浅低温对犬心脏停跳复苏后脑线粒体膜流动性及Na^＋—K^＋ATPa …

目的 研究全脑缺血再灌注损伤后脑线体膜流动性及Ｎａ＾＋－Ｋ＾＋ＡＴＰａｓｅ的变化及低温的影响。方法 健康家犬１６只随机分为三组：Ａ组（ｎ＝４），非缺血对照组，Ｂ组（ｎ＝６）?心脏停跳复苏后常温常规组；Ｃ组（ｎ＝６），心脏骤停复苏后，低温液灌注组。Ｂ、Ｃ两组动物心脏停跳１８分钟复苏后治疗观察８小时，Ａ组动物完成手术操作观察８小时，处死动物取脑组织测定线粒体膜浒性。Ｎａ＾＋－Ｋ＾＋ＡＴＰａｓｅ活性和Ｍ     

头部重点低温脱水综合治疗法对脑细胞膜功能的影响

作者采用“四血管”式兔脑缺血模型，观察了脑缺血３０分钟后再灌注３０，１８０和３６０分钟时脑细胞膜上Ｎａ＾＋，Ｋ＾＋－ＡＴＰａｓｅ，Ｃａ＾２＾＋－ＡＴＰａｓｅ，磷脂酶Ａ２和总磷脂的变化，比较了部重点低温，甘露醇脱水和头部重点低温水综合疗法对这些指标变化的影响。与正常动物比较，缺血再灌注后Ｎａ＾＋，Ｋ＾＋－ＡＴＰａｓｅ，Ｃａ＾２＾＋，Ｍｇ＾２＾＋－ＡＴＰａｓｅ活力进行性下降（Ｐ＜０．００１），磷脂酶Ａ     

头部重点低温脱水综合疗法对脑细胞膜功能的影响

作者采用“四血管”式兔脑缺血模型，观察了脑缺血３０分钟后再灌注３０、１８０和３６０分钟时脑细胞膜上Ｎａ￣＋，Ｋ￣＋－ＡＴＰａｓｅ、Ｃａ￣（２＋），Ｍｇ￣（２＋）－ＡＴＰａｓｅ、磷脂酶Ａ＿２和总磷脂的变化，比较了头部重点低温、甘露醇脱水和头部重点低温脱水综合疗法对这些指标变化的影响。与正常动物比较，缺血再灌注后Ｎａ￣＋，Ｋ￣＋－ＡＴＰａｓｅ、Ｃａ￣（２＋），Ｍｇ￣（２＋）－ＡＴＰａｓｅ活力进行性下降（Ｐ＜０．００１），磷脂酶Ａ＿２活力汁高（Ｐ＜０．００１），总磷脂在再灌注１８０和３６０分钟时减少（Ｐ＜０．０１）。头部重点低温和头部重点低温脱水综合疗法可抑制上述改变（Ｐ＜０．００１），而甘露醇脱水则几无效应。提示在再灌注开始后及早应用头部重点低温脱水综合疗法确能促进或有利于脑细胞膜功能的恢复，防止再灌注对脑细胞膜功能的进一步损害。     

严重烧伤早期心肌细胞内K~＋浓度和细胞膜Na~＋－K~＋－ATP酶活性的变化

为探讨严重烧伤后早期心肌细胞内Ｋ＋浓度的变化及其机制，采用Ｋ离子选择微电极技术，测定了大鼠３５％ＴＢＳＡⅢ度烧伤后第１、３、８和２４小时心室乳头肌细胞内Ｋ＋活度（并换算成浓度），同时测定了伤后８小时心肌细胞膜ＡＴＰ酶活性。结果表明：①严重烧伤后２４小时心肌细胞内Ｋ＋浓度均下降，伤后第１、３、８和２４小时分别降为正常值的９６．２％±１．３％、８５．８％±１．３％、６５．９％±１．０％和７３．７％±１．１％。伤后８小时达最低值，２４小时有所恢复，但仍低于伤后３小时水平；②伤后８小时心肌细胞膜总ＡＴＰａｓｅ，Ｍｇ２＋－ＡＴＰａｓｅ和Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ活性均降低。提示：烧伤促进Ｋ＋外流，抑制Ｋ＋内流，且烧伤后Ｋ＋内流减少与心肌细胞膜Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ活性显著降低有关。     

