Sendur R, Czarnobilski K, Pawlik W W, Konturek S J
Zakładu Fizjologii Doświadczalnej Instytutu Fizjologii, Akademii Medycznej im. M. Kopernika, Krakowie.
Folia Med Cracov. 1990;31(4):5-16.
These studies were conducted to assess whether cholecystokinin (CCK) play a role in the regulation of intestinal blood flow and metabolic activity. Anesthetized dogs were subjected to laparotomy and implantation of transducers to measured intestinal blood flow (MBF), intestinal oxygen extraction (AVO2) and intraluminal pressure (IP). Intestinal oxygen consumption (VO2) was calculated as the product of the AVO2 and MBF. CCK8 infused intraarterially in doses 12.5, 25, 50, 75 and 100 pmol/kg-h increased significantly MBF by 5, 8, 11, 15 and 19%. IP increased significantly with the last three doses of CCK by 55, 87 and 145%, respectively. Glucose and oleic acid increased MBF by 12 and 37% and VO2 by 26 and 17%, respectively. Pretreatment with a highly selective CCK-receptor antagonist L-364 718 (1 mg/kg i.v.) abolished the vascular and motor responses to exogenous CCK and significantly reduced intestinal hyperemia and increase in VO2 in response to luminal oleic acid but not glucose. These findings indicate that endogenous CCK may play a role in the intestinal hyperemia after fatty meal and that this effect is primarily mediated by the CCK receptors.
进行这些研究是为了评估胆囊收缩素（CCK）是否在肠血流量和代谢活性的调节中发挥作用。对麻醉的狗进行剖腹手术并植入传感器，以测量肠血流量（MBF）、肠氧摄取（AVO2）和腔内压力（IP）。肠氧消耗量（VO2）通过AVO2与MBF的乘积计算得出。以12.5、25、50、75和100 pmol/kg-h的剂量动脉内注入CCK8可使MBF分别显著增加5%、8%、11%、15%和19%。IP在CCK的最后三个剂量下分别显著增加55%、87%和145%。葡萄糖和油酸分别使MBF增加12%和37%，使VO2增加26%和17%。用高选择性CCK受体拮抗剂L-364 718（1 mg/kg静脉注射）预处理可消除对外源性CCK的血管和运动反应，并显著降低对腔内油酸而非葡萄糖的肠充血和VO2增加。这些发现表明内源性CCK可能在脂肪餐后的肠充血中发挥作用，并且这种作用主要由CCK受体介导。
