β1-Blocker improves survival and ventricular remodelling in rats with lethal crush injury

Crush injury/crush syndrome (CI/CS) is the second most common cause of death during earthquakes. Most studies of CI/CS have mainly focused on kidney injury after decompression. Few studies have focused on myocardial injury caused by crush injury and its potential mechanisms.

We first verified cardiomyocyte injury during compression in rats with a crush injury. The survival rate, electrocardiographic results, histological results, catecholamine changes and cardiac β1-AR expression were evaluated. Next, we explored the effects of pretreatment with a selective β1-blocker (bisoprolol) with or without fluid resuscitation on rats with a crush injury. In addition to evaluating the survival rates, biochemical and histological analyses and echocardiographic measurements were also performed.

Reduced heart rates, elevated ST segments, and tall-peaked T waves were observed in the rats with a crush injury. The changes in the myocardial enzymes and pathological results demonstrated that myocardial damage occurred during compression in rats with a crush injury. The levels of the catecholamine norepinephrine in both the serum and myocardial tissue were elevated during compression. Pretreatment with a selective β1-blocker combined with fluid resuscitation significantly improved the survival rates of the rats with lethal crush injury. The myocardial enzymes and pathological results showed that the combined therapy decreased myocardial damage. The echocardiography measurements showed that the rats that received the combined therapy exhibited decreased left ventricular mass (LVM), left ventricular volume at end-systole (LVVs) and left ventricular internal diameter (LVID) compared with the rats with a crush injury.

Our findings demonstrated the presence of myocardial injury in the early stage of compression in rats with a crush injury. Pretreatment with a β1-blocker (bisoprolol) with fluid resuscitation significantly reduced mortality, decreased myocardial tissue damage, and improved ventricular remodelling in rats with a lethal crush injury.