普鲁卡因对离体人红细胞膜ATPases活性的影响

盐酸普鲁卡因是静脉复合麻醉（ＩＢＡ）的常用药物之一。我们发现在ＩＰＢＡ下施行上腹部手 术时，术毕人红细胞膜ＡＴＰａｓｅｓ活性有所下降。本研究的目的是观察普鲁卡因对离体人红细胞膜ＡＴ－ Ｐａｓｅ活性是否有直接影响。结果；一定浓度的普鲁卡因对Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ活性有明显抑制作用，对 Ｍｇ２＋－ＡＴＰａｓｅ活性无明显作用，对Ｃａ２＋－Ｍｇ２＋－ＡＴＰａｓｅ活性有轻微保护作用。研究结果为临床合理应 用ＩＰＢＡ提供了一定的实验依据。     

芬太尼对离体红细胞膜ATPases活性的影响

选用静脉普鲁卡因复合麻醉（ＩＰＢＡ）中伍用镇痛药芬太尼，按一浓度作用于离体状态人体细胞膜，结果发现：当芬太尼浓度〉１０μｇ／Ｌ，对人红细胞膜Ｎａ＾＋－Ｋ＾＋－ＡＴＰａｓｅ活性开始出现轻微抑制；浓度〉５０μｇ／Ｌ有明显抑制作用（Ｐ〈０．０１）。任何浓度芬太尼对Ｍｇ＾２＋－ＡＴＰａｓｅ无明显影响，对Ｃａ＾２＋－Ｍｇ＾２＋－ＡＴＰａｓｅ有轻度抑制，抑制程度不随芬太尼浓度的增减而显著改变。     

浅低温对犬心脏停跳复苏后脑组织一氧化氮、一氧化氮合成酶和神经功能的影响

目的：一氧化氮参与机体的病理生理过程，本实验研究Ｌ－Ａｒｇ：ＮＯ通路在犬心脏停跳复苏后浅低温脑复苏中的作用。方法：１５只健康犬随机分为３组：手术对照组（Ａ组，ｎ＝４只），常规治疗组（Ｂ组，ｎ＝５只）和浅低温治疗组（Ｃ组，ｎ＝６只）。Ａ组动物只完成麻醉和手术，心脏不停跳，观察８小时；Ｂ、Ｃ两组动物完成麻醉和手术，心脏停跳１８分钟，心脏复苏成功后治疗８小时。Ｂ、Ｃ两组均给予激素和脱水治疗，Ｃ组动物在心肺复苏成功后１０分钟加用头部体表物理降温，２０分钟内将鼓膜温降至３４℃±０．５℃，维持８小时。各组动物在实验结束时行神经机能评分，开颅取右顶叶脑皮质，ＮＡＤＰＨ－ｄ组织化学显示ＮＡＤＰＨ阳性细胞、Ｇｒｉｅｓ法测定其亚硝酸盐含量。结果：（１）Ｂ组犬脑皮质ＮＡＤＰＨ阳性细胞数和亚硝酸盐含量显著高于Ａ组（Ｐ＜０．０１），Ｃ组犬脑皮质ＮＡＤＰＨ阳性细胞数和亚硝酸盐含量较Ｂ组显著降低（Ｐ＜０．０１），但ＮＡＤＰＨ阳性细胞数仍高于Ａ组（Ｐ＜０．０１）。（２）Ｃ组犬神经机能评分优于Ｂ组（Ｐ＜０．０５）。结论：浅低温具有脑复苏效应，其抑制犬心脏停跳复苏后脑组织Ｌ－Ａｒｇ：ＮＯ通路的激活，可能是其具有脑复苏效应的机理之一。     

吗啡哌替啶芬太尼对离体人红细胞膜ATPases活性的影响

目的：比较研究吗啡、哌替啶、芬太尼对离体人红细胞膜ＡＴＰａｓｅｓ活性的影响。方法：将不同浓度的药物分别与人红细胞孵育，以孔雀绿－磷钼酸复合比色法测定ＡＴＰａｓｅｓ活性。结果：随着药物浓度的增加，吗啡对Ｎａ＋，Ｋ＋－ＡＴＰａｓｅ活性有增强作用（Ｐ＜０．０５），芬太尼则呈明显地抑制作用（Ｐ＜０．０５），哌替啶仅具有轻微抑制作用；吗啡能明显抑制Ｍｇ２＋－ＡＴＰａｓｅ和Ｃａ２＋，Ｍｇ２＋－ＡＴＰａｓｅ活性（Ｐ＜０．０１或Ｐ＜０．０５），但哌替啶和芬太尼对Ｍｇ２＋－ＡＴＰａｓｅ活性均无影响；这两种药物仅轻微地抑制Ｃａ２＋，Ｍｇ２＋－ＡＴＰａｓｅ活性。结论：应用大剂量吗啡或芬太尼时，需注意他们对人红细胞膜ＡＴＰａｓｅｓ活性的影响。     

