共查询到16条相似文献,搜索用时 125 毫秒
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本实验在结扎大鼠盲肠并穿孔所复制的败血症休克模型上观察了早,晚期败血症休克时大鼠心肌M受体结构和功能的变化。结果发现:早期休克时M受体在质膜的分布增加,在轻囊的分布减少,表现为质膜^3H-QNB最大结合量增加33.3%;轻囊Bmax降低了26.90%;晚期休克时M受体在轻囊的分布增加,在质膜的分布减少。 相似文献
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烫伤大鼠远隔器官热休克抑制基因表达的研究 总被引:2,自引:0,他引:2
为了研究应激是否可诱导完整高等动物远隔器官细胞的热休克反应,在已发现烫伤大鼠肝,脑有热休克蛋白诱导的基础上,本文进一步研究了正常基因表达的抑制。雄性SD大鼠背部烫伤后,于10-240min分别断头处死,然后通过斑点印迹法分析热休克抑制基因-1信使核糖核酸的变化。 相似文献
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淋巴液对失血性休克大鼠心肌收缩功能的影响 总被引:1,自引:1,他引:0
淋巴液对失血性休克大鼠心肌收缩功能的影响*邱丽颖王德宝吕莉张静1(张家口医学院生理教研室,1病理生理教研室,张家口075029)淋巴系是组织液回流的主要途径,但我们发现淋巴液对失血性休克大鼠有明显的升压作用。为了围绕心脏功能探讨其抗休克机制及淋巴系的... 相似文献
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本文观察了失血性休克条件下大鼠白细胞介素1(IL-1)与内毒素的关系。结果表明:失血性休克早期血浆IL-1及ET均明显升高,前者升高在先;无菌大鼠失血性休克后IL-1活性也升高,但ET无明显变化;预先给大鼠口服乳果糖以清洁肠道,或静注内毒素抗体,休克后血浆IL-1活性仍然明显升高,而血浆ET无明显升高;大鼠失血后1h将失血回输再灌注后5d血浆IL-1与ET呈平行性变化,乳果糖或抗内毒素抗体治疗后, 相似文献
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用40、42、44℃分别处理清醒状态和麻醉状态大鼠30min,于正常饲养条件下恢复24h后,检测其肝脏热休克蛋白70(HSP70)的表达差异及酸性和中性蛋白水解酶活性变化。结果表明,当热休克温度为40-44℃时,清醒状态大鼠肝脏的HSP70合成能力逐渐下降,而麻醉大鼠肝脏HSP70合成能力逐渐增加,在42℃热休克条件下,麻醉状态大鼠肝脏的酸性蛋白水解酶活性最强,在44℃热休克条件下,清醒状态大鼠肝脏的酸性蛋白水解酶活性最强,在40-44℃热休克条件下,麻醉状态和清醒状态大鼠肝脏的45kD中性蛋白水解酶活性与对照相似,但40kD的中性蛋白水解酶活性随热休克温度升高而降低,另外,40℃热休克诱导麻醉状态大鼠肝脏出现一个高活性的35kD中性蛋白水解酶,根据实验结果推测,麻醉状态大鼠肝脏的热耐受性大于清醒大鼠,大鼠的热休克反应受整体水平和细胞水平的双重调控,并涉及除HSP70合成以外的其他生化活动。 相似文献
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目的:观察在大鼠左肝外叶切除+定容失血性休克模型制作过程中微量失血对最终大鼠生存率的影响。方法:45只SD大鼠按不同的放血比例分为三组,以Wigger改良法建立左肝外叶切除+定容失血性休克模型,严格标化放血前的各项手术操作和观测指标,比较三组大鼠最终生存率的差异。结果:在分别按2.4ml/100g(A组)、2.5ml/100g(B组)、2.6ml/100g(C组)比例定容失血的大鼠模型中,各组大鼠生存率分别为:A组66.67%,B组42.86%,C组7.69%,A、B两组与C组大鼠的生存率相比较存在明显差异(P<0.05)。结论:即使是0.1ml/100g的微量失血对于该模型大鼠的生存率也是有显著影响的,这一点在大鼠的定容失血性休克模型实验中是不应被忽视的。 相似文献
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目的:观察在大鼠左肝外叶切除+定容失血性休克模型制作过程中微量失血对最终大鼠生存率的影响。方法:45只SD大鼠按不同的放血比例分为三组,以Wigger改良法建立左肝外叶切除+定容失血性休克模型,严格标化放血前的各项手术操作和观测指标,比较三组大鼠最终生存率的差异。结果:在分别按2.4ml/100g(A组)、2.5ml/100g(B组)、2.6ml/100g(C组)比例定容失血的大鼠模型中,各组大鼠生存率分别为:A组66.67%,B组42.86%,C组7.69%,A、B两组与C组大鼠的生存率相比较存在明显差异(P〈0.05)。结论:即使是0.1ml/100g的微量失血对于该模型大鼠的生存率也是有显著影响的,这一点在大鼠的定容失血性休克模型实验中是不应被忽视的。 相似文献
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应用盲肠结扎法制备大鼠败血症休克模型,研究内源性一氧化碳(CO)在败血症休克时低血压发病中的作用。用血红素加氧酶(hemeoxygenase,HO)抑制剂2,4二甘油次卟啉锌(zincdeuteroporphyrin2,4bisglycol,ZnDPBG)处理大鼠后,观察动物动脉血压,同时测定主动脉平滑肌组织中HO活性和CO生成量。结果发现:败血症大鼠动脉收缩压、舒张压降低,同时血管平滑肌HO活性和CO生成明显增加。败血症大鼠用ZnDPBG处理后,动脉血压明显回升,同时HO活性和CO生成明显被抑制。实验表明败血症休克时低血压的发生与血管平滑肌细胞HO活性增加和内源性CO生成增多明显相关;应用HO抑制剂阻断HO活性能导致内源性CO生成减少,继而使败血症休克时大鼠血压明显回升。实验提示,内源性CO对血管张力具有重要的调节作用;HO活性和内源性CO生成增加是败血症休克时低血压发生的重要机制之一。 相似文献
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糖皮质激素受体减少在休克发生中的作用——一个新假说 总被引:18,自引:0,他引:18
用放射配体结合法和单抗测定结果表明,各种原因所致的应激在人、大鼠和狗的各脏器都引起糖皮质激素受体(GR)减少。给大鼠注射RU486阻断GR的实验结果证明,GR减少导致受体水平上的肾上腺皮质功能不全,从而使内毒素血症和失血大鼠的病变明显加重。由此,我们提出了休克发生的GR减少假说。关于应激时GR减少的机制,除了血浆糖皮质激素水平升高使GR减少之外;很可能还是热休克反应的一个表现。 相似文献
