Baker J F, Goode R C, Duffin J
Department of Physiology, University of Toronto, Ontario, Canada.
Eur J Appl Physiol Occup Physiol. 1996;72(5-6):537-41. doi: 10.1007/BF00242287.
We assessed the central-chemoreflex ventilatory responses to carbon dioxide in six male volunteers using a hyperoxic rebreathing technique. Hyperventilation prior to rebreathing allowed both the threshold and the sensitivity of the response to be measured. We used immersion in water to control the body temperature (tympanic). The water temperature was adjusted to be either thermo-neutral or hot so that body temperature either remained normal [+0.2 (0.04) degrees C, mean (SEM)] or was elevated by 1.5 (0.08) degrees C. The sensitivities of the central-chemoreflex ventilatory responses to carbon dioxide were increased at elevated body temperatures, changing from a mean of 1.8 (0.2) 1.min-1. Torr-1 to 2.7 (0.1) 1.min-1. Torr-1. However, the thresholds did not change with temperature, and the mean threshold was 48(1) Torr at both normal and elevated temperatures. For all of the volunteers, ventilation was increased at elevated body temperatures for all levels of carbon dioxide, mainly by changes in respiratory frequency due to reductions in expiratory times. At subthreshold levels of carbon dioxide, mean ventilation changed significantly from 6.3(1.1) 1.min-1 at normal temperatures to 10.8 (1.9) 1.min-1 at elevated temperatures. Heart rates also increased significantly with temperature, changing from a mean of 66 (4) beats.min-1 to 102 (3) beats.min-1 at threshold levels of carbon dioxide. The mean rates of rise of carbon dioxide partial pressure during rebreathing were significantly increased with temperature as well, changing from 0.075 (0.008) Torr.min-1 to 0.089 (0.004) Torr.min-1. We concluded that elevating the body temperatures of our subjects not only increased their ventilation, heart rates and metabolic rates at all levels of carbon dioxide, but it also increased the sensitivity of their central chemoreflex ventilatory responses to carbon dioxide. Despite these increases, the thresholds of the central-chemoreflex ventilatory responses to carbon dioxide remained unchanged.
我们采用高氧再呼吸技术评估了6名男性志愿者对二氧化碳的中枢化学反射性通气反应。再呼吸前的过度通气可使反应的阈值和敏感性均得以测量。我们通过让受试者浸入水中来控制体温(鼓膜温度)。水温被调节为中性或热,以使体温要么保持正常[+0.2(0.04)摄氏度,均值(标准误)],要么升高1.5(0.08)摄氏度。在体温升高时,对二氧化碳的中枢化学反射性通气反应的敏感性增加,从平均1.8(0.2)升·分钟⁻¹·托⁻¹变为2.7(0.1)升·分钟⁻¹·托⁻¹。然而,阈值并未随温度变化,正常体温和体温升高时的平均阈值均为48(1)托。对于所有志愿者,在体温升高时,所有二氧化碳水平下的通气量均增加,主要是由于呼气时间缩短导致呼吸频率改变。在低于阈值的二氧化碳水平下,平均通气量从正常体温时的6.3(1.1)升·分钟⁻¹显著变为体温升高时的10.8(1.9)升·分钟⁻¹。心率也随温度显著增加,在二氧化碳阈值水平时从平均66(4)次·分钟⁻¹变为102(3)次·分钟⁻¹。再呼吸期间二氧化碳分压的平均上升速率也随温度显著增加,从0.075(0.008)托·分钟⁻¹变为0.089(0.004)托·分钟⁻¹。我们得出结论,升高受试者的体温不仅在所有二氧化碳水平下增加了他们的通气量、心率和代谢率,还增加了他们对二氧化碳的中枢化学反射性通气反应的敏感性。尽管有这些增加,但对二氧化碳的中枢化学反射性通气反应的阈值仍保持不变。