内皮素1与一氧化氮对大鼠严重烧伤后早期心功能迅即变化的影响

目的 了解内皮素1和NO是否参与严重烧伤后早期心功能的迅即变化. 方法 (1)取31只Wistar大鼠,按随机数字表法分为假伤A组(7只)、烧伤A组(10只)、非选择性内皮素A/B受体拮抗剂PD142893组(7只)和选择性内皮素A受体拮抗剂BQ-123组(7只).后3组大鼠制成30%TBSA Ⅲ度烧伤模型,其中PD142893组和BQ-123组伤后即刻分别经静脉给予PD142893(0.1me,/kg)和BQ-123(30 nmol·kg~(-1)·min~(-1)).假伤A组除致假伤外,其余处理同烧伤A组.采用生理信号采集处理系统,监测假伤A组和烧伤A组大鼠伤前及伤后10、30、60、180 min时的左心室收缩压(LVSP)、心率、左心室压力最大上升/下降速率(LV±dp/dt max);计算4组大鼠伤后10 min上述各项心功能指标较各自伤前值变化的百分率.(2)另取20只Wistar大鼠,按随机数字表法分为假伤B组(4只)和烧伤B组(16只),同前致伤.烧伤B组分别于伤后10、30、60、180 min(每时相点4只)取心脏组织,假伤B组伤后即刻取心脏组织,用ELISA法检测内皮素1和NO含量. 结果 (1)与伤前值比较,烧伤A组大鼠伤后10 min LVSP、心率、LV+dp/dt max、LV-dp/dt max即明显下降(F值分别为7.14、16.40、14.09、14.98,P<0.05或P<0.01).假伤A组大鼠受伤前后4项心功能指标无明显变化(F值依次为0.59、0.51、1.03、1.04,P值均大于0.05).(2)与伤前值比较,伤后10 min烧伤A组LVSP下降27%、心率下降14%、LV+dp/dt max下降51%、LV-dp/dt max下降50%.PD142893组伤后10 min LVSP下降14%、心率升高4%、LV+dp/dt max下降31%、LV-dp/dt max下降14%,与烧伤A组相比各指标变化情况显著改善(F值分别为8.10、6.50、23.67、10.39,P<0.05或P<0.01).BQ-123组大鼠心率较伤前升高3%、LV-dp/dt max下降26%,与烧伤A组相比明显改善(F值分别为6.50、10.39,P<0.05或P<0.01);其LVSP和LV+dp/dt max变化百分率与烧伤A组接近(F值分别为8.10、23.67,P值均大于0.05).(3)与假伤B组相比,烧伤B组伤后10、60、180min心肌组织内皮素1含量均升高(F=2.85,P<0.05或P<0.01),NO含量于伤后60、180 min明显升高(F=1.87,P值均小于0.05). 结论 内皮素1可能参与了大鼠严重烧伤后早期心功能的迅即下降,在伤后立即出现的心肌损害中起重要作用.     

口服补液复苏对严重烧伤家兔心肌力学指标的改善作用

目的 了解口服补液复苏对严重烧伤家兔心脏功能的保护作用. 方法 150只家兔随机分为正常对照组(6只)、烧伤组(42只)、立即补液组(42只)、延迟补液组(30只)和延迟快速补液组(30只).正常对照组不致伤不补液.其余4组家兔均造成40%TBSAⅢ度烧伤,烧伤组不补液,余下3组伤后用灌胃的方式进行口服补液复苏.经家兔颈动脉左心室内置管,测量正常对照组及4组致伤家兔伤后2、6、8、12、24、36、48 h的平均动脉压(MAP)、左心室收缩压(LVSP)、左心室舒张末期压(LVEDP)以及左心室压力最大上升/下降速率(LV±dp/dt max),另检测休克期尿量. 结果烧伤组家兔LVSP、LV±dp/dt max较正常对照组显著下降.立即补液组和延迟快速补液组上述指标在伤后24 h内高于烧伤组,其中立即补液组LV+dp/dt max在伤后8 h达峰值[(892±116)kPa/s,1 kPa=7.5 mm Hg],LV-dp/dt max在伤后6 h达峰值[(724±149)kPa/s];伤后8 h,延迟快速补液组LV±dp/dt max均达峰值.延迟补液组伤后各时相点LVSP、LV±dp/dt max与烧伤组接近.各组家兔MAP、伤后第1个24 h尿量的比较情况大致与以上指标相似.烧伤组与其余4组比较,各时相点LVEDP差异无统计学意义(P>0.05). 结论严重烧伤家兔伤后24 h内给予有效的口服补液,可改善心肌力学指标;延迟复苏的家兔按照延迟复苏补液公式预估补液量,才能进行有效复苏.     

