ENDONEURIAL BLOOD-FLOW AND OXYGEN-TENSION IN THE SCIATIC-NERVES OF RATS WITH EXPERIMENTAL DIABETIC NEUROPATHY
ENDONEURIAL BLOOD-FLOW AND OXYGEN-TENSION IN THE SCIATIC-NERVES OF RATS WITH EXPERIMENTAL DIABETIC NEUROPATHY
复制标题
DOI：
10.1093/brain/107.3.935
复制
发表时间：
1984-01-01
期刊：
影响因子：
14.5
通讯作者：
LOW, PA
中科院分区：
文献类型：
--
作者：
TUCK, RR;SCHMELZER, JD;LOW, PA
神经内缺氧被认为在糖尿病周围神经病变的发病机制中很重要，可能是由于神经血流量减少所致。以前从未测量过糖尿病神经病变周围神经的血流量和氧张力。因此，我们测量了 8 只链脲佐菌素诱导糖尿病大鼠的坐骨神经的神经血流量和神经内氧张力，为期四个月，以及 8 只年龄匹配的对照组。 7 只糖尿病动物的平均神经血流量为 8.7±1.3 ml min−1100g−1，明显低于对照组的平均神经血流量（13.08 ± 0.8 ml min−1100g−1；P < 0.01）。在一只患有糖尿病的动物中，神经血流量太低而无法准确测量。糖尿病神经病变中神经血流量的减少是由于血流阻力增加所致，这可能是由于微血管病变和血液高粘度所致。在实验性糖尿病神经病变中，神经内氧张力也显着降低，其中 60% 的氧测量值低于 25 mmHg，而对照组为 19%。还测量了患有实验性半乳糖神经病的大鼠的神经血流量，其中与实验性糖尿病神经病相比，其中存在更明显的糖醇积累、神经内膜水肿和神经内液压力升高。在该神经病变中获得的结果表明，实验性糖尿病神经病变中发生的神经血流量减少主要是由于神经中糖醇积聚以外的因素造成的。我们假设神经内膜缺氧可能会在实验性糖尿病神经病变中产生许多观察到的形态和生化变化
Endoneurial hypoxia has been postulated to be important in the pathogenesis of diabetic peripheral neuropathy and may be due to reduced nerve blood flow. Neither blood flow nor oxygen tension have previously been measured in peripheral nerve in diabetic neuropathy. We have therefore measured both nerve blood flow and endoneurial oxygen tension in the sciatic nerves of 8 rats with streptozotocin-induced diabetes for four months, and in 8 age-matched controls. In 7 of the diabetic animals mean nerve blood flow was 8.7± 1.3 ml min−1100g−1which is significantly less than mean nerve blood flow in the controls (13.08 ± 0.8 ml min−1100g−1;P< 0.01). In one diabetic animal, nerve blood flow was too low to be accurately measured. The reduction in nerve blood flow in diabetic neuropathy is due to an increase in resistance to flow which may be due to microangiopathy and to blood hyperviscosity. Endoneurial oxygen tension was also significantly reduced in experimental diabetic neuropathy in which 60 per cent of the oxygen measurements were less than 25 mmHg, compared with 19 per cent in the controls. Nerve blood flow was also measured in rats with experimental galactose neuropathy in which there is more marked sugar-alcohol accumulation, endoneurial oedema and elevation of endoneurial fluid pressure than in experimental diabetic neuropathy. The results obtained in this neuropathy suggest that the reduction in nerve blood flow which occurs in experimental diabetic neuropathy is due largely to factors other than sugar-alcohol accumulation in nerve. We postulate that endoneurial hypoxia may produce many of the observed morphological and biochemical changes in experimental diabetic neuropathy