RESUMO
OBJECTIVE: To observe the effect of magnesium sulfate, Nifedipine Tablet (NT) combined Salvia Injection (SI) on endothelin-1 (ET-1), nitric oxide (NO), thromboxane A2(TXA2), prostacyclin I2(PG2), and hemorheology of preeclampsia patients. METHODS: Totally 704 preeclampsia patients were randomly assigned to the treatment group and the control group, 352 cases in each group. All patients were treated with magnesium sulfate combined NT (on the first day: slow intravenous injection of magnesium sulfate 5 g + intravenous dripping of magnesium sulfate injection 10 g + oral administration of NT 30 mg; on the second and third day, intravenous dripping of magnesium sulfate injection 10 g + oral administration of NT 30 mg), while those in the treatment group were dripped with SI additionally at 20 mL per day for 3 consecutive days. Before and after treatment plasma levels of endothelin-1 (ET-1), nitric oxide (NO), TXA2, PGi2, and hemorheology indicators [such as high blood viscosity (HBV), low blood viscosity (LBV), plasma viscosity (PV), erythrocyte rigidity index (ERI), fibrinogen (FIB)] of two groups were detected. RESULTS: Compared with the same group before treatment, serum levels of ET-1, TXA2, HBV, LBV, PV, ERI, and FIB decreased in the two groups after treatment (P <0. 05), but levels of NO and PG2 increased (P <0. 05). Compared with the control group in the same period, levels of ET-1, TXA2, HBV, LBV, PV, ERI, and FIB decreased in the treatment group after treatment (P <0. 05), but levels of NO and PGI2 increased (P <0. 05). CONCLUSION: Magnesium sulfate, NT combined SI could effectively regulate the balance of ET-1/NO and TXA2/PGI2, and improve hemorheology of preeclampsia patients.
Assuntos
Medicamentos de Ervas Chinesas/farmacologia , Sulfato de Magnésio/farmacologia , Nifedipino/farmacologia , Pré-Eclâmpsia/tratamento farmacológico , Salvia , Quimioterapia Combinada , Medicamentos de Ervas Chinesas/uso terapêutico , Endotelina-1/metabolismo , Epoprostenol/metabolismo , Feminino , Hemorreologia , Humanos , Injeções , Sulfato de Magnésio/administração & dosagem , Sulfato de Magnésio/uso terapêutico , Nifedipino/administração & dosagem , Nifedipino/uso terapêutico , Óxido Nítrico/metabolismo , Gravidez , Comprimidos , Tromboxano A2/metabolismoRESUMO
Four Ni-Ln-Ni heterometallic complexes, [Ni2LnL2]NO3·3H2O (H3L = tri(((3-methoxysalicylidene)amino)ethyl)amine, Ln = Gd for , Tb for and Dy for , respectively) and [Ni2DyL2]ClO4·MTBE·0.65H2O (, MTBE = methyl tert-butyl ether) have been synthesized by diffusion of methyl tert-butyl ether vapor into the reaction solution. The X-ray analyses demonstrated that the Gd(III) ion in exhibits rare seven-coordination, the Tb(III) and Dy(III) ions in display unusual six-coordination, and two Ni(II) ions and one Ln(III) ion are bridged by six phenolato atoms to form linear Ni-Ln-Ni heterotrinuclear complexes for . All complexes exhibit weak ferromagnetic interactions between Ni(II) and Ln(III) ions. Alternating current susceptibility measurements demonstrated that compounds and behave as single-molecule magnets with the effective energy barriers of 14.17 and 11.13 K under zero direct current field. They are rare single-molecule magnets containing six-coordinate Dy(III) ions.
RESUMO
OBJECTIVE: To investigate pulmonary vascular remodeling and protein kinase C-alpha (PKC-alpha) expression in chronic smoke exposure and/or hypoxia rats. METHODS: Fifty-six male Wistar rats were randomly divided into seven groups: control group (C group), smoke exposure groups (S(4W), S(8W) group), hypoxia groups (H(4W), H(8W) group), smoke exposure plus hypoxia groups (SH(4W), SH(8W) group). Wistar rats were exposed to cigarette smoke and/or hypoxia air [O2 (10.0 +/- 0.5)%] for 4 to 8 weeks. A method by right cardiac catheterization was used for measuring mean pulmonary artery pressure (mPAP). Right ventricle (RV), left ventricle (LV) plus interventricular septum (S) were split and weighed and right ventricular hypertrophy index (RVHI) was calculated. To evaluate vascular remodeling, alpha-smooth muscle actin (alpha-SM-actin) staining and count of the percentage of muscularized small pulmonary arteries which was determined by morphometric analysis of histological sections were used. Pulmonary artery smooth muscle cell (PASMC) apoptosis was detected by in situ end labeling technique (TUNEL), and proliferation by proliferating cell nuclear antigen (PCNA) staining. Reverse transcription-polymerase chain reaction (RT-PCR), immunofluorescence staining and Western blot analysis were used for the detection of PKC-alpha mRNA and protein expression in pulmonary arteries. RESULTS: mPAP in H(4W), H(8W), SH(4W), SH(8W) group [(31 +/- 7), (32 +/- 8), (32 +/- 9), (31 +/- 10) mm Hg, 1 mm Hg = 0.133 kPa] were higher than that in C group [(14 +/- 4) mm Hg, all P < 0.01], but mPAP in S(4W) and S(8W) group [(15 +/- 5), (16 +/- 6) mm Hg] were not increased (all P > 0.05). In S(4W), S(8W), H(4W), H(8W), SH(4W) and SH(8W) group, RVHI (0.258 +/- 0.024, 0.394 +/- 0.021, 0.374 +/- 0.020, 0.414 +/- 0.019, 0.434 +/- 0.023, 0.442 +/- 0.020, respectively), the percentage of muscularized arteries [(33.5 +/- 6.8)%, (41.1 +/- 9.8)%, (35.9 +/- 6.6)%, (46.0 +/- 6.3)%, (42.9 +/- 6.5)%, (50.2 +/- 9.9)%, respectively] and alpha-SM-actin expression (53 +/- 15, 75 +/- 14, 56 +/- 11, 82 +/- 17, 83 +/- 17, 98 +/- 16, respectively) were increased significantly (all P < 0.01). PASMC apoptosis was increased and proliferation was markedly increased. Apoptotic indices (AI, 2.5 +/- 1.0, 3.8 +/- 1.4, 2.3 +/- 1.1, 3.3 +/- 1.1, 3.5 +/- 1.4, 4.8 +/- 1.4, respectively) and proliferation indices (PI, 33.1 +/- 11.8, 43.8 +/- 11.0, 36.5 +/- 10.6, 46.3 +/- 12.1, 45.3 +/- 12.4, 53.3 +/- 13.4, respectively) were higher than those in C group (all P < 0.01). The expressions of PKC-alpha mRNA and protein were higher than those of C group (all P < 0.01). The differences were more significant between SH(4W) and H(4W) group, SH(8W) and H(8W) group (all P < 0.01). CONCLUSIONS: It is suggested that smoke is synergistic with hypoxia in aggravating pulmonary vascular remodeling. The possible mechanism is through PKC signaling transduction pathway activation.