依那普利拉对严重烫伤大鼠早期心肌力学的影响

目的 了解依那普利拉对严重烫伤大鼠早期心肌力学的影响.方法 将84只SD大鼠背部造成30%TBSA的Ⅲ度烫伤后,随机分为烫伤组,伤后按Parkland公式腹腔注射等渗盐水;小剂量治疗组、中剂量治疗组、大剂量治疗组,伤后即刻分别腹腔注射1、2、4 mg/kg依那普利拉.烫伤组、小剂量治疗组伤后1、3、6、12、24 h,中剂量治疗组、大剂量治疗组伤后6、12 h左心室置管检测大鼠左心室收缩压(LVSP)、左心室舒张末期压(LVEDP)、左心室压力最大上升/下降速率(±dp/dt max),并处死大鼠取心肌组织检测血管紧张素Ⅱ(AⅡ)含量.另取6只大鼠作为假伤组,模拟烫伤后检测以上指标.结果 伤后3～24 h,烫伤组及各剂量治疗组大鼠LVSP、LVEDP、±dp/dt max值普遍低于假伤组(P＜0.05或P＜0.01);而各剂量治疗组LVSP、LVEDP、±dp/dt max值普遍高于烫伤组(P＜0.05或P＜0.01);伤后6、12 h,大剂量治疗组±dp/dt max明显低于小、中剂量治疗组.伤后1 h,烫伤组心肌组织AⅡ含量[(53.0±2.6)pg/200 mg]明显高于假伤组[(14.8±0.7)pg/200 mg,P＜0.01],6 h达高峰,以后逐渐下降,伤后24 h仍明显高于假伤组(P＜0.01);伤后3～24 h.小剂量治疗组AⅡ含量均明显高于假伤组(P＜0.05或P＜0.01),但均低于烫伤组.伤后6 h烫伤组AⅡ含量为(145.2±14.5)pg/200 mg,高于小、中、大剂量治疗组[(65.1±0.9)、(53.6±1.1)、(34.2±0.9)pg/200 mg,P ＜0.01].结论 严重烫伤后早期心肌组织损害明显.心功能即明显下降,依那普利托注射液可以改善心肌力学指标、保护心功能,以小剂量效果最为明显.     

强化胰岛素治疗拮抗严重烫伤大鼠心肌细胞凋亡的作用

目的 了解强化胰岛素治疗对重度烫伤大鼠心肌细胞的抗凋亡作用及机制.方法 将18只SD大鼠分为3组,每组6只.烫伤组及强化组大鼠背部脱毛后造成30%TBSA的Ⅲ度烫伤.强化组伤后静脉注射胰岛素等渗盐水(15 mU·kg-5·min-1)和100 g/L葡萄糖;烫伤组给予等渗盐水(2 mL·kg-1·1%TBSA-1·8 h-1);假伤组模拟烫伤,伤后给予生理量的液体.记录3组大鼠伤后6 h的左心室压力最大上升/下降速率(±dp/dt max);采用原位末端标记法和DNA梯带法检测各组大鼠心肌细胞凋亡情况;蛋白质印迹法检测心肌组织中磷酸化蛋白激酶B(p-Akt)、Bcl-2的表达水平.结果 假伤组、强化组、烫伤组大鼠+dp/dt max值分别为(5.5±0.5)x 103、(3.4±0.4)×105、(2.5±0.5)×103mm Hg/s(1 mm Hg=0.133 kPa);-dp/dt max值分别为(4.55±0.34)× 103、(2.94±0.22)× 103、(2.05±0.19)× 103mm Hg/s.烫伤组大鼠±dp/dt max均低于强化组(P＜0.01).烫伤组大鼠心肌细胞凋亡指数[AI,(13.1±3.4)%]明显高于假伤组[(0.6±0.4)%,P＜0.01];强化组AI为(6.7±1.8)%,明显低于烫伤组(P＜0.01).假伤组大鼠心肌组织未见DNA断裂条带,烫伤组可见明显的DNA断裂形成梯带,而强化组梯带形成不明显,表示其凋亡细胞明显少于烫伤组.烫伤组心肌组织内p-Akt和Bcl-2蛋白表达水平明显低于强化组.结论 强化胰岛素治疗通过上调Akt活性,增加Bcl-2的表达,可能是其抗心肌细胞凋亡、保护心功能的机制之一.     

