Remifentanil Anesthesia on the Expression of Apoptosis-Related Proteins Bcl-2 and Bax in Rat Myocardial Cells with Ischemia-Reperfusion Injury

Abstract

Ischemia-reperfusion damage to the myocardium is inevitable. This study mainly explored the effect of remifentanil anesthesia on the expression of apoptosis-related proteins Bcl-2 and Bax in rat myocardial ischemia-reperfusion injury. Select 48 mice (n=6). First, prepare solutions of different concentrations of remifentanil. A model of ischemia-reperfusion cardiomyocytes was established, and 6 slices of tissue were taken from each specimen, and the positive cells were observed with an optical microscope and magnified 100 times. Bcl-2 and Bax were positive in the cytoplasm and yellowish-brown particles in the inner membrane. According to the distribution of positive cells, randomly select 3 clear fields of view from each part, count the number of positive cells in each field, and then take the average of the proportion of positive cells to get Bcl-2 or Bax protein-positive Index (PEI). Comparison of mRNA levels in each group: Compared with the R3 group, the ratio of the M, R1, and R2 groups increased, and the mRNA expression level of the M group increased almost 3 times, P<0.05. The results of the study show that remifentanil reduces the mortality of myocardial cells by regulating the appearance of Bcl-2 and Bax proteins, and has a certain protective effect on the rat heart during myocardial ischemia and reperfusion. There is no statistically significant difference in the protective effect of remifentanil on myocardial ischemia-reperfusion.

El postacondicionamiento del miocardio con remifentanil en el corazón aislado y perfundido de rata

“…Por otro lado, un mecanismo adicional de la cardioprotección inducida por los opioides es la inhibición del estrés del retículo endoplásmico mediante el mantenimiento de la homeostasis de zinc (42) ; además de sus efectos antiapoptóticos (43,44) . En este sentido, recientemente Lewinska y colaboradores informaron que, en cardiomiocitos humanos, el preacondicionamiento con remifentanil protege contra la senescencia celular y la necroptosis inducidas por la hipoxia que puede estar relacionada con la disminución de la isquemia miocárdica y la lesión inducida por reperfusión por el remifentanil en pacientes sometidos a cirugía cardíaca (45) .…”

Role of Remifentanil on MAC, Bcl-2, and Bax Levels in Traumatic Brain Injury Rat Models

“…It can regulate the balance of intracranial pressure by maintaining the Cerebral Metabolic Rate of Oxygen (CMRO 2 ) and Cerebral Blood Flow (CBF) to maintain hemodynamic stability. 10,11 With a faster onset of action, shorter half-life, and a more stable hemodynamic effect than its predecessor (fentanyl), remifentanil can be a new solution as balanced anesthesia in TBI cases. There is limited information on the administration of remifentanil in TBI cases.…”

“…The advantages of remifentanil include a fast onset of action, relatively short duration, and can regulate the balance of intracranial pressure by maintaining the Cerebral Metabolic Rate of Oxygen (CMRO 2 ) and Cerebral Blood Flow (CBF). 10 In the case of injury, remifentanil will lead to activated -receptors and release CD59 protein, reducing MAC levels. It also indirectly suppresses the apoptosis and homeostatic process as well as…”

High-dose remifentanil exacerbates myocardial ischemia-reperfusion injury through activation of calcium-sensing receptor-mediated pyroptosis

“…Some studies suggest that small amounts of RF protect the myocardium against hypoxia/reoxygenation (H/R) injury by enhancing autophagic flux or reducing lipid peroxidation [2,3]. Also, small amounts of RF can effectively reduce Ivyspring International Publisher myocardial cell injury caused by myocardial ischemia reperfusion in rats, improve cardiac function, decrease cleaved caspase-3 and increase the ratio of Bcl-2/Bax in myocardial cells [4]. Many researches focused on the protective effects of RF in MI/R, while ignoring its side effects in high doses.…”