اثرات ال- کارنیتین و آلفا- توکوفرول بر روی نقص دفع اسید ناشی از انسداد حاد میزنای در رت‌های بیهوش

Background: Ureteral obstruction has been shown to induce renal oxidative stress, suppressed energy metabolism and defected acid excretion. This study was aimed to examine the improving effects of L-carnitine, a facilitating cofactor for mitochondrial oxidation of fatty-acids as well as a scavenger of free-radicals, and -tocopherol as the most potent antioxidant on these renal disorders at early hours following release of unilateral ureteral obstruction. Methods: The left ureter was ligated in 60 anaesthetised rats, L-carnitine, -tocopherol, or their vehicles (normal saline and olive oil, respectively) were injected (i.p.) in four groups. Each rat was re-anesthetized and cannulated, and ureteral legation was released at exactly 24h after UUO-induction. A 30-min clearance period performed to separately collect urine from both kidneys. The collected urine and arterial blood samples were given to pH-gas analyzer and autoanalyzer, and malondialdehyde (MDA), ATP and ADP levels were assessed in preserved kidneys. There were also sham and control groups (n=8-10 in each).Results: In the post-obstructed kidney of vehicle-treated groups with respect to the equivalent kidney of sham group, there were increases in MDA (p<0.001), ADP (p<0.01), urinary pH (p<0.001), absolute (p<0.05) and fractional bicarbonate excretions (p<0.01), but decreases in ATP, ATP/ADP (both p<0.001), and urinary PCO2 (p<0.01). -tocopherol could normalize MDA level but did not affect the altered amounts of energy metabolic indices and acid-base excretions, while L-carnitine improved all of them except of decreased urinary PCO2.Conclusions: Increased bicarbonate-excretion in post-obstructed kidney is due to defected acid-secretion at collecting duct, which is not related to ureteral obstruction-induced renal oxidative stress and suppressed energy metabolism.