Dexmedetomidine protects against myocardial ischaemia/reperfusion-induced renal damage in rats

Background

Myocardial ischaemia/reperfusion (MI/R) may induce renal damage. Our aim was to investigate the effects of dexmedetomidine (DEX) administration at two different timings either before or after ischaemia on renal damage induced by MI/R.

Methods

MI/R injury was induced in a rat model. we ligated the left anterior descending coronary artery for 30?min (ischaemic period), then reperfusion occurred for 2?h (reperfusion period). A single dose of DEX (100?µg/kg) was given intraperitoneally, either 30?min before myocardial ischaemia or 5?min after reperfusion. With the end of reperfusion period, rats were sacrificed, then we collected the blood and removed both kidneys quickly for biochemical and histopathological analysis.

Results

MI/R caused an elevation in serum urea and creatinine, significant elevation in malondialdehyde (MDA) release and decrease in superoxide dismutase (SOD) activity in the rat kidney. There were also higher levels of serum tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). Treatment with dexmedetomidine, 30?min before induction of myocardial ischaemia, succeeded to improve all the tested parameters. The valuable changes in these biochemical parameters were linked with similar enhancement in the histopathological appearance of the kidney. Meanwhile, DEX given 5?min after reperfusion improved serum urea and creatinine only.

Conclusion

These findings imply that MI/R plays a fundamental role in kidney damage through increased production of oxygen radicals or deficiency in antioxidants, and DEX given before ischaemia exerts reno-protective effects probably by its radical scavenging antioxidant activity and anti-inflammatory mechanism.