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1.
Rev. esp. cardiol. (Ed. impr.) ; 77(3): 256-264, mar. 2024. ilus, tab, graf
Article in Spanish | IBECS | ID: ibc-231062

ABSTRACT

Introducción y objetivos La reperfusión coronaria produce un daño en la microcirculación y, en concreto, las células endoteliales. Este estudio evalúa el efecto del suero aislado tras la revascularización de pacientes con un infarto agudo de miocardio con elevación del segmento ST (IAMCEST) en la viabilidad celular, el grado de permeabilidad endotelial in vitro y la asociación de estos parámetros con una mayor extensión de los índices de resonancia magnética cardiaca (RMC) relacionados con el daño por reperfusión (edema, hemorragia y obstrucción microvascular). Métodos Se incubaron células endoteliales de arteria coronaria humana con suero aislado 24 h tras la revascularización de 43 pacientes con IAMCEST evaluados mediante RMC y 14 sujetos de control. Se testó el efecto del suero de pacientes con IAMCEST en la pérdida de viabilidad celular por activación de la apoptosis y la necrosis, así como en la permeabilidad y la estructura de la monocapa endotelial. Resultados El suero de pacientes con IAMCEST aumentó la apoptosis (p <0,01) y la necrosis (p <0,05) de células endoteliales de arteria coronaria humana y causó un incremento de la permeabilidad de la monocapa endotelial in vitro (p <0,01) debido a mayores espacios intercelulares (p <0,05 frente a los controles). Una mayor necrosis inducida por suero se asoció con más permeabilidad endotelial in vitro (p <0,05) y con una mayor extensión de los principales índices de daño tras reperfusión y mayor tamaño de infarto. Conclusiones El suero tras la reperfusión de pacientes con IAMCEST induce la apoptosis y la necrosis in vitro de las células endoteliales y la permeabilidad endotelial. Cuanto más potente sea el efecto inductor de necrosis, más deletéreas son las consecuencias en cuanto al daño estructural resultante. (AU)


Introduction and objectives Clinical and experimental studies have shown that, in patients with reperfused ST-segment elevation myocardial infarction (STEMI), abnormalities in the endothelial monolayer are initiated during ischemia but rapidly intensify upon restoration of blood perfusion to the ischemic area. We aimed to evaluate the effect of serum isolated after revascularization from STEMI patients on the degree of endothelial permeability in vitro, by promoting endothelial cell apoptosis and necrosis in vitro. We also investigated the association between the percentage of serum-induced endothelial cell apoptosis or necrosis in vitro and the extent of cardiovascular magnetic resonance (CMR)-derived parameters of reperfusion injury (edema, hemorrhage, and microvascular obstruction). Methods Human coronary artery endothelial cells were incubated with serum isolated 24hours after revascularization from 43 STEMI patients who underwent CMR and 14 control participants. We assessed the effect of STEMI serum on activation of apoptosis and necrosis, as well as on the permeability and structure of the endothelial monolayer. Results Serum from STEMI patients increased apoptosis (P <.01) and necrosis (P <.05) in human coronary artery endothelial cells and caused increased permeability of the endothelial monolayer in vitro (P <.01), due to enlarged intercellular spaces (P <.05 vs control in all cases). Higher serum-induced necrosis was associated with greater endothelial permeability in vitro (P <.05) and with more extensive CMR-derived indices of reperfusion injury and infarct size. Conclusions Postreperfusion serum activates necrosis and apoptosis in endothelial cells and increases the degree of endothelial permeability in vitro. The more potent the necrosis-triggering effect of serum, the more deleterious the consequences in terms of the resulting cardiac structure. (AU)


Subject(s)
Humans , Myocardial Infarction , Reperfusion Injury , Serum , Patients , Endothelial Cells , Magnetic Resonance Spectroscopy , Edema , Hemorrhage
2.
Rev Esp Cardiol (Engl Ed) ; 77(3): 254-264, 2024 Mar.
Article in English, Spanish | MEDLINE | ID: mdl-37696331

