Dabareiner R M, Sullins K E, White N A, Snyder J R
Marion duPont Scott Equine Medical Center at Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic and State Institute, Leesburg, VA, USA.
Vet Surg. 2001 Mar-Apr;30(2):114-25. doi: 10.1053/jvet.2001.21393.
To document morphologic changes that occur in equine intestinal serosa after experimentally induced ischemia and subsequent reperfusion (jejunum, ascending colon) or after intraluminal distention and decompression (jejunum).
Morphologic effects of ischemia-reperfusion or intraluminal distention-decompression determined on the serosal layer of the equine jejunum. The large colon serosa was evaluated after ischemia-reperfusion injury.
Seven adult horses.
After induction of general anesthesia and ventral median celiotomy, ischemia was created by arteriovenous (AVO) and lumen occlusion of a 20-cm segment of jejunum and ascending colon for 70 minutes, followed by a 60-minute reperfusion period. Intraluminal distention (25 cm H2O) was created in a second 20-cm jejunal segment and maintained within the abdomen for 120 minutes, followed by a 120-minute decompression period. Seromuscular biopsies were obtained upon entering the abdomen and after the ischemic and reperfusion periods, and after the distention and decompression periods along with corresponding control seromuscular biopsies. Samples were processed and examined by light microscopy, transmission electron, and scanning electron microscopy.
Ischemia and reperfusion, and intraluminal distention and decompression, resulted in severe morphologic changes in the seromuscular layer of equine jejunum. A similar period of ischemia-reperfusion caused minimal changes in the ascending colon serosa.
Adult equine jejunum sustains more serosal damage than the ascending colon after similar periods of ischemia-reperfusion injury. Intraluminal distention and subsequent decompression causes serosal damage in the equine jejunum.
The small intestine is more susceptible to seromuscular layer damage than the ascending colon.
记录实验诱导的缺血及随后的再灌注(空肠、升结肠)后或腔内扩张及减压(空肠)后马肠道浆膜发生的形态学变化。
确定缺血再灌注或腔内扩张减压对马空肠浆膜层的形态学影响。评估缺血再灌注损伤后大结肠浆膜。
7匹成年马。
诱导全身麻醉并进行腹正中剖腹术后,通过动静脉(AVO)和对20厘米长的空肠和升结肠段进行管腔闭塞造成缺血70分钟,随后进行60分钟的再灌注期。在另一段20厘米长的空肠段造成腔内扩张(25厘米水柱)并在腹腔内维持120分钟,随后进行120分钟的减压期。在进入腹腔时、缺血和再灌注期后以及扩张和减压期后获取浆肌层活检样本,并与相应的对照浆肌层活检样本一起进行检测。样本经过处理后通过光学显微镜、透射电子显微镜和扫描电子显微镜进行检查。
缺血再灌注以及腔内扩张减压导致马空肠浆肌层出现严重形态学变化。相似时长的缺血再灌注对升结肠浆膜造成的变化极小。
在相似时长的缺血再灌注损伤后,成年马空肠比升结肠承受更多的浆膜损伤。腔内扩张及随后的减压会导致马空肠浆膜损伤。
小肠比升结肠更容易受到浆肌层损伤。