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缺氧是否会导致对缺血性传导衰竭的抵抗?

Is resistance to ischaemic conduction failure induced by hypoxia?

作者信息

Masson E A, Church S E, Woodcock A A, Hanley S P, Boulton A J

机构信息

Manchester Royal Infirmary, UK.

出版信息

Diabetologia. 1988 Oct;31(10):762-5. doi: 10.1007/BF00274780.

Abstract

Resistance to ischaemic conduction failure is a recognised but unexplained property of diabetic peripheral nerve. We have studied matched groups of control, diabetic, and non-diabetic hypoxic subjects (hypoxia: arterial oxygen tension less than or equal to 60 mm Hg (8 kPa) on at least one occasion and secondary to chronic lung disease). Similar resistance to ischaemia was seen in the hypoxic and diabetic groups compared with control subjects (p less than 0.001). The degree of resistance correlated with arterial oxygen tension at the time of testing (r = 0.72, p less than 0.01). In all individuals with acute exacerbations of hypoxia, the resistance to ischaemia was normalised with improvement of respiratory function (p less than 0.02). These results are compatible with the hypothesis that endoneurial hypoxia may be a factor in the pathogenesis of diabetic neuropathy.

摘要

对缺血性传导衰竭的抵抗是糖尿病周围神经一种已被认识但尚未得到解释的特性。我们研究了对照组、糖尿病组和非糖尿病缺氧受试者的匹配组(缺氧:至少有一次动脉血氧分压小于或等于60 mmHg(8 kPa)且继发于慢性肺部疾病)。与对照组相比,缺氧组和糖尿病组对缺血的抵抗相似(p<0.001)。抵抗程度与测试时的动脉血氧分压相关(r = 0.72,p<0.01)。在所有缺氧急性加重的个体中,随着呼吸功能的改善,对缺血的抵抗恢复正常(p<0.02)。这些结果与神经内膜缺氧可能是糖尿病神经病变发病机制中的一个因素这一假说相符。

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