To investigate the effect and mechanism of isoprenaline, a β₁-adrenergic receptor agonist, on mitochondrial edema of cardiomyocytes induced by bupivacaine.

Six healthy pathogen-free male SD rats, weighing 180-220 g, were received enzymatic hydrolysis separation for myocardial cells, which were randomly divided into 4 groups: physiological saline group (control group), bupivacaine group, bupivacaine+isoprenaline group, and bupivacaine+isoprenaline+esmolol group. The myocardial cells were electrically stimulated to induce rhythmic contraction for 60 s. Electron microscopy of myocardial mitochondria was performed to assess the damage of the structure. The amount of mitochondrial reactive oxygen species (ROS) was quantitatively measured by ROS assay kit in the above cardiomyocytes. (Repeat 3 times and take the average) .

The mitochondrial edema score and ROS production was significantly higher in bupivacaine group than those in control group (4 719.95 vs. 3 921.94) (all P<0.05). The extent of myocardial mitochondrial edema and ROS production were significantly higher in bupivacaine+isoprenaline group than those in bupivacaine group (5 192.25 vs. 4 719.95) (all P<0.05). The mitochondrial edema score and ROS production was significantly lower in bupivacaine+isoprenaline+esmolol group than those in bupivacaine + isoprenaline group (4 709.68 vs. 5 192.25) (all P<0.05).

The excitation of β₁-adrenergic receptor induced by isoprenaline can interfere with mitochondrial metabolism and aggravate mitochondrial edema of cardiomyocytes caused by bupivacaine.

Electrical stimulation; Receptors, adrenergic, beta-1; Bupivacaine; Myocardium; Mitochondria