Abstract
Aim: The aim of this study was to investigate the effects of sodium nitroprussid (SNP) on ischemia-reperfusion injury in rats. Method: Twenty-four Sprague-Dawney rats were divided into four equal groups: group I without ischemia-reperfusion (I-R); group II with ischemia; group III with I-R; group IV with I-R and SNP. Complete bilateral hindlimb ischemia was produced by means of tourniquet occlusion of the upper thigh. Result: Blood creatine phosphokinase, lactate dehydrogenase, aspartate transaminase, urea, creatinine levels were not significantly different between groups 3 and 4. Malondialdehyde (MDA) levels were not significantly different between groups 3 and 4 in liver, soleus muscles and lung tissue. However, MDA levels were significantly lower in group 4 when compared with group 3 in renal tissue. Histological examination of the soleus muscles revealed that neutrophil leukocyte infiltration in group 3 was significantly less prominent than in group 4. Conclusion: These results have shown that SNP was not able to improve muscle ischemia-reperfusion injury in our study.
Highlights
It is known that long lasting ischemia for a definite period can cause cell death and tissue necrosis due to energy deficiency
These results have shown that sodium nitroprusside (SNP) was not able to improve muscle ischemia-reperfusion injury in our study
No statistically significant differences were found in pre-ischemic period measurements between groups (p>0.05).There were no statistically significant differences of serum creatine phosphokinase (CPK) levels when groups 1 and 2 and groups 3 and 4 were compared with each other (p>0.05); significant differences were found in CPK levels between groups 1 and 3 (p
Summary
It is known that long lasting ischemia for a definite period can cause cell death and tissue necrosis due to energy deficiency. Recent studies have shown that this tissue injury developes during ischemia period, and continues during reperfusion period. Many studies have been performed in order to prevent reperfusion injury; but a certain treatment modality couldn’t be determined because of the complex mechanism of reperfusion injury (1). We can see skeletal muscle ischemia-reperfusion (I-R) injury during vascular surgery after releasing across clamp, during orthopedic surgery after releasing tourniquet, after crush syndrome or extremity retransplantation (1). Different experimental studies have shown that NO can act dually and has both cytotoxic and cytoprotective effects. Treatment time and duration of NO and derivatives are not still clearly defined (2). We aimed to search regional and systemic protective effects of sodium nitroprusside (SNP) as a NO donor on muscle I-R injury
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