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本实验采用肠淋巴管引流术,在失血性休克大鼠模型的基础上,观察高渗盐水治疗失血性休克过程中肠淋巴流量及其蛋白含量的变化,旨在探讨高渗盐水对失血性休克大鼠治疗的淋巴机制。结果表明,休克大鼠输入高渗盐水或生理盐水后,两组大鼠的血压、肠淋巴流量及其蛋白输出量均比休克期明显升高,高渗盐水治疗组显著高于生理盐水对照组(P<0.01),而且治疗组大鼠肠淋巴流量及其蛋白输出量远远高于休克前水平(P<0.01)。结果提示,高渗盐水的抗休克机制可能与其恢复休克大鼠的淋巴流量及其蛋白输出量、改善休克时肠淋巴循环障碍有关。 相似文献
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为了阐明肠淋巴循环在出血性休克发生、发展和转归中的作用,应用wistar大鼠45只,分3组观察休克及补液过程中,肠淋巴流量及其蛋白含量的变化.结果表明,放血前,肠淋巴总流量为0.3±0.02ml/30min,淋巴蛋白浓度为3.30±0.13g/100ml,淋巴蛋白输出量为3.6±0.1mg/10min,无组间差异。休克早期,肠淋巴流量和淋巴蛋白输出量显著降低(P<0.001)P 0.休克晚期降低更为显著;淋巴蛋白浓度休克晚期才低于对照组。回输血液及输入生理盐水,肠淋巴流量且急升高,自补液20min起,肠淋巴流量相当于放血前及对照组的3—5倍,淋巴蛋白出量自输血后2min起恢复正常,输血后30min显著高于休克前,但停止补液后又降低.提示出血性休克及补液时淋巴液及其蛋白的变化,对休克的发展和康复具有一定的意义。 相似文献
3.
以少量胸导管淋巴液和肠淋巴液给予补液干予治疗的重症失血性休克大鼠,用生理盐水做对照,观察其对血压及存活时间的影响,以探讨不同部位淋巴液维持血压的共同特性。结果表明:胸导管淋巴液及肠淋巴液回升血压及延长存活时间作用均显著优于对照组(P<0.05～0.01),而两个治疗组间未见统计学差异(P>0.05)。结果提示:胸导管淋巴液和肠淋巴液对失血性休克大鼠均有较好的抗休克作用。 相似文献
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为探讨休克时血液和淋巴微循环超微结构的改变及其与细胞变化之间的关系,本文对14只大鼠,用透射电镜观察了正常肠系膜微淋巴管、微血管的超微结构和失血性休克不同时期的变化,以及去甲肾上腺素、酚苄明对肠系膜微循环超微结构的影响。结果发现:失血性休克时微血管和微淋巴管内皮细胞均有不同程度的损伤,尤以晚期严重,出现细胞器溶解,微血管内红细胞、血小板聚集,堵塞管腔,酚苄明和去甲肾上腺素均可减轻微淋巴管的损伤,前者对部分微血管有一定的保护作用。同时,对上述变化的意义和肠系膜淋巴管的构筑进行了讨论。 相似文献
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为探讨肠淋巴液对肠系膜上动脉闭塞性休克(SMAO休克)的影响,对SMAO休克大鼠给予肠淋巴液或血浆治疗,并以生理盐水作对照,观察其对血压及存活率的影响。结果表明,开夹后90min起,肠淋巴液治疗组的血压显著高于对照组(P<0.05),其4h存活率也显著优于对照组(P<0.05),而血浆组与对照组血压和存活率未见统计学差异(P>0.05),提示肠淋巴液对SMAO休克具有提升血压及延长存活时间的作用。 相似文献
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休克时体内有去甲肾上腺素含量的变化,临床对α受体阻断剂治疗休克看法不一。本文研究失血性休克大鼠肠系膜微血管和淋巴管对去甲肾上腺素反应性的变化,探讨休克的微循环变化及其与去甲肾上腺素的关系。结果发现,失血性休克时微血管的口径收缩,休克初期淋巴管收缩分数增加,休克晚期淋巴管总收缩活性指数降低,同时微血管及淋巴管对去甲肾上腺素的反应性降低,这可能是晚期微循环障碍、休克失代偿的机制之一,为临床选择药物提供了理论根据。 相似文献
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酚苄明的抗休克疗效各家报导不一,认为其机理是解除微血管痉挛,本文观察失血性休克时肠系膜微淋巴管、微血管的变化,以及酚苄明对其影响。发现失血性休克时,淋巴管的收缩频率和总收缩活性指数降低,晚期动力学指数降低;酚苄明使淋巴管总收缩活性指数及动力学指数增大,休克后该指数下降至给药前水平,至休克晚期方降低。而且血压维持40mmHg初期,可见淋巴管的收缩分数增大。休克时肠系膜细动脉和细静脉均收缩,出现流态改变,酚苄明可显著解除微血管痉挛,尤以二级细静脉明显,同时改善微血流,但对休克晚期的微循环障碍未见显著改善。提示早期应用酚苄明对防治休克有一定作用。 相似文献
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淋巴液对正常血压大鼠的平均动脉压[MAP]、左室收缩压[LVSP]及左室舒张末压[LVEDP]与生理盐水对照组各项指标相比无显著差异[P>>0.05];而对失血性休克大鼠的MAP、LVSP具有显著回升作用[P<0.01],而对休克时LVEP的恢复无明显作用[P>0.05]。提示:淋巴液只能提高休克心脏的收缩功能,在低血容量情况下对休克心脏的舒张功能无明显影响,对正常心脏的收缩和舒张功能均无明显影响。 相似文献
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大鼠重度失血性休克30min后,左心室内压的最大上升速率( dp/dt max)和左心室收缩压(LVSP)都显著下降(P<0.01),而左心室舒张末压(LVEDP)却有所增高(P<0.05)。说明心肌的收缩功能和舒张功能均出现障碍,给少量淋巴液后(用量为0.5ml/100g体重)使休克时下降的左心室内压的最大上升速率和左心室收缩压显著回升(P<0.05),而增高的左心室舒张末压回落不明显,提示淋巴液可改善休克心肌的收缩功能障碍,但对低血容量情况下的心肌舒张功能无明显改善。 相似文献
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Hypertonic saline resuscitation reduces apoptosis of intestinal mucosa in a rat model of hemorrhagic shock 总被引：1，自引：0，他引：1
