The Effect of a Nitric Oxide Donor on Microcirculation of Denervated Skeletal Muscle after Ischemia/Reperfusion Injury

PURPOSE. The protective effect of exogenous nitric oxide (NO) on innervat-ed skeletal muscle during early reperfusion has been proven in previous studies. This study evaluated the effect of exogenous NO donor on a denervated muscle model which is more relevant to clinical practice. METHODS. Twenty denervated rat cremaster muscles underwent 2 hours of ischemia followed by 90 minutes of reperfusion and were divided into two groups. One group received systemic infusion of s-nitroso-n-acetylcysteine (SNAC 100 nmol/min), and the other received an equal amount of phosphate-buffered saline (PBS). During reperfusion, the blood flow of the main vascular pedicle of the cremaster muscle was measured with laser Doppler flowmetry. RESULTS. The overall blood flow of the reperfused cremaster muscle in the SNAC group increased from 42% of baseline at 10 min to 107% at 30 min of reperfusion, and remained above baseline throughout the experiment, with a highest level of 168% at 60 min of reperfusion. In contrast, the average blood flow in the PBS group was only between 35% and 83% of baseline during 90 min of reperfusion. Compared to the PBS group, the average blood flow in the SNAC group was significantly (P＜0.03 to p＜0.001) greater from 30- to 90-min of reperfusion. CONCLUSIONS. (1) Exogenous NO donor (SNAC) improves microcircula-tion of reperfused denervated cremaster muscle. (2) This effect against reperfu-sion injury in skeletal muscle is independent of any degree of intact innervation. (3) The difference between SNAC and control groups was more prominent after 30 minutes of reperfusion, when the detrimental effect of reperfusion reaches its peak.

並列關鍵字

Ischemia/reperfusion ； Nitric oxide ； Denervation ； Skeletal mus-cle

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