To investigate the protective effect and specific mechanism of esmolol on sepsis-induced acute cardiac injury in rats.

A total of 26 adult male Sprague-Dawley rats were randomly divided into the sham group (6 rats), sepsis group (10 rats) and esmolol group (10 rats), and 6 rats in each group were guaranteed for follow-up experimental analysis. In the esmolol group, esmolol (15 mg·kg^-1·h^-1) was continuously pumped through the left internal jugular vein, and the same amount of isotonic NaCl solution was continuously pumped into the sham group and sepsis group. After 30 min of injection, the sepsis-induced acute cardiac injury model was reproduced by intraperitoneal injection of lipopolysaccharide (10 mg/kg) in the sepsis group and esmolol group, and rats in the sham group only received an equivalent amount of isotonic NaCl solution. The death of rats in each group was observed at 24 h after modeling, and the abdominal aorta blood was collected to test the serum cardiac troponin I (cTnI). The rats were sacrificed after blood collection. The cardiac tissues were collected to observe the pathological structure changes under the hematoxylin-eosin staining by light microscope, and the expression levels of Beclin-1, microtubule-associated protein 1 light 3-Ⅱ (LC3-Ⅱ) and Parkin proteins were tested by Western-blotting.

There were no deaths in the sham group, 4 in the sepsis group and 2 in the esmolol group at 24 h after modeling. Under light microscope, in the sham group, the myocardium structure was complete, the myocardium fibers were arranged in order, and the morphology of myocardium cells was normal; in the sepsis group, myocardial fibers were disordered, inflammatory cells infiltrated, cell swelling was obvious, and tissue necrosis was observed; in the esmolol group, the myocardial fibers were relatively regular, the infiltration of inflammatory cells reduced, and the swelling of myocardial cells improved. The levels of cTnI, Beclin-1, LC3-Ⅱ and Parkin proteins among the three groups all showed significant differences (F = 17.300, 110.00, 57.670, 14.980; all P < 0.001). Compared with the sepsis group, the level of cTnI was much lower [(3.2 ± 0.8), (1.4 ± 0.6), (1.4 ± 0.7) ng/L], and the levels of Beclin-1 [(0.21 ± 0.07), (1.01 ± 0.13), (0.98 ± 0.11)], LC3-Ⅱ [(0.29 ± 0.11), (1.02 ± 0.16), (0.99 ± 0.13)] and Parkin [(0.73 ± 0.09), (1.00 ± 0.13), (1.13 ± 0.16)] proteins were much higher in the sham group and esmolol group (all P < 0.05).

Esmolol has a significant protective effect on acute myocardial injury in sepsis rats, and its mechanism is related to the promotion of Parkin-mediated mitochondrial autophagy.