Van Hoogmoed L, Rakestraw P C, Snyder J R, Harmon F A
Department of Surgical and Radiological Sciences, University of California, Davis 95616, USA.
Am J Vet Res. 1999 Aug;60(8):1004-9.
To determine the in vitro effect of various prostaglandins (PG) and nonsteroidal anti-inflammatory drugs (NSAID) on contractile activity of the large-colon taenia of horses.
14 healthy horses.
The taenia was collected from the ventral colon, cut into strips (2 X 10 mm), and mounted in a tissue bath system (20-ml capacity) that contained oxygenated Krebs buffer solution warmed to 37.5+/-0.5 C. After equilibration, incremental doses of PGE2, PGF2alpha, PGl2, flunixin meglumine, carprofen, ketoprofen, and phenylbutazone were added to the baths, and contractile activity was recorded. Magnitude of the response was calculated by comparing contractile activity before and after administration of the PG or NSAID to the tissue baths.
PGE2 and PGF2alpha, caused a significant increase in contractile activity, whereas PGI2 induced an inhibitory response. Activity of NSAID on contraction was predominantly inhibitory. At low concentrations, ketoprofen induced an excitatory effect, which then became inhibitory at high concentrations. Compared with the other NSAID, carprofen significantly reduced contractile activity at lower concentrations.
PGE2 and PGF2alpha appear to enhance contractility of large-colon taenia of horses, whereas PGI2 was inhibitory in the in vitro model. Administration of NSAID also inhibited contractility, with carprofen having the most potent effect.
Administration of NSAID in combination with liberation of endogenous PG may predispose horses to development of intestinal stasis and subsequent impaction.
确定各种前列腺素（PG）和非甾体抗炎药（NSAID）对马的结肠带收缩活性的体外作用。
14匹健康马。
从腹侧结肠采集结肠带，切成条（2×10毫米），安装在容量为20毫升的组织浴系统中，该系统含有加热至37.5±0.5℃的含氧 Krebs 缓冲溶液。平衡后，将递增剂量的前列腺素E2、前列腺素F2α、前列环素、氟尼辛葡甲胺、卡洛芬、酮洛芬和保泰松添加到浴液中，并记录收缩活性。通过比较向组织浴中加入PG或NSAID前后的收缩活性来计算反应幅度。
前列腺素E2和前列腺素F2α使收缩活性显著增加，而前列环素诱导抑制反应。NSAID对收缩的作用主要是抑制性的。在低浓度时，酮洛芬诱导兴奋作用，而在高浓度时则变为抑制作用。与其他NSAID相比，卡洛芬在较低浓度时能显著降低收缩活性。
前列腺素E2和前列腺素F2α似乎增强了马结肠带的收缩性，而在体外模型中前列环素具有抑制作用。NSAID的给药也抑制了收缩性，其中卡洛芬的作用最显著。
NSAID与内源性PG释放联合给药可能使马易发生肠道淤滞及随后的阻塞。
