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1.
Clin Hemorheol Microcirc ; 77(4): 425-433, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-33386797

RESUMEN

OBJECTIVE: The aim of the present study was to observe the effect of sacubitril valsartan on cardiac function and vascular endothelial function in patients with chronic heart failure with reduced ejection fraction (HFrEF). METHODS: A total of 80 patients with HFrEF were randomly divided into an observation group and a control group, with 40 patients in each group. Sacubitril valsartan was added to the conventional treatment in the observation group, and perindopril was added to the conventional treatment in the control group. Both groups were treated continuously for 12 weeks. The left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), flow-mediated vasodilatory function (FMD) of the brachial artery, and levels of plasma Ang II, endothelin 1 (ET-1), and calcitonin gene-related peptide (CGRP), together with the serum nitric oxide (NO) and NO synthase (NOS) were compared before and after treatment in the groups. RESULTS: Before the treatment, the levels of LVEF, LVEDD, FMD, Ang II, ET-1, CGRP, NO, and NOS in the observation group were not significantly different from those in the control group (P > 0.05). However, the levels of LVEF, FMD, CGRP, NO, and NOS in both groups were significantly higher after the treatment than those before the treatment (P < 0.05) and significantly higher in the observation group than those in the control group. The difference was statistically significant (P < 0.05). Meanwhile, the levels of LVEDD, Ang II, and ET-1 in both groups decreased significantly after the treatment (P < 0.05) and were significantly lower in the observation group than those in the control group. The difference was statistically significant (P < 0.05). CONCLUSION: Sacubitril valsartan might improve endothelial function while increasing cardiac function in HFrEF patients.


Asunto(s)
Aminobutiratos/uso terapéutico , Compuestos de Bifenilo/uso terapéutico , Insuficiencia Cardíaca/tratamiento farmacológico , Volumen Sistólico/efectos de los fármacos , Valsartán/uso terapéutico , Función Ventricular Izquierda/efectos de los fármacos , Anciano , Aminobutiratos/farmacología , Compuestos de Bifenilo/farmacología , Combinación de Medicamentos , Femenino , Humanos , Masculino , Persona de Mediana Edad , Resultado del Tratamiento , Valsartán/farmacología
2.
Asian Pac J Trop Med ; 8(10): 864-9, 2015 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-26522304

RESUMEN

OBJECTIVE: To study the mechanism and significance of pH change in the coronary artery microthrombosis of rats. METHODS: After the sodium laurate-induced model of coronary artery microthrombosis of rats was constructed, the vascular endothelial cells were separated and then cultured in the mediums with different pH values for 24 h. Enzyme linked immunosorbent assay was used to detect the content of von Willebrand factor (vWF) in the medium; while the real-time PCR and western blot assay were used to detect the expression of fibrinogen-like protein 2 (FGL2) at the mRNA and protein level. The comprehensive evaluation was performed to discuss the effect of pH change on the coronary artery microthrombosis of rats. RESULTS: The expression level of vWF detected by enzyme linked immunosorbent assay was 336.67 ± 24.95, 311.33 ± 14.98, 359.67 ± 39.63, 354.67 ± 49.01 and 332.00 ± 33.42 (pg/mL) respectively; while the expression of vWF in the model group was 570.00 ± 57.94, 524.67 ± 57.94, 437.00 ± 95.38, 415.33 ± 44.38 and 444.67 ± 74.31 respectively. Being cultured under the different pH values, the relative expression level of FGL2 mRNA in the model group was 7.93 ± 0.93, 6.70 ± 0.70, 5.03 ± 0.32, 5.13 ± 0.40 and 5.57 ± 0.83 respectively. CONCLUSIONS: The coronary artery microthrombosis of rats can cause the high expression and secretion of vWF. Meanwhile, FGL2 is also up-regulated in the thrombosis and such up-regulation is more significant in the condition with low pH, which indicates that the low pH condition may be one of factors that contribute to the cardiovascular diseases.

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