血管紧张素(1-7)和依那普利拉对烧伤血清离体灌注大鼠心脏功能的影响

目的 了解血管紧张素(1-7)[Ang(1-7)]和依那普利托对烧伤血清离体灌注大鼠心脏功能的影响.方法 选取80只SD大鼠制备烧伤血清.另取24只SD大鼠心脏建立Langendofff离体灌注模型.根据灌注液不同,将大鼠心脏分为K-H液组、含体积分数20%烧伤血清的K-H液组(烧伤血清组)、含体积分数20%烧伤血清和2μg/mL依那普利拉的K-H液组(依那普利托组)、含体积分数20%烧伤血清和1 nmoL/mL Ang(1-7)的K-H液组[Ang(1-7)组].各组大鼠心脏连续灌注30min上述溶液后,检测其左心室收缩压(LVSP)、左心室舒张末期压(LVEDP)、左心室压力最大上升/下降速率(±dp/dt max),以及冠状动脉血流量(CF)和冠状动脉流出液中肌酸激酶(CK)、乳酸脱氢酶(LDH)的含量.结果 与K-H液组LVSP[(11.2±1.0)kPa,1 kPa=7.5 mm Hg]、+dp/dt max[(642±53)kPa/s]、-dp/dt max[(380±61)kPa/s]及CF值比较,烧伤血清组、依那普利拉组和Ang(1.7)组LVSP[(5.9±0.8)、(8.0±1.1)、(8.9±1.3)kPa]、+dp/dt max[(275±37)、(454±48)、(479±63)kPa/s]、-dp/dt max[(135±35)、(219±47)、(277±58)kPa/s]及CF值均明显降低(P<0.05或P<0.01),LVEDP和冠状动脉流出液中CK、LDH的含量升高.与烧伤血清组比较,依那普利拉组和Ang(1-7)组CF、LVSP及±dp/dt max均明显升高(P<0.05或P<0.01),LVEDP和冠状动脉流出液中CK、LDH的含量明显降低(P<0.01).结论 Ang(1-7)和依那普利拉均能有效改善烧伤血清离体灌注大鼠左心功能,减轻心肌损伤.     

严重烫伤大鼠早期心肌抑制对肝肾肠损害的影响

目的 了解严重烫伤大鼠早期心肌抑制对肝、肾、肠损害及血流灌注的影响.方法 将32只Wistar大鼠按随机数字表分为假伤组、普萘洛尔组、烫伤对照组和烫伤+普萘洛尔组,每组8只.各组大鼠腹腔注射10 g/L戊巴比妥钠(30 mg/kg)麻醉后,假伤组、普萘洛尔组置于37℃水中18 s致假伤,其余2组置于97℃水浴中18 s,造成30%TBSAⅢ度烫伤.伤后30 min按Parkland公式腹腔注射复方乳酸钠林格液(4 mL·kg-1·1%TBSA-1).普萘洛尔组、烫伤+普萘洛尔组补液的同时静脉注射普萘洛尔0.75 mg/kg.伤后6 h以多道生理信号采集仪检测大鼠动脉收缩压(SBP)、动脉舒张压(DBP)、平均动脉压(MAP)以及左心室收缩压(LVSP)、左心室舒张末期压(LVEDP)、左心室压力最大上升/下降速率(±dp/dt max);以激光多普勒血流仪检测肝、肾、肠血流量;同时抽取大鼠静脉血检测血清心肌肌钙蛋白I(cTnI)、总胆汁酸(TBA)、β2-微球蛋白(β2-MG)浓度和二胺氧化酶(DAO)活性.结果 普萘洛尔组除LVEDP外,SBP、DBP、MAP、LVSP、±dp/dt max均低于假伤组(P<0.05).烫伤对照组与假伤组比较,心肌力学指标均下降(P<0.05).烫伤+普萘洛尔组与烫伤对照组比较,各项心肌力学指标均明显下降(P<0.05).与假伤组比较,烫伤对照组肝、肾、肠血流量显著降低(P<0.05);与烫伤对照组比较,烫伤+普萘洛尔组肝、肾、肠血流量降低(P<0.05).烫伤对照组血清cTnI、TBA、β2-MG和DAO值分别为(4.86±0.29)μg/L、(83.6±18.2)μmol/L、(2.75±0.19)mg/L、(1.45±0.09)×103U/L,均高于假伤组[(1.73±0.09)μg/L、(24±2.4)μmol/L、(1.15±0.18)mg/L、(0.87±0.13)×103U/L,P<0.05];与烫伤对照组比较,烫伤+普萘洛尔组血清cTnI(5.95±0.42)μg/L、TBA(125.8±21.3)μmol/L、β2-MG(3.25±0.17)mg/L、DAO(1.83±0.13)×103U/L均明显升高(P<0.05).结论 严重烫伤大鼠早期心肌抑制能加剧肝、肾、肠损害,提示"休克心"可能是严重烧伤后早期肝、肾、肠血流量减少和损害的启动因素之一.     