浅低温对犬心脏停跳复苏后脑组织一氧化氮,一氧化氮合成酶和…

一氧化氮参与机体的病理生理过程，本实验研究Ｌ－Ａｒｇ：ＮＯ通路在犬以及地停跳复苏后浅低温脑复苏中的作用。１５只健康犬随机分为３组；手术对照且（Ａ组，ｎ＝４只），常规治疗组（Ｂ组，ｎ＝５只）和浅低温治疗且（Ｃ组，ｎ＝６只）。Ａ组动物只完成麻醉和手术，心脏不停跳，观察８小时；Ｂ、Ｃ两组动物完成麻醉和手术，心脏停跳１８分钟以及地得苏成功后治疗８小时Ｂ、Ｃ两组均给予激素和脱水治疗，Ｃ组动物在心脏复苏成功后     

体外循环红细胞钙运转异常

体外循环红细胞钙运转异常王涛张青高鲁燕为了探索体外循环中红细胞钙运转变化，我们测定了３０例体外循环患儿的Ｃａ２＋，Ｍｇ２＋－三磷酸腺苷酶（ＡＴＰａｓｅ）与Ｎａ＋，Ｋ＋－ＡＴＰａｓｅ活性，发现体外循环中红细胞存在严重的钙运转异常。１资料与方法１．１一般...     

体外循环对瓣膜置换术病人红细胞膜功能的影响

目的：观察体外循环对红细胞膜的损伤作用。方法：利用ＤＰＨ荧光标记测定１０例瓣膜置换术病人红细胞膜流动性，并测定红细胞膜三磷酸腺苷（ＡＴＰ）酶活性和丙二醛含量。结果：转流３０分红细胞膜平均微粘度（η）、各向异性（γ）和丙二醛均明显增加（Ｐ＜０．０１），而膜上Ｎａ＋，Ｋ＋－ＡＴＰ酶、Ｃａ艹－ＡＴＰ酶和Ｍｇ艹－ＡＴＰ酶活性明显降低（Ｐ＜０．０１）。停机后３０分上述各值仍未恢复到转流前水平。结论：ＣＰＢ可通过引起红细胞膜脂质过氧化反应增强，降低膜流动性和膜上ＡＴＰ酶活性，对红细胞产生损伤。     

巴曲酶复合低温对全脑缺血再灌注期间ATP酶活性的影响

目的 观察低温，巴英酶及巴曲酶复合低温对沙土鼠全脑缺血后海马组织Ｎａ＾＋－Ｋ＾＋－ＡＴＰ酶，Ｃａ６２＋－ＡＴＰ酶活性的影响。方法 利用沙土鼠全脑缺血模型，观察全脑缺血１０分及再灌２０分，６０分时，低温，巴曲酶及巴曲酶复合低温对海马组织Ｎａ＾＋－Ｋ＾＋－ＡＴＰ酶，Ｃａ＾２＋－ＡＴＰ酶活性的影响。     

