Abstract
Sepsis is a life-threatening organ dysfunction syndrome with a high rate of mortality. It is caused by an abnormal immune response to infection, and the occurrence of sepsis-induced cardiomyopathy is the primary cause of death. The present study was designed to examine the effects of adenosine on lipopolysaccharide- (LPS-) induced cardiac anomalies and the underlying mechanisms involved. Adenosine (25, 50, and 100 mg/kg, i.g., 2 times/day) was administered for three days, followed by the induction of sepsis by intraperitoneal injection of LPS (10 mg/kg/2h). The effects of adenosine on inflammatory factors, LVEF, LVFS, and MAPK in septic rats (half male and half female) were observed. Subsequently, the effect of adenosine (10 μM) on the mitochondrial function of H9c2 cells stimulated with LPS (20 μg/mL, 24 h) was observed in the presence and absence of the estrogen receptor-specific antagonist ICI182,780. The results show that medium to high doses of adenosine can significantly promote cardiac function (LVEF and LVFS) and reduce the levels of inflammatory factors (TNF-α, IL-6, PCT, and cTnI) and p-JNK in septic rats, with a significant difference seen between male and female rats. The results of flow cytometry show that adenosine significantly inhibited increases in ROS levels, mitochondrial membrane potential, and the swelling degree of mitochondria in H9c2 cells stimulated with LPS, but this effect could be blocked by ICI182,780, indicating that adenosine attenuated LPS-induced cardiac dysfunction by inhibiting mitochondrial function via the ER pathway.
Highlights
Sepsis is a life-threatening organ dysfunction syndrome caused by an abnormal immune response to infection [1] and is one of the major causes of death in critically ill patients
Ultrasound revealed that LPS challenge significantly decreased left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS), the effect of which was abrogated by adenosine
The results show that HQ (2000 mg/kg) and adenosine (50 and 100 mg/kg) can significantly improve LVEF and LVFS in septic rats, promoting their cardiac function
Summary
Sepsis is a life-threatening organ dysfunction syndrome caused by an abnormal immune response to infection [1] and is one of the major causes of death in critically ill patients. According to the latest statistical data [2], the mortality rate of patients with sepsis is as high as 24.3%, and the occurrence of sepsis-induced cardiomyopathy is the primary cause of death. In a study by Pulido et al [3], the recorded incidence of sepsis-induced cardiomyopathy was reported to be as high as 64%. With the development of technology monitoring cardiac function, a greater understanding of sepsis-induced cardiomyopathy has been reached. The heart is an organ rich in mitochondria, and the mitochondrial dysfunction in sepsis is receiving increasing attention [4].
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