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目的:观察失血性休克(HS)大鼠淋巴管与血管对去甲肾上腺素(NE)反应性的变化,探讨淋巴管与血管反应性的关系。方法:大鼠行左侧腹部手术,分离胸导管,测量淋巴管压力(LP);股部手术,经股动脉测量平均动脉血压(MAP)。休克组经股动脉放血复制HS模型(维持MAP40mmHg左右,3h),假手术(sham)组仅手术。在休克不同时间点(或相当),股静脉注射NE(5μg/kg.bw),观察给予NE前后两组大鼠LP以及MAP的变化。结果:休克即刻淋巴管对NE的反应性与sham组无明显差异,到休克0.5h时淋巴管对NE的升压反应开始减弱,至休克3h依然维持低反应性;与sham组相比,休克组血管对NE反应性呈双相表现,休克即刻血管高反应性,休克1h后对NE的升压作用开始减弱,表现为血管低反应性;休克后二者的反应性相关。结论:大鼠HS后淋巴管出现低反应性,且出现在血管低反应性之前;休克发展进程中淋巴管与血管对NE的低反应性呈正相关。 相似文献
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L. M. Kozhevnikova P. P. Avdonin I. L. Zharkikh P. V. Avdonin 《Biochemistry (Moscow) Supplemental Series A: Membrane and Cell Biology》2017,11(1):82-86
Previously we have shown that at traumatic shock in rats the force of contraction of isolated aorta in response to angiotensin II, vasopressin, endothelin 1, or norepinephrine is decreased. On the contrary, vasoconstriction caused by serotonin is increased. A possible reason of the alterations of neuroendocrine regulation of vascular tone in shock may be a change in the expression of the receptors of these agonists in blood vessels. In the present study, using real-time PCR, we demonstrated that a day after injury the contents of mRNA encoding receptors V1A for vasopressin, ETA for endothelin 1, and AT1 for angiotensin II are not changed in aorta. There was a slight increase of the serotonin 5-HT2A receptor mRNA (36 ± 16%; p = 0.41). The level of the 5-HT2B receptor mRNA in aorta, initially low (2% of the content of the mRNA of receptors 5-HT2A), after the injury increased 15.8 ± 0.3 times (p < 0.01). However, at traumatic shock there was no contraction of aorta in response to 5-HT2B receptor agonist BW723C86, while vasodilation of the isolated aorta preconstricted with norepinephrine in response to BW723C86 was similar to that of the vessel isolated from control rats. The data obtained suggest that the observed 5-HT2B receptor overexpression is not related to the increased serotonin-induced vasoconstriction and might cause other vascular pathological changes at traumatic shock. 相似文献
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Summary When the body temperature of rats is elevated to 42°C, four heat shock proteins, with the molecular weights of 70000, 71000, 85000, and 100000 (hsp 70, hsp 71, hsp 85, and hsp 100, respectively), are induced in various tissues of rats (Fujio et al., J Biochem 101, 181–187, 1987). Heat shock proteins are induced by various stresses other than heat in varieties of cultured cells, so we studied whether heat shock proteins are induced in intact rats by different treatments. Analysis of the translation products of poly(A) + RNA isolated from the livers of rats recovering from ischemia of the liver showed that mRNAs for hsp 70, hsp 71, and hsp 85 were induced. These hsp-mRNAs were also induced in the livers of rats 6 h after a partial hepatectomy, and had returned to control levels 24 h after the surgery. These results suggested that heat shock proteins have not only the function of protection against various stresses but also physiological functions in the normal growth and development of animals. 相似文献