"休克心"对严重烫伤大鼠早期肝肾肠损害的启动作用

目的 了解"休克心"对严重烫伤大鼠早期肝、肾、肠损害是否具有启动作用.方法 将56只Wistar大鼠随机分为对照组(8只),不予烫伤;烫伤组(48只),大鼠背部造成30%TBSA Ⅲ度烫伤,设伤后0.5、1.0、3.0、6.0、12.0和24.0 h观察时相点,每时相点8只大鼠.伤后30 min按Park-land公式腹腔注射乳酸林格液(4 mL·kg-1·1%TBSA-1).检测大鼠肝、肾、肠血流量;动脉收缩压(SBP)、动脉舒张压(DBP)、平均动脉压(MAP)、左心室收缩压(LVSP)、左心室舒张末期压(LVEDP)、左心室压力最大上升/下降速率(±dp/dt max);抽取各组大鼠静脉血检测其血清心肌肌钙蛋白I(cTnI)、总胆汁酸(TBA)、β2微球蛋白(β2-MG)、二胺氧化酶(DAO)含量.结果 伤后1.0 h烫伤组大鼠肝、肾、肠血流量均明显降低.伤后12.0 h内均呈持续下降趋势,至伤后24.0 h仍显著低于对照组(P＜0.05或P＜0.01).烫伤组大鼠伤后1.0 h,LVSP和±dp/dt max即明显下降;伤后3.0 h,SBP、DBP、MAP明显下降;伤后6.0 h所有心脏功能指标均降低,至伤后24.0 h仍低于对照组(P＜0.01).与对照组[(1.71±0.07)μg/L]比较,伤后0.5 h烫伤组大鼠血清cTnI[(2.22±0.08)μg/L]即明显升高,伤后12.0 h[(7.07±0.44)μg/L]达峰值,伤后24.0 h[(4.57±0.30)μg/L]仍保持在较高水平(P＜0.01);伤后3.0 h血清TBA及伤后1.0 h血清β2-MG、DAO开始明显升高,并超过对照组(P＜0.05或P＜0.01),至伤后12.0 h仍呈上升趋势.结论 严重烫伤后心肌损害在时间上明显早于其他脏器,且与其他脏器损害指标和血流量呈显著相关,提示"休克心"可能是严重烫伤后早期肝、肾、肠血流量减少和损害的启动因素之一,但还需深入研究以进一步证明.     

液体复苏加1-6-FDP对严重烧伤家兔心肌功能变化的研究

采用家兔25％Ⅲ度烫伤模型,分别于伤前、伤后即刻、伤后1、3、5、7 h 测定左心室内压峰值、左心室内压最大变化速率及血浆容量(不测伤后即刻值),并观察了液体复苏加1-6-FDP 对严重烧伤休克期家兔 LVSP、LV±dp/dt max 的影响,结果表明严重烧伤后心肌的收缩性和舒张性均立即受到抑制,并呈进行性减退,单纯的液体复苏并不能明显改善心肌的收缩性和舒张性;单用1-6-FDP 治疗可在伤后一定时间内对心功能有支持作用;而在液体复苏同时给予1-6-FDP 可使心肌的收缩性和舒张性得到明显改善,其与烧伤未治疗组和液体复苏组比较差异有非常显著性意义,提示在液体复苏的同时.应用1-6-FDP,可改善心肌功能,有利于休克的复苏。     

