| Co-Investigator(Kenkyū-buntansha) |
KOHROGI Hirotugu KUMAMOTO UNIVERSITY SCHOOL OF MEDICINE, FIRST DEPARTMENT OF INTERNAL MEDICINE, LECTURER, 医学部・附属病院, 講師 (00178237)
MASAYUKI Ando KUMAMOTO UNIVERSITY SCHOOL OF MEDICINE, FIRST DEPARTMENT OF INTERNAL MEDICINE, PROFESSOR, 医学部, 教授 (00040204)
岡部 紘明 熊本大学, 医学部, 教授 (20185466)
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| Research Abstract |
Although autonomic dysfunction (AD) has been described in many medical disorders, there are little recognized clinica sequelae of AD involving respiratory system. To investigate the effect of systemic peripheral AD on ventilatory response in human, we measured the responsiveness to hyperoxic progressive hypercapnia in 12 healthy subjects and 8 patients with familial amyloidotic polyneuropathy and AD (type I FAP). Spirometry were performed in all subjects and arterial blood gas analysis was done in each patient breathing room air at rest. The hypercapnic responsiveness, measured by using a system in which end-tidal PCO2 (PETCO2) and PO2 (PETO2) were automatically regulated, were assessed in terms of the slope of ventilation as a function of the PETCO2. The resting pH and PaO2 of the patients were almost in normal range, but PaCO2 in five were elevated over 44 mmHg, and this was limited in patients with advanced AD.Furthermore the mean base line minute ventilation (VE) of patients was si
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gnificantly lower than that of normal subjects (p<0.01), however the difference of mean respiratory frequency was not significant (p>0.7). There was significant correlation between resting PaCO2 and the severity of of AD (p <0.01) and significant negative correlation between base line VE and AD (p<0.03) in patients with FAP.The magnitudes of responsiveness to CO2 of these patients were significantly lower than those of normal subjects (p<0.05). These findings suggest systemic peripheral autonomic functions may play a role in regulating ventilation during hypercapnia. We concluded FAP with peripheral AD should be listed as a cause of hypoventilation.
Although autonomic dysfunction (AD) has been described in many medical disorders, there are little recognized clinica (sequelae of AD involving respiratory system. To investigate the effect of systemic peripheral AD on ventilatory response in human, we measured the responsiveness to hyperoxic progressive hypercapnia in 12 healthy subjects and 8 patients with familial amyloidotic polyneuropathy and AD (type l FAP). Spirometry were performed in all subjects and arterial blood gas analysis was done in each patient breathing roomair at rest. The hypercapnic responsiveness, measured by using a system in which end-tidal PCO2 (PETCO2) and PO2 (PETO2) were automatically regulated, were assessed n terms of the slope of ventilation as a function of the PETCO2. The resting pH and PaO2 of the patients were almost in normal range, but PaCO2 in five were elevated over 44 mmHg, and this was limited in patients with advanced AD.Furthermore the mean base line minute ventilation (VE) of patients was significantly lower than that of normal subjects (p<0.01), however the difference of mean respiratory frequency was not significant (p>0.7). There was significant correlation between resting PaC02 and the severity of of AD (p <0.01) and sinificant negative correlation between base line VE and AD (p<0.03) in patients with FAP.The magnitudes of responsiveness to CO2 of these patients were significantly lower than those of normal subjects (p<0.05). These findings suggest systemic perjpheraj autonomic functions may play a role in regualting ventilation during hypercapnia. We concluded FAP with peripheral AD should be listed as a cause of hypoventilation. Less
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