Cook Vanessa L, Meyer Colleen T, Campbell Nigel B, Blikslager Anthony T
Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606, USA.
Am J Vet Res. 2009 Aug;70(8):992-1000. doi: 10.2460/ajvr.70.8.992.
To determine whether treatment of horses with firocoxib affects recovery of ischemic-injured jejunum, while providing effective analgesia.
18 horses.
Horses (n = 6 horses/group) received saline (0.9% NaCl) solution (1 mL/50 kg, IV), flunixin meglumine (1.1 mg/kg, IV, q 12 h), or firocoxib (0.09 mg/kg, IV, q 24 h) before 2 hours of jejunal ischemia. Horses were monitored via pain scores and received butorphanol for analgesia. After 18 hours, ischemic-injured and control mucosa were placed in Ussing chambers for measurement of transepithelial resistance and permeability to lipopolysaccharide. Histomorphometry was used to determine denuded villus surface area. Western blots for cyclooxygenase (COX)-1 and COX-2 were performed. Plasma thromboxane B(2) and prostaglandin E(2) metabolite (PGEM) concentrations were determined.
Pain scores did not significantly increase after surgery in horses receiving flunixin meglumine or firocoxib. Transepithelial resistance of ischemic-injured jejunum from horses treated with flunixin meglumine was significantly lower than in saline- or firocoxib-treated horses. Lipopolysaccharide permeability across ischemic-injured mucosa was significantly increased in horses treated with flunixin meglumine. Treatment did not affect epithelial restitution. Cyclooxygenase-1 was constitutively expressed and COX-2 was upregulated after 2 hours of ischemia. Thromboxane B(2) concentration decreased with flunixin meglumine treatment but increased with firocoxib or saline treatment. Flunixin meglumine and firocoxib prevented an increase in PGEM concentration after surgery.
Flunixin meglumine retarded mucosal recovery in ischemic-injured jejunum, whereas firocoxib did not. Flunixin meglumine and firocoxib were effective visceral analgesics. Firocoxib may be advantageous in horses recovering from ischemic intestinal injury.
确定用氟尼辛葡甲胺治疗马匹是否会影响缺血性损伤空肠的恢复，同时提供有效的镇痛作用。
18匹马。
在空肠缺血2小时前，马匹（每组6匹马）分别接受生理盐水（0.9%氯化钠）溶液（1毫升/50千克，静脉注射）、氟尼辛葡甲胺（1.1毫克/千克，静脉注射，每12小时一次）或伐地考昔（0.09毫克/千克，静脉注射，每24小时一次）。通过疼痛评分对马匹进行监测，并给予布托啡诺用于镇痛。18小时后，将缺血性损伤和对照黏膜置于尤斯灌流小室中，以测量跨上皮电阻和对脂多糖的通透性。采用组织形态计量学方法确定裸露绒毛表面积。进行环氧化酶（COX）-1和COX-2的蛋白质免疫印迹分析。测定血浆血栓素B2和前列腺素E2代谢物（PGEM）浓度。
接受氟尼辛葡甲胺或伐地考昔治疗的马匹术后疼痛评分未显著增加。用氟尼辛葡甲胺治疗的马匹缺血性损伤空肠的跨上皮电阻显著低于用生理盐水或伐地考昔治疗的马匹。用氟尼辛葡甲胺治疗的马匹缺血性损伤黏膜的脂多糖通透性显著增加。治疗未影响上皮修复。缺血2小时后，COX-1呈组成性表达，COX-2上调。氟尼辛葡甲胺治疗后血栓素B2浓度降低，但伐地考昔或生理盐水治疗后升高。氟尼辛葡甲胺和伐地考昔可防止术后PGEM浓度升高。
氟尼辛葡甲胺延缓了缺血性损伤空肠的黏膜恢复，而伐地考昔则没有。氟尼辛葡甲胺和伐地考昔是有效的内脏镇痛药。伐地考昔可能对从缺血性肠损伤中恢复的马匹有利。
