To examine the effects of prenatal tetrandrine (Tet) therapy on pulmonary arterial structural remodeling in nitrofen-induced congenital diaphragmatic hernia (CDH) Methods CDH was induced in fetal rats by materna...To examine the effects of prenatal tetrandrine (Tet) therapy on pulmonary arterial structural remodeling in nitrofen-induced congenital diaphragmatic hernia (CDH) Methods CDH was induced in fetal rats by maternal administration of 100*!mg nitrofen by gavage on day 9 5 of gestation (term, day 22) Control animals received olive oil (OO) Tet (24*!mg/kg per day) or normal saline (NS) was given by gavage every day from 16 to 20 days of gestation, and fetuses were delivered by caesarean section on day 21 5 Lung sections from 3 fetuses in each group were studied The number of vessels were calculated, the external diameter (ED), medial wall thickness (MT), percent of medial wall thickness, and wall structure were evaluated by image analysis software Results In the pre-acinar arteries, CDH-NS pups had a significantly increased %MT compared with the OO-NS group ( P <0 05), while CDH-Tet animals had a reduced %MT compared with the CDH-NS rats ( P <0 05) Similar results were seen in the intra-acinar level Significant differences were observed between CDH-NS animals and OO-NS controls in the percentage of muscularized intra-acinar blood vessels ( P <0 001) Tet-treated CDH pups had a reduced percentage of muscularized intra-acinar arteries compared with CDH-NS animals Conclusions Medial hypertrophy is present in both the pre-acinar and intra-acinar arteries in the nitrofen-induced CDH rat model Tet treatment inhibits medial hypertrophy and reduces the percentage of muscularized intra-acinar vessels Prenatal Tet therapy may be efficacious in reducing the risk of PH in human newborns with CDH展开更多
Objective To investigate the expression of inducible heme oxygenase (HO-1) gene in pulmonary artery smooth muscle cells (PASMCs) exposed to hypoxia, and the influence of carbon monoxide (CO) on the proliferation of PA...Objective To investigate the expression of inducible heme oxygenase (HO-1) gene in pulmonary artery smooth muscle cells (PASMCs) exposed to hypoxia, and the influence of carbon monoxide (CO) on the proliferation of PASMCs under hypoxic conditions. Methods Primary culture of rat PASMCs were passed every 3 days, and the 3-5 passages were used. After exposure to hypoxic conditions (95% N 2, 5% CO 2) 0, 12, 24 and 48 hours, the level of HO-1 mRNA was examined by reverse transcriptase polymerase chain reaction (RT-PCR). The volume of COHb in the medium was measured spectrophotometrically. The cyclic guanosine mono-phosphate (cGMP) concentration of cell extracts was determined by radioimmunoassay. PASMCs were divided into 5 groups, cultured under normoxia and hypoxia and treated with hemin, hemoglobin (Hb) and exogenous CO respectively. Then 3-(4, 5-cimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) colorimetric assay and immunocytochemical staining were used to study the energy metabolism and the expression of proliferating cell nuclear antigen (PCNA) in PASMCs. Flow cytometry was used to analyze the cell cycle of PASMCs.Results After exposure to hypoxic conditions for 12, 24, and 48 hours, the HO-1 mRNA increased by 2.7%, 5.7% and 27.1% respectively (P<0.01). The carboxy-hemoglobin (COHb) in the medium increased by 13.8%, 31.0% and 93.1% (P<0.01); the cGMP concentrations were 2.7, 4.0 and 6.8-fold compared with the control group (P<0.01 and P<0.05). In comparison with the control group, the value of MTT colorimetric assay, the immunocytochemical staining of PCNA and the percentages of PASMCs in S and G 2M phases in the hypoxic group were significantly higher (P<0.01). After treatment with Hemin and CO, the results of the above analysis decreased significantly (P<0.01 and P<0.05), but increased significantly after treatment with Hb (P<0.01 and P<0.05). Conclusions The expression of HO-1 gene in PASMCs is upregulated by hypoxia and the production of endogenous CO is elevated as well. The endogenous CO s展开更多
<strong>OBJECTIVE:</strong> <span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">To determine the types o...<strong>OBJECTIVE:</strong> <span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">To determine the types of major maternal-perinatal morbidity associated with prolonged, acute-onset severe systolic hypertension during pregnancy and postpartum.</span></span></span><span><span><span style="font-family:""> </span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><b><span style="font-family:Verdana;">METHODS: </span></b></span></span><span><span><span style="font-family:""><span style="font-family:Verdana;">A medicolegal database retaining only medical record data was created from all cases involving women with medical/hypertensive disorders of pregnancy evaluated by the first author between 1986-2015. Case files of women that experienced severe systolic hypertension (SSH) sustained for many hours to days were identified for study. </span><b><span style="font-family:Verdana;">RESULTS: </span></b><span style="font-family:Verdana;">Sixty six pregnant/postpartum women met study criteria. Stroke secondary to intracranial hemorrhage or thrombosis (65.2) and acute pulmonary edema (33%) were the leading causes of maternal morbidity and mortality, most often antepartum as a component of early-onset preeclampsia (</span></span></span></span><span><span><span style="font-family:""><span style="font-family:Verdana;">≤</span><span style="font-family:Verdana;">34 weeks). Eclampsia, abruptio placenta and injury to heart, liver and/or kidneys were other frequent co-morbidities. Seven postpartum women developed sudden new-onset postpartum SSH and suffered a stroke 4</span></span></span></span><span><span><span style="font-family:""> </span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">-</span></span></span><span><span><span style="font-family:""> </span></span></span><span><span><span style="font-family:""><span style="font-family:Verdana;">13 days after delivery. Maternal mo展开更多