经颅高压电烧伤对大鼠肠系膜微血管白细胞流变行为的影响及乌司他丁干预作用

目的 了解经颅高压电烧伤对大鼠肠系膜微血管内白细胞流变行为的影响,以及乌司他丁(UTI)对其的干预作用.方法 将45只SD大鼠按随机数字表法分为假伤组、电伤组和治疗组,每组15只.电伤组和治疗组大鼠均用调压器及实验变压器制成高压电烧伤模型;假伤组大鼠接相同装置但不通电,致假伤.假伤组和电伤组伤后2 min内腹腔注射生理盐水2 mL,治疗组于伤后2 min内按2×104 U/kg腹腔注射UTI 2 mL.用布氏显微镜及微循环图像分析系统观测3组大鼠伤前15 min及伤后5 min、lh、2h、4h、8h肠系膜微血管内滚动白细胞数、白细胞滚动速度、白细胞黏附数、白细胞-内皮细胞接触时间(TLECT).对实验数据行t检验.结果 (1)微静脉滚动白细胞数:电伤组和治疗组大鼠伤后各时相点滚动白细胞数较伤前增多,伤后5 min分别剧增至(51.4±3 2)、(24.6±1 9)个/min,多于假伤组的(1 1±0 7)个/min(t值分别为59 28、44.99,P值均小于0.05);治疗组伤后各时相点滚动白细胞数均少于电伤组,伤后5 min组间比较,t=27.97,P ＜0.05.(2)微静脉白细胞滚动速度:电伤组和治疗组伤后各时相点白细胞滚动速度较伤前下降,伤后5 min最慢,分别为(90±9)、(175±13) μm/s,均慢于假伤组的(277±12) μm/s(t值分别为47 97、21.59,P值均小于0 05);治疗组伤后各时相点白细胞滚动速度均快于电伤组,伤后5 min组间比较,t=20.55,P＜0 05.(3)微静脉白细胞黏附数:电伤组和治疗组伤后各时相点白细胞黏附数较伤前增多,伤后5 min即达每100微米血管(23.27±3.20)、(5.80±1.61)个,均多于假伤组的每100微米血管0个(t值分别为28.16、13 95,P值均小于0.05);治疗组伤后各时相点白细胞黏附数少于电伤组,伤后5 min组间比较,t=18.89,P＜0.05.(4)微静脉TLECT:电伤组和治疗组伤后各时相点TLECT较伤前增高,伤后5 min即达(14.45±1.99)、( 3.66±0 96) s/min,均多于假伤组的0 s/min(t值分别为28.12、14 77,P值均小于0 05),治疗组伤后各时相点TLECT低于电伤组,伤后5 min组间比较,t=18.91,P＜0.05.(5)3组大鼠伤前及伤后微动脉、毛细血管血流中,均未见白细胞滚动或者贴壁黏附.结论 经颅高压电烧伤可导致大鼠肠系膜微静脉白细胞流变行为异常,UTI对此有明显改善作用.     

高张盐溶液与中分子右旋糖酐复苏烧伤休克对犬心肌功能的影响

采用含 Na~ 250mmol/L 的乳酸钠高张盐溶液与6%中分子右旋糖酐(HLD)复苏烧伤休克,与乳酸钠林格氐液(LR)比较,综合评价其复苏效果并探讨其部分机制。结果表明 HLD 组心脏指数(CI) 在伤后4、8、12、24h 均明显高于 LR 组(P<0.05)。HLD 组心肌收缩功能(dp/dtmax),心肌舒张功能(—dp/dt max)在伤后12、24h 也高于 LR 组(P<0.05)。HLD 组在伤后24h 的心肌 MDA 含量(1.74±0.28×10~(-2)mol/g 组织)明显低于 LR 组(3.23±0.56×10~(-2)mol/g 组织,P<0.05)。而其心肌 SOD 活力(157.49±32·23u/mg 组织)明显高于 LR 组(46.88±16.28u/mg,P<0.01)。提示:与 LR 复苏相比,HLD 复苏烧伤休克能明显改善心肌功能,并可持续到伤后24h。HLD 可能通过提高心肌组织 SOD 活力从而降低心肌组织脂质过氧化物含量,减轻脂质过氧化物对细胞膜的损伤,进而起到保护心肌、改善心肌功能的作用。     

Sevoflurane preserves endocardial blood flow during coronary ligation in dogs: comparison with adenosine