ABSTRACT

INTRODUCTION AND OBJECTIVES: Clinical and experimental studies have shown that, in patients with reperfused ST-segment elevation myocardial infarction (STEMI), abnormalities in the endothelial monolayer are initiated during ischemia but rapidly intensify upon restoration of blood perfusion to the ischemic area. We aimed to evaluate the effect of serum isolated after revascularization from STEMI patients on the degree of endothelial permeability in vitro, by promoting endothelial cell apoptosis and necrosis in vitro. We also investigated the association between the percentage of serum-induced endothelial cell apoptosis or necrosis in vitro and the extent of cardiovascular magnetic resonance (CMR)-derived parameters of reperfusion injury (edema, hemorrhage, and microvascular obstruction). METHODS: Human coronary artery endothelial cells were incubated with serum isolated 24hours after revascularization from 43 STEMI patients who underwent CMR and 14 control participants. We assessed the effect of STEMI serum on activation of apoptosis and necrosis, as well as on the permeability and structure of the endothelial monolayer. RESULTS: Serum from STEMI patients increased apoptosis (P <.01) and necrosis (P <.05) in human coronary artery endothelial cells and caused increased permeability of the endothelial monolayer in vitro (P <.01), due to enlarged intercellular spaces (P <.05 vs control in all cases). Higher serum-induced necrosis was associated with greater endothelial permeability in vitro (P <.05) and with more extensive CMR-derived indices of reperfusion injury and infarct size. CONCLUSIONS: Postreperfusion serum activates necrosis and apoptosis in endothelial cells and increases the degree of endothelial permeability in vitro. The more potent the necrosis-triggering effect of serum, the more deleterious the consequences in terms of the resulting cardiac structure.


Subject(s)
Percutaneous Coronary Intervention , Reperfusion Injury , ST Elevation Myocardial Infarction , Humans , ST Elevation Myocardial Infarction/diagnosis , ST Elevation Myocardial Infarction/surgery , ST Elevation Myocardial Infarction/etiology , Endothelial Cells , Magnetic Resonance Imaging/methods , Necrosis/etiology , Reperfusion Injury/etiology , Percutaneous Coronary Intervention/adverse effects , Treatment Outcome
3.
Med. crít. (Col. Mex. Med. Crít.) ; 37(2): 134-140, Feb. 2023. graf
Article in Spanish | LILACS-Express | LILACS | ID: biblio-1558401

ABSTRACT

Resumen: La atención a pacientes con quemaduras extensas es compleja, la quemadura condiciona efectos en el sitio de la lesión y a nivel sistémico. A nivel de la microcirculación se presenta respuesta de mediadores químicos inflamatorios y excesiva producción de especies reactivas de oxígeno y nitrógeno, además condiciona disminución de la capacidad antioxidante de vitamina C, por lo que se altera el balance fisiológico de óxido-reducción, dando paso al estado de estrés oxidativo, esto trae como consecuencia un incremento en la inflamación, disfunción endotelial e incremento de la permeabilidad capilar. Uno de los objetivos de la reanimación del paciente quemado es restaurar el volumen intravascular generado por el estado de choque, en el cual se implementan estrategias como el uso de cristaloides, coloides, plasma, terapias dialíticas, uso limitado de opioides y la administración de vitamina C. El objetivo de este trabajo es dar a conocer a la comunidad médica las características físicas y químicas, los mecanismos moleculares de la vitamina C en los que se encuentra implicada en condiciones de quemaduras graves, con la finalidad de la implementación durante la fase de reanimación del quemado.


Abstract: The care of patients with extensive burns is complex, the burn conditions effects at the site of the injury and at the systemic level. At the microcirculation level, there is a response of inflammatory chemical mediators and excessive production of reactive oxygen and nitrogen species, which also causes a decrease in the antioxidant capacity of vitamin C, which is why the physiological balance of oxide-reduction is altered, giving way to the state of oxidative stress, this results in an increase in inflammation, endothelial dysfunction and an increase in capillary permeability. One of the objectives of the resuscitation of the burned patient is to restore the intravascular volume generated by the state of shock, in which strategies such as the use of crystalloids, colloids, plasma, dialysis therapies, limited use of opioids and the administration of vitamins are implemented C. The objective of this work is to make known to the medical community, the physical and chemical characteristics, the molecular mechanisms of vitamin C in which it is involved in severe burn conditions, with the purpose of implementation during the resuscitation phase of burn.


Resumo: O atendimento a pacientes com queimaduras extensas é complexo, a queimadura condiciona efeitos no local da lesão e em nível sistêmico. Ao nível da microcirculação, há uma resposta de mediadores químicos inflamatórios e produção excessiva de espécies reativas de oxigénio e nitrogênio, condiciona também uma diminuição da capacidade antioxidante da vitamina C, que altera o equilíbrio fisiológico de oxidação-redução, dando lugar a o estado de estresse oxidativo, isso resulta em aumento da inflamação, disfunção endotelial e aumento da permeabilidade capilar. Um dos objetivos da ressuscitação do paciente queimado é restaurar o volume intravascular gerado pelo estado de choque, no qual se implementam estratégias como o uso de cristalóides, colóides, plasma, terapias dialíticas, uso limitado de opióides e administração de vitamina C. O objetivo deste trabalho é dar a conhecer à comunidade médica as características físicas e químicas, os mecanismos moleculares da vitamina C em que está envolvida em condições de queimaduras graves, com vista à sua aplicação durante a fase de reanimação do paciente queimado.

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