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Adjuvant arthritis in Lewis rats is induced by the subcutaneous injection of Mycobacterium tuberculosis in mineral oil, and the predominant T cell immune reactivity is against the heat shock protein 65 derived peptide 176-190. We treated Lewis rats with human recombinant G-CSF followed by (i.v) administration of peptide 176-190 after induction of adjuvant arthritis (AA), and observed decreased disease severity, joint destruction, new bone formation and joint ankylosis. Treatment with G-CSF alone was also effective, but to a lesser extent. In addition, we found that splenocytes from rats treated with G-CSF had reduced antigen presenting capacity compared with splenocytes from vehicle treated rats. Primed lymph node cells from G-CSF plus peptide treated rats showed a marked reduction in proliferation and secretion of IFN-gamma after stimulation with the heat shock protein peptide in vitro as compared to controls. 相似文献
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内皮素在实验性主动脉狭窄—高盐摄入性高血压发病中的作用 总被引:2,自引:1,他引:1
内皮素是血管内皮释放的生物活性多肽,具有强烈的收缩血管和促进血管平滑肌细胞增生肥大的效应。本工作在大鼠腹主动脉狭窄和高盐摄入引起的高血压模型上,观察到高血压动物血浆内皮素水平成倍增加(9.70±0.68vs。假手术动物4.11±0.33pg/ml,P<0.01)。应用特异的内皮素抗血清治疗,显著缓解了动物血压的升高(18.97±1.32vs.27.33±0.90kPa,P<0.01)和心肌肥大损伤。实验结果提示:内皮素是高血压的重要发病因素之一;拮抗内皮素可能是高血压病防治的新途径。 相似文献
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Atsushi Kobayashi Soichiro Mimuro Takasumi Katoh Kensuke Kobayashi Tsunehisa Sato Truong Sang Kien Yoshiki Nakajima 《Experimental Animals》2022,71(3):281
Hemorrhagic shock causes vascular endothelial glycocalyx (EGCX) damage and systemic inflammation. Dexmedetomidine (DEX) has anti-inflammatory and EGCX-protective effects, but its effect on hemorrhagic shock has not been investigated. Therefore, we investigated whether DEX reduces inflammation and protects EGCX during hemorrhagic shock. Anesthetized Sprague-Dawley rats were randomly assigned to five groups (n=7 per group): no shock (SHAM), hemorrhagic shock (HS), hemorrhagic shock with DEX (HS+DEX), hemorrhagic shock with DEX and the α7 nicotinic type acetylcholine receptor antagonist methyllycaconitine citrate (HS+DEX/MLA), and hemorrhagic shock with MLA (HS+MLA). HS was induced by shedding blood to a mean blood pressure of 25–30 mmHg, which was maintained for 30 min, after which rats were resuscitated with Ringer’s lactate solution at three times the bleeding volume. The survival rate was assessed up to 3 h after the start of fluid resuscitation. Serum tumor necrosis factor-alpha (TNF-α) and syndecan-1 concentrations, and wet-to-dry ratio of the heart were measured 90 min after the start of fluid resuscitation. The survival rate after 3 h was significantly higher in the HS+DEX group than in the HS group. Serum TNF-α and syndecan-1 concentrations, and the wet-to-dry ratio of heart were elevated by HS, but significantly decreased by DEX. These effects were antagonized by MLA. DEX suppressed the inflammatory response and serum syndecan-1 elevation, and prolonged survival in rats with HS. 相似文献