基金ThissubjectwassupportedbytheFoundationofScienceandTechnologyCommitteeofSichuanProvince (No G970 15 )
文摘To examine the effects of prenatal tetrandrine (Tet) therapy on pulmonary arterial structural remodeling in nitrofen-induced congenital diaphragmatic hernia (CDH) Methods CDH was induced in fetal rats by maternal administration of 100*!mg nitrofen by gavage on day 9 5 of gestation (term, day 22) Control animals received olive oil (OO) Tet (24*!mg/kg per day) or normal saline (NS) was given by gavage every day from 16 to 20 days of gestation, and fetuses were delivered by caesarean section on day 21 5 Lung sections from 3 fetuses in each group were studied The number of vessels were calculated, the external diameter (ED), medial wall thickness (MT), percent of medial wall thickness, and wall structure were evaluated by image analysis software Results In the pre-acinar arteries, CDH-NS pups had a significantly increased %MT compared with the OO-NS group ( P <0 05), while CDH-Tet animals had a reduced %MT compared with the CDH-NS rats ( P <0 05) Similar results were seen in the intra-acinar level Significant differences were observed between CDH-NS animals and OO-NS controls in the percentage of muscularized intra-acinar blood vessels ( P <0 001) Tet-treated CDH pups had a reduced percentage of muscularized intra-acinar arteries compared with CDH-NS animals Conclusions Medial hypertrophy is present in both the pre-acinar and intra-acinar arteries in the nitrofen-induced CDH rat model Tet treatment inhibits medial hypertrophy and reduces the percentage of muscularized intra-acinar vessels Prenatal Tet therapy may be efficacious in reducing the risk of PH in human newborns with CDH
基金ThisworkwassupportedbytheNationalNaturalScienceFoundationofChina (No 3 9970 3 3 2 )
文摘Objective To investigate the expression of inducible heme oxygenase (HO-1) gene in pulmonary artery smooth muscle cells (PASMCs) exposed to hypoxia, and the influence of carbon monoxide (CO) on the proliferation of PASMCs under hypoxic conditions. Methods Primary culture of rat PASMCs were passed every 3 days, and the 3-5 passages were used. After exposure to hypoxic conditions (95% N 2, 5% CO 2) 0, 12, 24 and 48 hours, the level of HO-1 mRNA was examined by reverse transcriptase polymerase chain reaction (RT-PCR). The volume of COHb in the medium was measured spectrophotometrically. The cyclic guanosine mono-phosphate (cGMP) concentration of cell extracts was determined by radioimmunoassay. PASMCs were divided into 5 groups, cultured under normoxia and hypoxia and treated with hemin, hemoglobin (Hb) and exogenous CO respectively. Then 3-(4, 5-cimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) colorimetric assay and immunocytochemical staining were used to study the energy metabolism and the expression of proliferating cell nuclear antigen (PCNA) in PASMCs. Flow cytometry was used to analyze the cell cycle of PASMCs.Results After exposure to hypoxic conditions for 12, 24, and 48 hours, the HO-1 mRNA increased by 2.7%, 5.7% and 27.1% respectively (P<0.01). The carboxy-hemoglobin (COHb) in the medium increased by 13.8%, 31.0% and 93.1% (P<0.01); the cGMP concentrations were 2.7, 4.0 and 6.8-fold compared with the control group (P<0.01 and P<0.05). In comparison with the control group, the value of MTT colorimetric assay, the immunocytochemical staining of PCNA and the percentages of PASMCs in S and G 2M phases in the hypoxic group were significantly higher (P<0.01). After treatment with Hemin and CO, the results of the above analysis decreased significantly (P<0.01 and P<0.05), but increased significantly after treatment with Hb (P<0.01 and P<0.05). Conclusions The expression of HO-1 gene in PASMCs is upregulated by hypoxia and the production of endogenous CO is elevated as well. The endogenous CO s
文摘<strong>OBJECTIVE:</strong> <span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">To determine the types of major maternal-perinatal morbidity associated with prolonged, acute-onset severe systolic hypertension during pregnancy and postpartum.</span></span></span><span><span><span style="font-family:""> </span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><b><span style="font-family:Verdana;">METHODS: </span></b></span></span><span><span><span style="font-family:""><span style="font-family:Verdana;">A medicolegal database retaining only medical record data was created from all cases involving women with medical/hypertensive disorders of pregnancy evaluated by the first author between 1986-2015. Case files of women that experienced severe systolic hypertension (SSH) sustained for many hours to days were identified for study. </span><b><span style="font-family:Verdana;">RESULTS: </span></b><span style="font-family:Verdana;">Sixty six pregnant/postpartum women met study criteria. Stroke secondary to intracranial hemorrhage or thrombosis (65.2) and acute pulmonary edema (33%) were the leading causes of maternal morbidity and mortality, most often antepartum as a component of early-onset preeclampsia (</span></span></span></span><span><span><span style="font-family:""><span style="font-family:Verdana;">≤</span><span style="font-family:Verdana;">34 weeks). Eclampsia, abruptio placenta and injury to heart, liver and/or kidneys were other frequent co-morbidities. Seven postpartum women developed sudden new-onset postpartum SSH and suffered a stroke 4</span></span></span></span><span><span><span style="font-family:""> </span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">-</span></span></span><span><span><span style="font-family:""> </span></span></span><span><span><span style="font-family:""><span style="font-family:Verdana;">13 days after delivery. Maternal mo
