Henninger D D, Granger D N, Aw T Y
Department of Physiology, Louisiana State University Medical Center, Shreveport 71130.
Am J Physiol. 1995 Jan;268(1 Pt 1):G116-20. doi: 10.1152/ajpgi.1995.268.1.G116.
The purpose of our study was to investigate the changes in enterocyte cellular and mitochondrial respiration rates subsequent to ischemia of graded duration. The small intestine of anesthetized adult cats was assigned to one of five treatment regimens: control or ischemia of 15-, 30-, 60-, or 90-min duration. Cellular and mitochondrial respiration was measured using a Clark-type O2 electrode at 0 and 4 h postharvest. Ischemia of increasing duration caused a progressive decrease in cellular and mitochondrial respiration in enterocytes at 0 h postharvest. By 4 h postharvest, cellular and mitochondrial respiration rates for the 15-, 30-, and 60-min ischemic groups had recovered to near control levels, whereas the 90-min group showed minimal recovery. These data suggest that ischemia suppresses cellular and mitochondrial respiration of intestinal epithelial cells, the magnitude of which is related to the ischemic duration. The ischemia-induced suppression in cellular respiration primarily reflects a reduction in mitochondrial respiration.
我们研究的目的是调查不同时长缺血后肠上皮细胞的细胞呼吸和线粒体呼吸速率的变化。将麻醉成年猫的小肠分为五种处理方案之一：对照或缺血15、30、60或90分钟。在收获后0小时和4小时使用Clark型氧电极测量细胞呼吸和线粒体呼吸。缺血时间延长导致收获后0小时肠上皮细胞的细胞呼吸和线粒体呼吸逐渐下降。到收获后4小时，缺血15、30和60分钟组的细胞呼吸和线粒体呼吸速率已恢复到接近对照水平，而90分钟组的恢复则微乎其微。这些数据表明，缺血会抑制肠上皮细胞的细胞呼吸和线粒体呼吸，其程度与缺血持续时间有关。缺血诱导的细胞呼吸抑制主要反映了线粒体呼吸的降低。