氯胺酮联合亚低温对窒息性心跳骤停大鼠复苏后脑缺血再灌注损伤的影响

目的 探讨氯胺酮联合亚低温对窒息性心跳骤停大鼠复苏后脑缺血再灌注损伤的影响.方法 健康Wistar大鼠50只,4.0～4.5个月,雌雄各半,体重410～510 g,随机分为5组(n=10):假手术组(S组)仅经动、静脉穿刺置管;窒息性心跳骤停组(ACA组)制备窒息性脑缺血模型;氯胺酮组(K组)窒息前5 min腹腔注射氯胺酮100 mg/kg;亚低温组(MH组):窒息开始后维持直肠温30～35℃;氯胺酮+亚低温组(K+MH组):窒息前5 min腹腔注射氯胺酮100 mg/kg,窒息开始后维持直肠温30～35 ℃.成功复苏后,取脑组织,测定脑含水量和海马神经元p-caspase-3的表达水平.结果 与S组比较,ACA组和K组脑含水量升高,p-caspase-3表达上调,MH组和K+MH组p-caspase-3表达上调(P＜0.01),脑含水量差异无统计学意义(P＞0.05);与ACA组比较,MH组和K+MH组脑含水量降低,p-caspase-3表达下调,K组p-caspase-3表达下调(P＜0.01),脑含水量差异无统计学意义(P＞0.05);与K组比较,K+MH组脑含水量降低,p-caspase-3表达下凋,MH组脑含水量降低(P＜0.01),p-caspase-3表达差异无统计学意义(P＞0.05);与MH组比较,K+MH组p-caspase-3表达下调(P＜0.01),脑含水量差异无统计学意义(P＞0.05).结论 氯胺酮联合亚低温可减轻窒息性心跳骤停大鼠复苏后的脑缺血再灌注损伤,该效应较两者单独应用时增强.     

丹参注射液对胃黏膜Na+-K+-ATPase活性和胃黏膜屏障功能的影响

目的探讨丹参注射液对严重腹腔感染状态下大鼠胃黏膜Na -K -ATPase活性变化和电位差的影响。方法将180只大鼠随机分为感染组(盲肠穿孔)、丹参组(盲肠穿孔感染后注射复方丹参注射液)和对照组,每组60只。用紫外分光光度计检测穿孔前和穿孔后3、6、12、24和48h各时相组大鼠胃黏膜Na -K -ATPase活性。应用电生理记录仪检测穿孔前和穿孔后3、6、12、24和48h胃黏膜电位差(GTPD)的变化。结果感染组在盲肠穿孔后3hNa -K -ATPase活性显著降低(P<0.05),12h降至最低(P<0.01),48h仍未恢复正常;丹参组12h、24hNa -K -ATP酶活性比感染组显著升高(P<0.05)。GTPD穿孔后3h即有下降,6h显著下降(P<0.05),12h下降至最低(P<0.01),24h和48h仍然显著低于对照组(P<0.05);丹参组12h、24h比感染组明显升高(P<0.05)。结论严重腹腔感染状态下胃黏膜Na -K -ATPase活性降低,可能是引起胃黏膜屏障功能受损的主要原因,提示早期应用丹参能有效地预防应激性溃疡的发生。     

一氧化碳对脑缺血脂质过氧化物及Na+-K+ATP酶的影响及其限速酶在脑缺血中的表达

目的 观察一氧化碳(CO)对局灶性脑缺血脑组织脂质过氧化物及Na+-K+ATP酶的影响以及血红素氧合酶(HO-1)在脑缺血中的表达.方法 将SD大鼠随机分为3组,使用HO诱导剂、HO抑制剂腹腔注射为实验组,对照组注入生理盐水,12 h后制备大鼠局灶性脑缺血模型.缺血后24 h检测CO浓度、丙二醛(MDA)、超氧化物歧化酶(SOD)及Na+-K+ATP酶活性.对大鼠脑缺血后早期不同时间点进行HO-1免疫组织化学及病理学研究,并应用计算机图像分析技术检测HO-1表达的强弱.结果 与对照组比较,HO诱导剂组CO浓度显著升高1.36倍(P<0.01),HO抑制剂组CO浓度显著降低26.4%(P<0.01).HO诱导剂组MDA减少11.3%(P<0.01),SOD及Na+-K+ATP酶活性分别升高6.8%和20.1%(P均<0.05),而HO抑制剂组MDA增加12.4%(P<0.05),SOD及Na+-K+ATP酶活性分别降低8.2%和18.9%(P均<0.05).免疫组织化学显示缺血后30 min神经元和胶质细胞即有HO-1阳性表达,随着时间推移,HO-1的表达逐渐增强.结论 CO可对局灶性缺血的脑组织起保护作用.脑缺血时脑内HO-1的表达可能是脑组织对自身损伤的恢复机制之一.     

