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卡托普利所致糖尿病自主神经病变的明显改善。

Apparent improvement in diabetic autonomic neuropathy induced by captopril.

作者信息

Moore M V, Jeffcoate W J, Macdonald I A

机构信息

Department of Medicine, City Hospital, Nottingham, UK.

出版信息

J Hum Hypertens. 1987 Dec;1(3):161-5.

PMID:3333529
Abstract

Eight diabetic subjects with moderately elevated blood pressure (BP) (systolic (SBP) greater than 140 and/or diastolic (DBP) greater than 90 mmHg) were studied. Each had evidence of mild asymptomatic autonomic neuropathy (impairment of forced sinus arrhythmia). The effect of a single oral 25 mg dose of captopril on BP and some aspects of autonomic function was compared with matched placebo in a double-blind, cross-over study. Resting supine SBP and DBP fell significantly (P less than 0.01) over 90 minutes following captopril, indicating that the hypotensive effect of the drug was not dependent on intact autonomic function. There was no significant change in resting heart rate. The bradycardic response to apnoeic face immersion was significantly (P less than 0.01) enhanced following captopril. Sinus arrhythmia did not change. The BP responses to standing and to the cold pressor test were unaffected. There was no exacerbation of postural hypotension. The ingestion of a single dose of captopril appears to increase vagal function, without affecting sympathetic nervous function, in diabetics with evidence of mild vagal impairment.

摘要

对8名血压中度升高(收缩压(SBP)大于140和/或舒张压(DBP)大于90 mmHg)的糖尿病患者进行了研究。每个人都有轻度无症状自主神经病变(强迫性窦性心律失常受损)的证据。在一项双盲、交叉研究中,将单次口服25 mg卡托普利对血压和自主神经功能某些方面的影响与匹配的安慰剂进行了比较。服用卡托普利后90分钟内,静息仰卧位SBP和DBP显著下降(P小于0.01),表明该药物的降压作用不依赖于完整的自主神经功能。静息心率无显著变化。服用卡托普利后,对屏气面部浸入的心动过缓反应显著增强(P小于0.01)。窦性心律失常没有改变。对站立和冷加压试验的血压反应未受影响。体位性低血压没有加重。在有轻度迷走神经损伤证据的糖尿病患者中,单次服用卡托普利似乎会增加迷走神经功能,而不影响交感神经功能。

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