Stroma-free hemoglobin increases blood pressure and GFR in the hypotensive rat: role of nitric oxide.
Stroma-free hemoglobin increases blood pressure and GFR in the hypotensive rat: role of nitric oxide.
复制标题
无基质血红蛋白增加低血压大鼠的血压和 GFR：一氧化氮的作用。
DOI：
10.1152/jappl.1994.77.5.2348
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Lieberthal,W
中科院分区：
文献类型：
--
作者：
Thompson,A;McGarry,AE;Valeri,CR;Lieberthal,W
在失血性低血压后的麻醉大鼠中检查了两种无基质血红蛋白（SFH）溶液（一种未经修饰，另一种经过交联修饰）的短期全身和肾脏血流动力学影响。两种形式的 SFH 均使平均动脉压 (MAP) 和肾小球滤过率 (GFR) 升高至基线（出血前）值。由未修饰的SFH引起的MAP增加大于由与未修饰的SFH溶液等渗的白蛋白溶液引起的MAP增加。类似地，由修饰的SFH引起的MAP增加也显着大于胶体渗透压与修饰的SFH溶液相当的白蛋白溶液诱导的MAP增加。未修饰和修饰的 SFH 均增加了 GFR。与 MAP 一样，两种 SFH 溶液诱导的 GFR 增加均大于与溶瘤匹配的白蛋白溶液相关的增加。在单独的实验中，还检查了失血性低血压和随后输注未修饰的 SFH 或白蛋白后，N omega-硝基-L-精氨酸甲酯 (L-NAME) 抑制一氧化氮 (NO) 对 MAP 的影响。在输注白蛋白的大鼠中，L-NAME 增加了 MAP。与此形成鲜明对比的是，SFH 后输注时，L-NAME 抑制 NO 对 MAP 没有进一步影响。我们得出的结论是，未经修饰和修饰的 SFH 溶液均通过蛋白质胶体效应引起的血管内容积扩张和 NO 失活的综合作用，显着改善了 MAP 和 GFR。
The short-term systemic and renal hemodynamic effects of two stroma-free hemoglobin (SFH) solutions, one unmodified and the other modified by cross-linking, were examined in anesthetized rats after hemorrhagic hypotension. Both forms of SFH increased mean arterial pressure (MAP) and glomerular filtration rate (GFR) to baseline (prehemorrhage) values. The increase in MAP induced by unmodified SFH was greater than the increase in MAP caused by an albumin solution isoncotic to the unmodified SFH solution. Similarly, the increase in MAP caused by the modified SFH was also substantially greater than that induced by an albumin solution of comparable oncotic pressure to the modified SFH solution. Both unmodified and modified SFH increased GFR. As with MAP, the increase in GFR induced by both SFH solutions was greater than that associated with the oncotically matched albumin solutions. In separate experiments, the effects of nitric oxide (NO) inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) on MAP after hemorrhagic hypotension and subsequent infusion of unmodified SFH or albumin were also examined. In the albumin-infused rats, L-NAME increased MAP. In marked contrast, NO inhibition with L-NAME had no further effect on MAP when infused after SFH. We conclude that both unmodified and modified SFH solutions acutely improve MAP and GFR by the combined effects of intravascular volume expansion resulting from the colloid effect of the protein and by inactivation of NO.