intragastrically administrated with misoprostol (100 microg x kg(-1)) and mifepristong (8.3 mg x kg(-1)) to established the incomplete-abortion model. The incomplete-abortion rats were randomly divided into the model group (the same volume of distilled water), the positive control group (at the daily dose of 4.3 g x kg(-1) Motherwort Particles), and THSWD-treated groups (at the daily dose of 18.0, 9.0 and 4.5 g x kg(-1)). Pregnant rats were taken as the control group (the same volume of distilled water). After the successive oral administration for 7 days, blood was collected from aorta abdominalis, and rat uterine tissues were collected. The content of serum Ang-1 and Ang-2 were detected by ELISA; And the levels of Tie-2 and MVD in uterine tissues were detected by SP immunohistochemistry.

RESULTTHSWD remarkably increased the levels of MVD in uterus of medicine-induced abortion rats, the content of Ang-1 and Ang-2 in serum, and the expression of Tie-2 in uterine tissues.

CONCLUSIONTHSWD has the effect in markedly promoting angiogenesis in incomplete-abortion rats. Its mechanism may be related to the regulation of concentrations of Ang-1 and Ang-2 in serum and Tie-2 in uterine tissues.

Abortion, Incomplete ; blood ; drug therapy ; genetics ; Angiopoietin-1 ; blood ; genetics ; Angiopoietin-2 ; blood ; genetics ; Animals ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Gene Expression ; drug effects ; Humans ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Receptor, TIE-2 ; genetics ; metabolism ; Uterus ; blood supply ; drug effects ; metabolism