Estrous cycle phase affects myocardial infarction through reactive oxygen species and nitric oxide


Por: Ramírez-Hernández D., López-Sanchez P., Rosales-Hernández M.C., Fonseca-Coronado S., Flores-Monroy J.

Publicada: 1 ene 2021
Resumen:
Introduction: Myocardial infarction is the leading cause of death in women worldwide. Several studies have shown that estrogens play a cardioprotective role in women by decreasing reactive oxygen species (ROS) and increasing nitric oxide (NO). The aim of this work was to determine whether the evolution of myocardial infarction depends on the phase of the estrous cycle. Methods: Female Wistar rats were randomized into the following groups with an (n = 7 per group): (1) ovariectomized (OVX-sham); (2) OVX-48 h coronary occlusion (CO); (3) OVX-2 w CO; (4) proestrus-sham; (5) proestrus-48 h CO; (6) proestrus-2 w CO; (7) estrus-sham; (8) estrus-48 h CO; and (9) estrus-2 w CO. We measured the percentage of myocardial necrosis, cardiac hypertrophy, hemodynamic parameters, and the production of NO and ROS, after acute and chronic myocardial infarction was induced in proestrus or estrus or ovariectomized female rats. Results: The infarct area was reduced in the proestrus groups, while it was increased in the estrus and OVX groups. The left ventricular systolic pressure (LVSP) and ± dP/dt were reduced, but left ventricular diastolic pressure (LVDP) was increased in the OVX groups. NO was increased in the OVX + CO and estrus + CO groups. Production of ROS was increased in OVX rats after myocardial infarction but remained unchanged in proestrus and estrus. Conclusion: The phase of the estrous cycle in which the myocardial infarction occurs is important. When the coronary occlusion occurs during the proestrus phase, it prevents changes in cardiac function, the development of hypertrophy, oxidative stress and changes in NO levels, and reduces the extent of infarction. © 2021 The Author(s).

Filiaciones:
Ramírez-Hernández D.:
 Laboratorio de Farmacologia del Miocardio, Facultad de Estudios Superiores Cuautitlan, Universidad Nacional Autonoma de Mexico, México, 54740, Mexico

 Laboratorio de Farmacologia Molecular, Escuela Superior de Medicina, Instituto Politecnico Nacional, Ciudad de México, 11340, Mexico

López-Sanchez P.:
 Laboratorio de Farmacologia Molecular, Escuela Superior de Medicina, Instituto Politecnico Nacional, Ciudad de México, 11340, Mexico

Rosales-Hernández M.C.:
 Laboratorio de Biofísica y Biocatalisis, Seccion de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politecnico Nacional, Ciudad de México, 11340, Mexico

Fonseca-Coronado S.:
 Laboratorio de Farmacologia del Miocardio, Facultad de Estudios Superiores Cuautitlan, Universidad Nacional Autonoma de Mexico, México, 54740, Mexico

Flores-Monroy J.:
 Laboratorio de Farmacologia del Miocardio, Facultad de Estudios Superiores Cuautitlan, Universidad Nacional Autonoma de Mexico, México, 54740, Mexico
ISSN: 27686701
Editorial
Bioscience Research Institute, 7 TEMZASEK BLVD, SUNTEC TOWER ONE, SINGAPORE, SINGAPORE, Singapur
Tipo de documento: Article
Volumen: 26 Número: 12
Páginas: 1434-1443
WOS Id: 000742514300007
ID de PubMed: 34994158
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