Golab F, Kadkhodaee M, Zahmatkesh M, Ghaznavi R, Arab H A, Seifi B, Soleimani M
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Transplant Proc. 2009 Sep;41(7):2749-50. doi: 10.1016/j.transproceed.2009.07.006.
Recent studies have suggested that ischemic damage to the kidneys causes liver tissue alterations. Thus, the morbidity and mortality in patients with acute renal failure (ARF) may be related to liver complications as well as to renal injury. The aim of the present study was to assess the hepatic changes during various periods of reperfusion after induction of renal ischemia.
Forty male rats were subjected to either a sham operation or to a 45-minute ischemia followed by 1, 3, 6, or 24 hours of reperfusion. Arterial pressure was continuously monitored. Blood samples were drawn to measure serum creatinine and blood urea nitrogen (BUN).
We evaluated hepatic concentrations of interleukin (IL)-10 and tumor necrosis factor (TNF)-alpha. Ischemia reperfusion (IR) caused significant reductions in renal function as demonstrated by increased values of serum creatinine and BUN. These rats also showed significant increases in hepatic TNF-alpha and IL-10 concentrations. The most significant changes among inflammatory factors in the liver were observed at 3 hours of reperfusion: TNF-alpha, 616 +/- 41 vs 215 +/- 16, and IL-10, 926 +/- 73 vs 125 +/- 34, pg/100 mg tissue (P <or= .05). Twenty-four-hour reperfusion reduced the extent of liver injury.
Renal IR affects liver inflammatory status, possibly due to increased renal production or impaired clearance of mediators of tissue injury, namely proinflammatory cytokines. The reduction in liver injury at 24 hours of reperfusion compared with the other groups, suggested activation of late-protective mechanisms. These observations may be important for clinical interventions to reduce the morbidity and mortality of ARF.
近期研究表明，肾脏缺血性损伤会导致肝脏组织改变。因此，急性肾衰竭（ARF）患者的发病率和死亡率可能与肝脏并发症以及肾脏损伤有关。本研究的目的是评估肾缺血诱导后不同再灌注时期的肝脏变化。
40只雄性大鼠接受假手术或45分钟缺血，随后再灌注1、3、6或24小时。持续监测动脉血压。采集血样以测量血清肌酐和血尿素氮（BUN）。
我们评估了肝脏中白细胞介素（IL）-10和肿瘤坏死因子（TNF）-α的浓度。缺血再灌注（IR）导致肾功能显著降低，血清肌酐和BUN值升高即表明了这一点。这些大鼠肝脏中的TNF-α和IL-10浓度也显著升高。在再灌注3小时时观察到肝脏中炎症因子的变化最为显著：TNF-α，616±41对215±16，IL-10，926±73对125±34，pg/100mg组织（P≤0.05）。24小时再灌注减轻了肝脏损伤程度。
肾IR影响肝脏炎症状态，可能是由于肾脏产生增加或组织损伤介质（即促炎细胞因子）清除受损。与其他组相比，24小时再灌注时肝脏损伤减轻，提示晚期保护机制被激活。这些观察结果可能对降低ARF发病率和死亡率的临床干预具有重要意义。
