Preventive effect of ginger (Zingiber officinale) pretreatment on renal ischemia-reperfusion in rats.

BACKGROUND/AIMS: The present study examined the preventive effect of ginger against renal ischemia-reperfusion (I-R) injury. METHODS: 30 adult male rats were used. The animals were allocated to five groups of 6 rats: (1) normal (N), (2) normal + ginger (N+G), (3) right nephrectomy (Sham), (4) I-R, and (5) I-R + ginger (I-R+G). To induce renal ischemia, animals were unilaterally nephrectomized and subjected to 45 min of left renal pedicle occlusion with 24 h reperfusion. Ginger was administered orally 24 h and just before ischemia. At the end of the experiment, blood samples and urine were collected. The following renal functional parameters were studied: serum and urinary levels of creatinine and urea, fractional excretion of sodium, and creatinine clearance. Histopathological examination of the kidney was also performed. RESULTS: Rats with renal I-R showed a significant increase in creatinine and urea concentration in serum and also a significant decrease in creatinine clearance compared with the other groups. In addition, renal histopathology in the I-R group showed severe alterations such as tubular dilatation and tubular epithelial necrosis. However, these changes were significantly reduced in the I-R+G group. CONCLUSION: This study suggests that ginger is a useful agent for the prevention of renal ischemia reperfusion-induced injury.

The role of nitric oxide in iron-induced rat renal injury.

Iron overload and enhanced hydroxyl radical (*OH) formation have been implicated as the causative factors of oxidative stress in different organs. Both pro-oxidant and anti-oxidant properties have been reported for nitric oxide (NO) in iron-mediated tissue injury. To determine the contribution of NO to iron-induced renal injury, eight groups of rats (eight in each group) were studied as follows: control (normal saline), L-Arg (L-arginine as a substrate of NO synthase, 400 mg/kg), L-NAME (an inhibitor of NO synthase, 8 mg/kg), Fe (iron dextran, 600 mg/kg), DFO (deferroxamine as a chelator of iron, 150 mg/kg), Fe+L-Arg, Fe+L-NAME, DFO+L-Arg. Twenty-four hours after the injections, blood samples were taken and kidneys removed for biochemical analysis. Plasma creatinine and urea were used to stimulate renal function. Renal tissue and plasma vitamin E levels, the most important endogenous fat soluble antioxidant, were measured by HPLC and UV detection. In this study, renal function was markedly reduced in the Fe group compared to controls (creatinine, 1.02+/-0.05 mg/dL versus 0.78+/-0.04 P <0.05; urea, 49.59+/-1.69 mg/dL versus 40.75+/-0.86, P <0.01). Vitamin E levels were significantly lower in the Fe group compared to controls (plasma P <0.01; renal tissue P <0.05). Administration of L-Arg to Fe-treated groups prevented these reductions. L-NAME increased iron-induced toxicity significantly, demonstrated by further reduction in the vitamin E levels and renal function compared to the Fe group alone. We concluded that NO plays an important role in protecting the kidney from iron-induced nephrotoxicity. NO synthase blockade enhances iron-mediated renal toxicity in this model.

Surgical relief of progressive upper limb paralysis in Arnold-Chiari malformation.

Two cases of delayed progressive paralysis of the upper limbs in an adult and a teenage patient, without neurological deficits in other regions of the body, are presented. In both cases, the pathology appeared to be a traction lesion of the middle cervical and lower cervical nerve roots, due to abnormal angulation of the nerve roots, which first ran up and then downward in the neural foramina and canal. Re-routing of the nerve roots by removing part of the floor of the neural canal, or by a facetectomy, appeared to offer extensive improvement or full recovery.