高血糖导致肾脏高灌注的机制研究

The mechanisn of renal hyperperfusion induced byhyperglycemia

探讨了高血糖对整体大鼠和离体灌注鼠肾（ＩＰＲＫ）血流动力学的影响及其机制。结果显示：高血糖在整体大鼠和ＩＰＲＫ均可引起肾血浆流量（ＲＰＦ）、肾小球滤过率（ＧＦＲ）的增加；在ＩＲＰＫ阻断管－球反馈后，高血糖不再能诱发上述改变；结构和葡萄糖相似的Ｄ－α－甲基－葡萄糖苷在ＩＰＲＫ可引起与相同渗透浓度的葡萄糖相似的ＲＰＦ，ＧＦＲ增加；血红蛋白不改变高血糖对肾血流动力学的影响。提示：高血糖可支接引起肾脏高灌注、高滤过，其机制主要是对管一球反馈的抑制，此抑制效应可能与葡萄糖的结构相关。内皮由来性舒张因子（ＥＤＲＦ）在高血糖导致的ＩＰＲＫ高灌注中不起主要作用。

sing whole body clearance technique as well asisolated perfusedrat kidney (IPRK). We studied theeffect of hyperglycemia on renai hemodynamics andthe possible mechanism involved. Hyperglycemia in-creased renal plasma flow (RPF) and glomerularfiltration rate (GFR). In nonfiltering isolated perfusedrat kidney or after adding furosemide to the perfusate,both techniques were believed to abolish thetubuloglomerular feedback, the renal hemodynamicchanges induced by hyperglyeemia disappeared, butadding sodium nitroprusside increased RPF and de-creased renal vascular resistance (RVR). D-α-methyl- glucoside, a glucose derivative, increased RPFand GFR in IPRK. but had no influence on renalhemodynamics in whole body clearance study.Hemoglobin, which could block the action ofendotheliumderived relaxing factor (EDRF), did notchange the effects of hyperglycemia on renalhemodvnamics in IPRK. These results indicated thathyperglycemia could directly induce hyperperfusionand hyperfiltration, which is mainly mediated by sup-pression of tubuloglomerular feedback. EDRF do notplay the major role in the changes of hemodynamicsinduced by hyperglycemia.