论文部分内容阅读
选择营养中等的成龄健康蒙古马10匹,分为两组,均实验性地造成体表软组织伤(长12cm,深3cm切口),分别立即及24h后进行冷冻。对冷冻诱起马体表局部软组织坏死及其修复特点,以及冷冻性免疫作用进行了系统观察。结果:①体表软组织冷冻性坏死的性质,最初属凝固性坏死,以后呈干性或湿性坏疽变化;②在冷冻性损伤修复过程中,损伤深部健康组织首先形成肉芽组织分界面,成为防止感染的屏障和修复损伤的肉芽组织基础;在坏死组织脱落后,伤面pH为7.0～7.7,有利于肉芽再生和防止化脓性感染;修复过程明显见有组织坏死及肉穿组织生成,属第二期愈合,但愈合后不留功能障碍;③冷冻性坏死能诱起T淋巴细胞显著增多(冷冻后第三周t=2.8068,P<0.05,第四周t=6.4869, P<0.01),可作为冷冻性免疫力增强的指标之一。
Ten moderately healthy, aged Mongolian horses were selected and divided into two groups, all of which caused experimental soft tissue injury (12cm in length and 3cm in depth) experimentally, which were frozen immediately and 24h later. The frozen-induced local necrosis of the hippocampal surface of soft tissue and its repair characteristics, as well as the role of cryogenic immunity were systematically observed. Results: (1) The frozen-necrotic necrosis of body surface was originally caused by coagulation necrosis and later showed dry or wet gangrene; (2) In the process of the repair of frozen injury, the damaged deep healthy tissue first formed granulation tissue interface, Of the barrier and repair damaged granulation tissue foundation; necrotic tissue shedding, wound surface pH of 7.0 to 7.7, is conducive to granulation regeneration and prevent suppurative infection; repair process was found to have tissue necrosis and meat wear tissue formation, is second (3 weeks after freezing, t = 2.8068, P <0.05, t = 6.4869 in the fourth week, P <0.01), but no significant difference was found between the two groups As one of the indicators of enhanced immunity.