Objective: To investigate the early effects of hypertonic and isotonic saline solutions on apoptosis of intestinal mueosa in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock was established in 21 Spragne-Dawley (SD) rats. The rats were randomly divided into the sham group, normal saline resuscitation (NS) group, and hypertonic saline resuscitation (HTS) group, with 7 in each group. We detected and compared the apoptosis in small intestinal mucosa of rats after hemorrhagic shock and resuscitation by terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL), FITC (fluo-rescein-iso-tbiocyanate)-Annexin V/PI (propidium iodide) double staining method, and flow cytometry. Results: In the early stage of hemorrhagic shock and resuscitation, marked apoptosis of small intestinal mucosa in the rats of both NS and HTS groups was observed. The numbers of apoptotic cells in these two groups were significantly greater than that in the sham group (P＜0.01). In the HTS group, the apoptic cells significantly decreased, compared with the NS group (P＜0.01). Conclusion: In this rat model of severe hemorrhagic shock, the HTS resuscitation of small volume is more effective than the NS resuscitation in reducing apoptosis of intestinal mucosa in rats, which may improve the prognosis of trauma. 相似文献
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目的:探讨HSP_(27)在消化道癌中的表达状况和意义。方法:收集食道癌、胃癌和大肠癌标本168例,用SP免疫组织化学方法染色。结果:HSP在食道癌、胃癌和大肠癌中的表达率分别为66.04％、37.04％和34.43％;在食道癌中高分化组阳性率(75％)明显高于低分化组(38.46％)。HSP表达与性别、年龄、癌侵润深度、淋巴有无转移的相关性不显著。结论:HSP在食道、胃、大肠癌中表达率依次下降,HSP表达率与癌分化程度有一定相关性。 相似文献
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Lu Yuan-qiang Cai Xiu-jun Gu Lin-hui Fan Yu-jing Wang Qi Bao De-guo 《浙江大学学报(A卷英文版)》2005,6(9):907-912
Objective: To observe the effects of three fluid resuscitation methods on apoptosis of visceral organs in rats with hemorrhagic
shock. Methods: A model of rat with severe hemorrhagic shock and active bleeding was established in 32 SD (Sprague-Dawley)
rats. The rats were randomly divided into control group, no fluid resuscitation group (NF group), controlled fluid resuscitation
group (NS40 group) and rapid large scale fluid resuscitation group (NS80 group). Each group contained 8 rats. The curative
effects were compared. At the same time, the apoptosis in liver, kidney, lung and small intestinal mucosa of survivors after
hemorrhage and resuscitation was detected by light microscopy in HE (hematoxylin and eosin) stained tissue sections, flow
cytometry and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL). Results: The survival rate of early fluid
resuscitation (14/16) was markedly higher than that of NF group (3/8). There was some apoptosis in liver, kidney, lung and
small intestinal mucosa of all survivors. Compared with NF and NS40 groups, the apoptosis of liver, kidney and small intestinal
mucosa of NS80 group was obviously increased. Conclusions: Among three fluid resuscitation methods, controlled fluid resuscitation
can obviously improve the early survival rate and the apoptosis of liver, kidney and small intestinal mucosa in rats with