Effect of hypothermia on cellular membrane function during low-flow extracorporeal circulation

The use of systemic hypothermia is known to allow recovery from potentially lethal states of profound hypoperfusion or total circulatory arrest. While the cellular alterations accompanying states of decreased perfusion in skeletal muscle are well defined, little is known regarding the impact of coexistent hypothermia. To investigate this issue, nine dogs were placed on total cardiopulmonary bypass (CPB) and perfused in nonpulsatile fashion. The following flow and temperature parameters were used in three different perfusion models: 3.5 L/min/m2 at 23 degrees C (group A, n = 3), 1.6 L/min/m2 at 37 degrees C (group B, n = 3), and 1.6 L/min/m2 at 23 degrees C (group C, n = 3). Assessment of cellular function in a hind limb adductor muscle by measurement of resting transmembrane potential difference (Em) and determination of tissue electrolyte distribution in a biopsy specimen was performed in the control state and again after 60 minutes of total CPB. Low-flow/hypothermic CPB (group C) was associated with depolarization of resting Em to -63.3 +/- 3.2 mV from a control value of -87.0 +/- 1.3 mV (p less than 0.05), an increase in the calculated intracellular Na ([Na]i) to 16.4 +/- 4.0 mEq/L from a control value of 7.6 +/- 1.4 mEq/L (p less than 0.05), and an increase in the ratio of the selective membrane permeabilities of Na+ to K+ (pNa/pK), to 0.067 +/- 0.013 from a control value of 0.013 +/- 0.002 (p less than 0.05). In contrast, resting Em was maintained at -86.4 +/- 6.1 mv during normal-flow/hypothermic CPB (group A), while low-flow/normothermic CPB (group B) produced an intermediate depolarization to -75.2 +/- 3.0 mV (p less than 0.05). Neither [Na]i or pNa/pK was altered significantly in group A or group B dogs. These data characterize a physiologic alteration in the cellular membrane function of skeletal muscle during low-flow/hypothermic CPB, which is similar in many respects to that accompanying hemorrhagic shock. This suggests that during periods of profound hypothermia certain flow-related derangements in skeletal muscle are not obviated and may be exacerbated.     

大鼠股薄肌早期压疮局部腺苷三磷酸酶活性与兰尼碱受体1mRNA表达

目的 了解ATP酶活性与兰尼碱受体1(RyR1)mRNA表达变化在早期压疮形成过程中的作用机制.方法 将36只雄性SD大鼠按照随机数字表法分为3组,每组12只:(1)未施压组,大鼠股薄肌部位未施予压强.(2)3次缺血再灌注(IR)组,用特制压力装置对大鼠一侧大腿股薄肌持续施压(22.47 kPa)2.0 h模拟缺血状态,继而停止施压0.5 h模拟再灌注变化,如此进行3次即完成3个IR循环.(3)5次IR组,处理条件同3次IR组但重复操作5次.处理结束后处死各组大鼠,取受压中心(未施压组取相同解剖部位)肌肉组织标本,用比色法检测总ATP酶、Ca2+-Mg2+-ATP酶和Na+-K+-ATP酶活性,用ELISA法检测丙二醛含量,实时荧光定量RT-PCR法测定RyR1 mRNA表达水平.对实验数据行单因素方差分析,用Pearson相关分析法分析总ATP酶活性分别与丙二醛含量、RyR1 mRNA表达水平的相关性,RyR1 mRNA表达水平与丙二醛含量的相关性.结果 未施压组总ATP酶、Ca2+-Mg2+-ATP酶、Na+-K+-ATP酶活性分别为(1.629±0.004)、(0.907±0.061)、(0.697±0.083)U/mg,均高于3次IR组[(1.365±0.004)、(0.784±0.020)、(0.581±0.017)U/mg,F值分别为1707.0、29.8、15.2,P<0.05或P<0.01]以及5次IR组[(1.055±0.049)、(0.619±0.016)、(0.436±0.039)U/mg,F值分别为1107.0、169.9、65.7,P值均小于0.01];5次IR组此3项指标明显低于3次IR组(F值分别为322.8、341.7、94.0,P值均小于0.01).未施压组丙二醛含量为(7.5±0.6)nmol/L,明显低于3次IR组[(9.9±0.6)nmol/L,F=53.2,P<0.01]和5次IR组[(13.7±1.3)nmol/L,F=76.9,P<0.01];后2组比较,差异有统计学意义(F=82.9,P<0.01).实时荧光定量RT-PCR 结果表明,未施压组RyR1 mRNA表达水平为8.5±4.2,与3次IR组(3.3±2.1)接近(F=0.9,P>0.05),但明显高于5次IR组(0.6±0.5,F=23.6,P<0.05);5次IR组明显低于3次IR组(F=39.3,P<0.05).总ATP酶活性与丙二醛含量呈显著负相关,r=-0.918,P<0.01;总ATP酶活性与RyR1 mRNA表达水平呈显著正相关,r=0.713,P<0.01;RyR1 mRNA表达水平与丙二醛含量呈显著负相关,r=-0.702,P<0.01.结论 能量代谢障碍可能是早期压疮发生的始动因素;RyR1 mRNA表达降低初步反映局部组织受压一定时间后存在钙超载损伤.

