Tantucci C, Bottini P, Dottorini M L, Puxeddu E, Casucci G, Scionti L, Sorbini C A
Clinica di Semeiotica Metodologia Medica, University of Ancona, Ospedale Regionale Torrette, Italy.
J Appl Physiol (1985). 1996 Nov;81(5):1978-86. doi: 10.1152/jappl.1996.81.5.1978.
We have used diabetic autonomic neuropathy as a model of chronic pulmonary denervation to study the ventilatory response to incremental exercise in 20 diabetic subjects, 10 with (Dan+) and 10 without (Dan-) autonomic dysfunction, and in 10 normal control subjects. Although both Dan+ and Dan- subjects achieved lower O2 consumption and CO2 production (VCO2) than control subjects at peak of exercise, they attained similar values of either minute ventilation (VE) or adjusted ventilation (VE/maximal voluntary ventilation). The increment of respiratory rate with increasing adjusted ventilation was much higher in Dan+ than in Dan- and control subjects (P < 0.05). The slope of the linear VE/VCO2 relationship was 0.032 +/- 0.002, 0.027 +/- 0.001 (P < 0.05), and 0.025 +/- 0.001 (P < 0.001) ml/min in Dan+, Dan-, and control subjects, respectively. Both neuromuscular and ventilatory outputs in relation to increasing VCO2 were progressively higher in Dan+ than in Dan- and control subjects. At peak of exercise, end-tidal PCO2 was much lower in Dan+ (35.9 +/- 1.6 Torr) than in Dan- (42.1 +/- 1.7 Torr; P < 0.02) and control (42.1 +/- 0.9 Torr; P < 0.005) subjects. We conclude that pulmonary autonomic denervation affects ventilatory response to stressful exercise by excessively increasing respiratory rate and alveolar ventilation. Reduced neural inhibitory modulation from sympathetic pulmonary afferents and/or increased chemosensitivity may be responsible for the higher inspiratory output.
我们将糖尿病自主神经病变作为慢性肺去神经支配的模型，以研究20名糖尿病患者（其中10名有自主神经功能障碍[Dan+]，10名无自主神经功能障碍[Dan-]）以及10名正常对照者对递增运动的通气反应。尽管Dan+组和Dan-组患者在运动峰值时的耗氧量和二氧化碳产生量（VCO2）均低于对照组，但他们的分钟通气量（VE）或校正通气量（VE/最大自主通气量）值相似。随着校正通气量增加，Dan+组的呼吸频率增加幅度远高于Dan-组和对照组（P<0.05）。Dan+组、Dan-组和对照组中，VE/VCO2线性关系的斜率分别为0.032±0.002、0.027±0.001（P<0.05）和0.025±0.001（P<0.001）ml/min。与VCO2增加相关的神经肌肉和通气输出在Dan+组中均逐渐高于Dan-组和对照组。在运动峰值时，Dan+组的呼气末PCO2（35.9±1.6 Torr）远低于Dan-组（42.1±1.7 Torr；P<0.02）和对照组（42.1±0.9 Torr；P<0.005）。我们得出结论，肺自主神经去神经支配通过过度增加呼吸频率和肺泡通气来影响对压力性运动的通气反应。交感肺传入神经的神经抑制调节降低和/或化学敏感性增加可能是吸气输出增加的原因。
