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  • 學位論文

人工密閉環境中二氧化碳對人類生理反應之研究

Research of physiological responses to carbon dioxide concentration in an airtight room

指導教授 : 蕭子健

摘要


根據布朗運動定律與室內空氣品質標準,通風不良將造成環境二氧化碳濃度與溫度升高,而人體呼吸與代謝是室內環境二氧化碳的主要來源,為了探討環境二氧化碳濃度對於人體的影響,本研究模擬一間通風不良的環境,藉此觀察與分析其效應。受測者部分,徵求10位自願受測者參與,在連續1小時的實驗過程,監測環境訊號為二氧化碳濃度與空間溫度,生理訊號之擷取則包含:臉部表面溫度、血氧濃度與心電圖。初步實驗結果顯示,二氧化碳濃度升高使血液中的血氧濃度下降,臉部表面溫度升高,心臟跳動加快,使得中樞化學反射器感受到血液中氧與二氧化碳分壓的變化,改變心、肺循環系統進呼吸,以達到體內平衡。綜合本研究之實驗結果,通風不良的室內環境將影響人類一般生理狀態。

並列摘要


According to Brownian motion and indoor air quality (IAQ) standard, the carbon dioxide concentration (CCO2) and air temperature (Ta) increase when ventilation is poor. The main source of CO2 pollution indoor is human respiration. This study simulates an airtight condition and uses 10 volunteer subjects to study the physiological responses to three CCO2. Facial temperature (Tf), saturation of peripheral oxygen (SpO2), and electrocardiography were spontaneously acquired while subjects were inside an airtight room. Analytical results indicate that SpO2 decreased as CCO2 increased. Those results further demonstrate a positive correlation between CCO2/heart rate and CCO2/Tf, implying that the central-chemoreflex can stimulate the respiratory system since SpO2 variance and an increased heart rate can promote pulmonary gas exchange. Notably, differences in Tf and Ta increased under low CCO2 and then reversed and stabilized. The antagonistic pattern accelerated rapidly initially and decelerated finally stabilized. These findings also imply that the internal body responded to changes in the external environment rapidly, attempted to homeostasis, and reached equilibrium slowly. Results of this study demonstrate that IAQ affects physiological responses in the symbiotic relationship between the human body and surrounding environment.

參考文獻


[1] ASHRAE standard, “Ventilation for Acceptable Indoor Air Quality,” pp. 62-1989, ISSN 1041-2336, 1999.
[2] Baker, J. F., R. C. Goode, and J. Duffin, “The effect of a rise in body temperature on the central-chemoreflex ventilatory response to carbon dioxide,” Eur. J. Appl. Physiol, vol. 72, pp. 537- 541, 1996.
[3] Boden, A. G., M. C. Harris, and M. J. Parkes, “A respiratory drive in addition to the increase in CO2 production at raised body temperature in rats,” Exp. Physiol, vol. 85, no. 3, pp. 309-319, 2000.
[4] Brundage, J. F., R. M. Scott, W. M. Lednar, D. W. Smith, and R. N. Miller, “Building-associated risk of febrile acute respiratory diseases in army trainees,” J. American Med. Assoc., vol. 259, pp. 2108–2112, 1988.
[6] Cotes, J. E., “The role of body temperature in controlling ventilation during exercise in one normal subject breathing oxygen,” J. Physiol., vol. I29, pp. 554-563, 1995.

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