Abstract：

Objective To investigate changes in adenosine triphosphatase (ATPase) activity and expression of ryanodine receptor 1 (RyR1) mRNA in formation of pressure ulcer at early stage,and to analyze its mechanism. Methods Thirty-six male Sprague-Dawley rats were divided into three groups according to the random number table as follows,with 12 rats in each group. (1) Ischemia-reperfusion (IR) for 3 times (3IR) group: unilateral gracilis of rats were loaded with 22.47 kPa pressure with a special pressure apparatus for 2.0 h to simulate ischemia,and unloaded for 0.5 h to simulate reperfusion. All rats were treated with above-mentioned manoeuvre for 3 times. (2) IR for 5 times (5IR) group: rats were treated with the same manoeuvre as that in 3IR group except for IR for 5 times. (3) Control group: gracilis of rats were subjected to a load of 0 kPa pressure. Rats in 3IR,5IR groups were sacrificed,and then central part of pressured tissue was harvested for detection of activity of total ATPase,Ca2+-Mg2+-ATPase,and Na+-K+-ATPase with spectrophotometer colorimetry,the level of malondialdehyde (MDA) with enzyme linked immunosorbent assay (ELISA),and the level of RyR1 mRNA with real-time fluorescence quantitative RT-PCR. The same part of gracilis muscle of rats in control group was harvested for determination of indexes as above. Data were processed with one-way analysis of variance. Pearson correlation analysis was respectively performed between total ATPase activity and MDA level,total ATPase activity and RyR1 mRNA expression level,and RyR1 mRNA expression level and MDA level. Results Activity of total ATPase,Ca2+-Mg2+-ATPase,Na+-K+-ATPase in control group was respectively (1.629±0.004),(0.907±0.061),(0.697±0.083) U/mg,all significantly higher than those in 3IR group[(1.365±0.004),(0.784±0.020),(0.581±0.017) U/mg,with F value respectively 1707.0,29.8,15.2,P<0.05 or P<0.01]and 5IR group[(1.055±0.049),(0.619±0.016),(0.436±0.039) U/mg,with F value respectively 1107.0,169.9,65.7,P values all below 0.01],and the values of 3 indexes in 5IR group were obviously lower than those in 3IR group (with F value respectively 322.8,341.7,94.0,P values all below 0.01). The level of MDA in control group[(7.5±0.6) nmol/L]was lower than that in 3IR group[(9.9±0.6)nmol/L,F=53.2,P<0.01]and 5IR group[(13.7±1.3) nmol/L,F=76.9,P<0.01]. There was also statistical difference in MDA level between 3IR group and 5IR group (F=82.9,P<0.01). Expression level of RyR1 mRNA in control group (8.5±4.2),which was similar to that in 3IR group (3.3±2.1,F=0.9,P>0.05),was significantly higher than that in 5IR group (0.6±0.5,F=23.6,P<0.05);while the RyR1 mRNA expression level was lower in 5IR group than in 3IR group (F=39.3,P<0.05). Activity of total ATPase was negatively correlated with MDA level (r=-0.918,P<0.01). Activity of total ATPase was positively correlated with RyR1 mRNA expression level (r=0.713,P<0.01). RyR1 mRNA expression level was negatively correlated with MDA level (r=-0.702,P<0.01). Conclusions Energy dysbolism may be an initial factor in the development of pressure ulcer at early stage. Calcium overload injury in pressure tissue can be identified by determination of RyR1 mRNA expression.     

