Effects of hemoglobin-based oxygen-carrying solutions in anesthetized rats with acute ischemic renal failure

Effects of hemoglobin-based oxygen-carrying solutions in anesthetized rats with acute ischemic renal failure
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DOI:
10.1016/s0022-2143(00)70023-0
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发表时间:
2000-01-01
期刊:
JOURNAL OF LABORATORY AND CLINICAL MEDICINE
影响因子:
--
通讯作者:
Valeri, CR
Valeri, CR
中科院分区:
其他
文献类型:
--
作者:
Lieberthal, W;Fuhro, R;Valeri, CR

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在缺血性肾功能衰竭大鼠和假手术对照组中,比较了三种血红蛋白溶液与异嗜酸性人血清白蛋白的作用。未修饰和α-α交联血红蛋白均增加平均动脉压和全身血管阻力,并显著降低心输出量,且程度相当。相比之下,o-棉子糖交联血红蛋白对这些参数中的任何一个都没有有害影响。在假手术大鼠中,未修饰的血红蛋白使肾小球滤过率(GFR)降低约30%,而这两种交联血红蛋白对该组中的GFR都没有任何不利影响。三种血红蛋白溶液均未加重缺血再灌注损伤所致GFR降低的程度。此外,缺血再灌注损伤诱导的肾小管坏死程度在所有组中也相当。我们得出以下结论:(1)O-棉子糖交联,而不是α-α交联,改善了未修饰的血红蛋白对血管阻力和心输出量的作用;(2)两种形式的交联都降低了假手术大鼠中未修饰的血红蛋白所表现出的肾毒性;和(3)没有一种血红蛋白溶液加剧了由缺血-再灌注诱导的肾损伤。
The effects of three hemoglobin solutions were compared with those of iso-oncotic human serum albumin in rats with ischemic renal failure and sham-operated controls. Unmodified and alpha-alpha cross-linked hemoglobins both increase mean arterial pressure and systemic vascular resistance and reduce cardiac output substantially and to a comparable extent. In contrast, o-raffinose cross-linked hemoglobin has no deleterious effect on any of these parameters, In sham-operated rats unmodified hemoglobin reduces the glomerular filtration rate (GFR) by approximately 30%, whereas neither of the two cross-linked hemoglobins has any adverse effect on GFR in this group. None of the three hemoglobin solutions exacerbated the degree to which GFR was reduced by ischemia-reperfusion injury. Also, the degree of tubular necrosis induced by ischemia-reperfusion injury was also comparable in all groups. We conclude the following: (1) o-raffinose cross-linking, but not alpha-alpha cross-linking, ameliorates the effects of unmodified hemoglobin on vascular resistance and cardiac output; (2) both forms of cross-linking reduce the nephrotoxicity exhibited by unmodified hemoglobin in sham-operated rats; and (3) none of the hemoglobin solutions exacerbate renal injury induced by ischemia-reperfusion.