Feldman G M, Arnold M A, Charney A N
Am J Physiol. 1984 Jun;246(6 Pt 1):G687-94. doi: 10.1152/ajpgi.1984.246.6.G687.
The mechanism of the increase in luminal CO2 tension (PCO2) that accompanies jejunal HCO-3 absorption is unknown. One possibility is that mucosal metabolism and the reaction of absorbed HCO-3 with blood buffers in mucosal capillaries govern luminal PCO2. To evaluate this possibility, jejunal segments of anesthetized adult male Sprague-Dawley rats were perfused in vivo with modified Ringer solutions with varying PCO2 levels (0-141 mmHg). Arterial PCO2 was varied by mechanical ventilation (20-70 mmHg). The net flux of CO2 gas into bulk luminal fluid varied directly with the transmucosal PCO2 gradient both in the absence (r = 0.98, P less than 0.001) and presence of net HCO-3 absorption (r = 0.97, P less than 0.001). The apparent permeability coefficient for CO2 gas across the jejunal mucosa was relatively low (2 X 10(-4) cm3 X s-1 X cm length -1) and was not affected by net HCO-3 absorption. Under conditions of equal arterial blood and perfusate PCO2 levels (40 mmHg), the PCO2 in mucosa and effluent was 51 and 44 mmHg, respectively, in the absence and 62 and 48 mmHg, respectively, in the presence of net HCO-3 absorption. These results suggest that CO2 diffuses from the mucosal region into bulk liminal fluid during net HCO-3 absorption in the rat jejunum. In addition, we found in vitro that the elevation of mucosal PCO2 above arterial PCO2 during net HCO-3 absorption can be quantitatively accounted for by metabolism and the admixture of absorbed HCO-3 with blood buffers.
空肠吸收HCO₃⁻时伴随的管腔内二氧化碳张力（PCO₂）升高的机制尚不清楚。一种可能性是黏膜代谢以及吸收的HCO₃⁻与黏膜毛细血管中的血液缓冲物质的反应决定了管腔内的PCO₂。为了评估这种可能性，对麻醉的成年雄性Sprague-Dawley大鼠的空肠段进行体内灌注，使用不同PCO₂水平（0 - 141 mmHg）的改良林格溶液。通过机械通气改变动脉PCO₂（20 - 70 mmHg）。在没有净HCO₃⁻吸收（r = 0.98，P < 0.001）和存在净HCO₃⁻吸收（r = 0.97，P < 0.001）的情况下，CO₂气体进入大量管腔液的净通量均与跨黏膜PCO₂梯度直接相关。CO₂气体穿过空肠黏膜的表观渗透系数相对较低（2×10⁻⁴ cm³×s⁻¹×cm长度⁻¹），并且不受净HCO₃⁻吸收的影响。在动脉血和灌注液PCO₂水平相等（40 mmHg）的条件下，在没有净HCO₃⁻吸收时，黏膜和流出液中的PCO₂分别为51和44 mmHg，在存在净HCO₃⁻吸收时分别为62和48 mmHg。这些结果表明，在大鼠空肠净吸收HCO₃⁻期间，CO₂从黏膜区域扩散到大量管腔液中。此外，我们在体外发现，在净HCO₃⁻吸收期间，黏膜PCO₂高于动脉PCO₂的升高可以通过代谢以及吸收的HCO₃⁻与血液缓冲物质的混合来定量解释。