Rapid hypothermic aortic flush can achieve survival without brain damage after 30 minutes cardiac arrest in dogs

BACKGROUND: Neither exsanguination to pulselessness nor cardiac arrest of 30 min duration can be reversed with complete neurologic recovery using conventional resuscitation methods. Techniques that might buy time for transport, surgical hemostasis, and initiation of cardiopulmonary bypass or other resuscitation methods would be valuable. We hypothesized that an aortic flush with high-volume cold normal saline solution at the start of exsanguination cardiac arrest could rapidly preserve cerebral viability during 30 min of complete global ischemia and achieve good outcome. METHODS: Sixteen dogs weighing 20-25 kg were exsanguinated to pulselessness over 5 min, and circulatory arrest was maintained for another 30 min. They were then resuscitated using closed-chest cardiopulmonary bypass and had assisted circulation for 2 h, mild hypothermia (34 degrees C) for 12 h, controlled ventilation for 20 h, and intensive care to outcome evaluation at 72 h. Two minutes after the onset of circulatory arrest, the dogs received a flush of normal saline solution at 4 degrees C into the aorta (cephalad) via a balloon catheter. Group I (n = 6) received a flush of 25 ml/kg saline with the balloon in the thoracic aorta; group II (n = 7) received a flush of 100 ml/kg saline with the balloon in the abdominal aorta. RESULTS: The aortic flush decreased mean tympanic membrane temperature (Tty) in group I from 37.6 +/- 0.1 to 33.3 +/- 1.6 degrees C and in group II from 37.5 +/- 0.1 to 28.3 +/- 2.4 degrees C (P = 0.001). In group 1, four dogs achieved overall performance category (OPC) 4 (coma), and 2 dogs achieved OPC 5 (brain death). In group II, 4 dogs achieved OPC 1 (normal), and 3 dogs achieved OPC 2 (moderate disability). Median (interquartile range [IQR]) neurologic deficit scores (NDS 0-10% = normal; NDS 100% = brain death) were 69% (56-99%) in group I versus 4% (0-15%) in group II (P = 0.003). Median total brain histologic damage scores (HDS 0 = no damage; > 100 = extensive damage; 1,064 = maximal damage) were 144 (74-168) in group I versus 18 (3-36) in group II (P = 0.004); in three dogs from group II, the brain was histologically normal (HDS 0-5). CONCLUSIONS: A single high-volume flush of cold saline (4 degrees C) into the abdominal aorta given 2 min after the onset of cardiac arrest rapidly induces moderate-to-deep cerebral hypothermia and can result in survival without functional or histologic brain damage, even after 30 min of no blood flow.     

温血停搏液术终灌注对缺血再灌注心肌的保护作用

利用猫体外循环模型观察含甘露醇的温血停搏液术终灌注对缺血再灌注心肌的保护作用。心肌缺血恢复正常血液灌注前，从主动脉根部以５～６ｋＰａ的压力注入３７℃含甘露醇的低钾温血停搏液５０ｍｌ。结果显示用含甘露醇的温血停搏液术终灌注可保护缺血后再灌注心肌的功能，提高心肌能量储备，降低线粒体丙二醛含量。结论：含甘露醇的温血停搏液术终灌注，可提高心肌对氧自由基的清除能力，减轻线粒体膜脂质过氧化，提高心肌能量储备，有利于再灌注后心肌功能的恢复     

幼年雄性大鼠双侧睾丸切除后体内Na~＋、K~＋－ATP酶活性的动态观察

采用雄性大鼠６４只作为研究对象，实验组６周龄时切除双侧睾丸，同时设对照组。分别于术后１、３、６和９个月收集标本，测定Ｎａ￣＋Ｋ￣＋－ＡＴＰ酶活性和血浆睾酮含量。结果表明：（１）去双侧睾丸后红细胞膜Ｎａ￣＋Ｋ￣＋－ＡＴＰ酶活性明显低于同月龄正常对照组（Ｐ＜０．０１）；并且随去睾月龄的增加，去睾组红细胞膜Ｎａ＋Ｋ＋－ＡＴＰ酶活性无明显上升。大鼠红细胞膜Ｎａ＋Ｋ＋－ＡＴＰ酶活性的高低与血浆睾酮含量呈直线相关（ｒ＝０．９４），表明雄激素对雄性动物的Ｎａ＋Ｋ＋－ＡＴＰ酶活性具有兴奋作用。