severe and uncontrolled hemorrhagic shock, and may benefit improvement of prognosis. 相似文献
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Barpress suppression in a 1-min interval following CS trials was investigated using 16 rats in a conditioned suppression procedure with a two-stage design. For one group, each CS co-terminated with a brief shock US in Stage 1; then, in Stage 2, only half the CSs ended with a shock, which in turn was followed 1 min later by a second shock. For a second group, the two stages were reversed. When CSs were followed by single shocks in Stage 1, posttrial suppression weakened across trials; but when, in Stage 2, double shocks followed half the CSs, posttrial suppression grew stronger. When half the trials were followed by double shocks in Stage 1, posttrial suppression was maintained at initial levels but weakened in Stage 2 when single shocks followed each trial. In both stages, posttrial suppression was stronger on nonreinforced than on reinforced trials. Two factors were hypothesized to control posttrial suppression. First, posttrial suppression weakens with training under the single-shock procedure because post-shock temporal stimuli come to inhibit fear unless themselves paired with shock. Second, posttrial suppression is stronger on nonreinforced trials than on reinforced trials because freezing behaviors initiated during the CS are not disrupted by a US and so persist into the posttrial interval. 相似文献
15.
D. Chris Anderson Charles R. Crowell Martin B. Wikoff J. Victor Lupo 《Learning & behavior》1980,8(4):664-672
Two experiments investigated the relationship between activity during shock and the magnitude of subsequent impairment of shock-elicited fighting in the rat. Different levels of intra-shock activity were engendered in two ways. In Experiment 1, differing temporal forms of inescapable shock were employed to produce markedly different levels of activity. In Experiment 2, a passive-escape procedure was used to explicitly reinforce nonmovement during shock relative to a yoked, inescapable shock control. Results indicated that relative to the performance of subjects not previously shocked, fighting impairment was produced only by those prior treatments that promoted reduced intrashock activity. Since one of the prior shock treatments involved inescapable shock but the other did not, these findings may be viewed as strong support for the notion that behavior during shock, rather than uncontrollability, is the critical determinant of the observed impairment effects. There was some suggestion in both studies that shock treatments that resulted in sustained or increased intrashock activity tended to produce augmentation of fighting. Both inhibitory and facilitative effects of prior shock exposure are discussed in terms of an interacting response theory of shock treatment effects. 相似文献