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糖尿病自主神经病变中的脑血管反应性与高碳酸血症呼吸驱动

Cerebrovascular reactivity and hypercapnic respiratory drive in diabetic autonomic neuropathy.

作者信息

Tantucci C, Bottini P, Fiorani C, Dottorini M L, Santeusanio F, Provinciali L, Sorbini C A, Casucci G

机构信息

Semeiotica e Metodologia Medica, University of Ancona, 60020 Ancona, Italy.

出版信息

J Appl Physiol (1985). 2001 Mar;90(3):889-96. doi: 10.1152/jappl.2001.90.3.889.

DOI:10.1152/jappl.2001.90.3.889
PMID:11181597
Abstract

Because abnormalities in cerebrovascular reactivity (CVR) in subjects with long-term diabetes could partly be ascribed to autonomic neuropathy and related to central chemosensitivity, CVR and the respiratory drive output during progressive hypercapnia were studied in 15 diabetic patients without (DAN-) and 30 with autonomic neuropathy (DAN+), of whom 15 had postural hypotension (PH) (DAN+PH+) and 15 did not (DAN+PH-), and in 15 control (C) subjects. During CO(2) rebreathing, changes in occlusion pressure and minute ventilation were assessed, and seven subjects in each group had simultaneous measurements of the middle cerebral artery mean blood velocity (MCAV) by transcranial Doppler. The respiratory output to CO(2) was greater in DAN+PH+ than in DAN+PH- and DAN- (P < 0.01), whereas a reduced chemosensitivity was found in DAN+PH- (P < 0.05 vs. C). MCAV increased linearly with the end-tidal PCO(2) (PET(CO(2))) in DAN+PH- but less than in C and DAN- (P < 0.01). In contrast, DAN+PH+ showed an exponential increment in MCAV with PET(CO(2)) mainly >55 Torr. Thus CVR was lower in DAN+ than in C at PET(CO(2)) <55 Torr (P < 0.01), whereas it was greater in DAN+PH+ than in DAN+PH- (P < 0.01) and DAN- (P < 0.05) at PET(CO(2)) >55 Torr. CVR and occlusion pressure during hypercapnia were correlated only in DAN+ (r = 0.91, P < 0.001). We conclude that, in diabetic patients with autonomic neuropathy, CVR to CO(2) is reduced or increased according to the severity of dysautonomy and intensity of stimulus and appears to modulate the hypercapnic respiratory drive.

摘要

由于长期糖尿病患者脑血管反应性(CVR)异常部分可归因于自主神经病变且与中枢化学敏感性有关,因此我们对15例无自主神经病变的糖尿病患者(DAN-)、30例有自主神经病变的糖尿病患者(DAN+,其中15例有体位性低血压(PH)(DAN+PH+),15例无体位性低血压(DAN+PH-))以及15例对照(C)受试者进行了研究,观察在渐进性高碳酸血症期间的CVR和呼吸驱动输出。在重复吸入二氧化碳期间,评估了阻断压和分钟通气量的变化,每组中有7名受试者通过经颅多普勒同时测量大脑中动脉平均血流速度(MCAV)。DAN+PH+组对二氧化碳的呼吸输出大于DAN+PH-组和DAN-组(P<0.01),而DAN+PH-组的化学敏感性降低(与C组相比,P<0.05)。在DAN+PH-组中,MCAV随呼气末二氧化碳分压(PET(CO(2)))呈线性增加,但低于C组和DAN-组(P<0.01)。相反,DAN+PH+组中,当PET(CO(2))主要>55 Torr时,MCAV随PET(CO(2))呈指数增加。因此,当PET(CO(2))<55 Torr时,DAN+组的CVR低于C组(P<0.01),而当PET(CO(2))>55 Torr时,DAN+PH+组的CVR大于DAN+PH-组(P<0.01)和DAN-组(P<0.05)。高碳酸血症期间的CVR和阻断压仅在DAN+组中相关(r = 0.91,P<0.001)。我们得出结论,在患有自主神经病变的糖尿病患者中,对二氧化碳的CVR根据自主神经功能障碍的严重程度和刺激强度而降低或增加,并且似乎调节高碳酸血症呼吸驱动。

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