Background : Sevoflurane has been reported to attenuate ischaemia-induced changes of myocardial metabolism, but the mechanism is still unclear. We examined the effect of sevoflurane on regional myocardial blood flow (RMBF) in the ischaemic area and compared the flow with that in the presence of adenosine.
Method : Twenty-seven mongrel dogs were anaesthetized with fentanyl infused at the rate of 1μg.kg^-1.min^-1 throughout the experiment. Then they were divided into 4 groups; 0, 1, 2 MAC sevoflurane groups and adenosine group. Adenosine was infused into the left ventricle at a rate of 14.5 mg.kg^-1.h^-1. The left anterior descending coronary artery (LAD) was ligated for 3 min. RMBF in the endo- and epicardial layers were measured using coloured microspheres.
Results : Sevoflurane decreased both systolic and diastolic blood pressures and LV dp/dt max. Adenosine increased heart rate and coronary flow. The endocardial blood flow in 2 MAC sevoflurane was almost the same as that in the 0 MAC group. Adenosine significantly increased the myocardial blood flow. During 3-min ischaemia, endocardial blood flow in the ischaemic area under 2 MAC sevoflurane was essentially the same as those in 0 MAC and adenosine groups, though myocardial work in 2 MAC sevoflurane was lower compared with that of the other groups.
Conclusion : Preservation of endocardial blood flow related to the myocardial work during ischaemia occurred during 2 MAC sevoflurane. The decrease in LV dp/dt max induced by 2 MAC sevoflurane is one of the factors responsible for the preservation of the endocardial blood flow during ischaemia.     

Effects of hypocapnia on hemodynamics and myocardial metabolism in anesthetized dogs

The authors previously reported that hypocapnia increased myocardial oxygen demand under droperidol-fentanyl (D-F) anesthesia. In this study, we observed myocardial oxygen tension, hemodynamics, and coronary arterial-venous blood content differences of oxygen and lactate before and after hyperventilation in dogs with and without a narrowed coronary artery under halothane anesthesia. We studied the functional and metabolic responses of the heart to hypocapnia under halothane in comparison with D-F anesthesia. In the intact heart, heart rate, LV dp/dt max and myocardial energy demand (heart rate x systolic aortic pressure x LV dp/dt max), which increased during hypocapnia under D-F anesthesia, were unchanged during hypocapnia under halothane anesthesia. Aortic pressure and coronary flow were unchanged under both types of anesthesia. Though subendocardial oxygen tension decreased significantly, myocardial lactate extraction was unchanged under both types of anesthesia. In the heart with a constricted coronary artery, subendocardial oxygen tension and lactate extraction ratio decreased significantly during hypocapnia under both types of anesthesia. Myocardial lactate production was observed in six of eleven dogs in which myocardial energy demand increased under D-F anesthesia. Myocardial lactate production was observed in one dog under halothane anesthesia. Coronary arterial-venous blood oxygen content difference increased under D-F anesthesia, but not under halothane anesthesia. In summary, hypocapnia increased myocardial oxygen demand under D-F anesthesia but not under halothane anesthesia. In the intact heart under both types of anesthesia, hypocapnia deteriorated myocardial oxygen supply-demand relations, but the evidence of myocardial anaerobic metabolism was not observed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in systemic circulation and organ blood flow during induced total spinal block

Total spinal block with lidocaine was performed in adult mongrel dogs, and circulatory changes or changes in organ blood flow were investigated. Dogs were divided into group A (5.1 mg.kg-1) and group B (10.0 mg.kg-1) according to the dose of lidocaine. During total spinal block, HR (79% and 78%), MAP (64% and 69%), LV dp/dt max (58% and 49%) and CI (67% and 67%) decreased significantly compared with the control values in groups A and B respectively. However, SVR was unchanged. The circulatory change occurred more rapidly in group B. Organ blood flow was measured in group A. Blood flow was measured in four areas during total spinal block. It was significantly decreased at liver and slightly decreased at cerebral cortex and medullary substance. However, renal cortex blood flow was not altered.     

Evaluation of dopamine and dobutamine for use in circulatory depression associated with induced total spinal block

We carried out total spinal block (T.S.B.) in adult mongrel dogs with 0.5 ml.kg-1 of 2% lidocaine, and compared the effects of dopamine (DOA) and dobutamine (DOB) to correct the circulatory depression produced by T.S.B. HR, MAP, LV dp/dt max. and CI decreased significantly by T.S.B. under continuous infusion of 2.5 mcg.kg-1.min-1 of both DOA and DOB. During DOA infusion these circulatory values decreased significantly compared with those of control period, while during DOB infusion they were unchanged. MAP, LV dp/dt max. and CI decreased significantly by T.S.B. under 5 mcg.kg-1.min-1 of DOA infusion, while influence was hardly observed by T.S.B. under DOB infusion. From the results, it is concluded that DOB is more effective than DOA to correct the circulatory depression by T.S.B., and in order to correct it more than 5 mcg.kg-1.min-1 of DOA and approx. 2.5 mcg.kg-.min-1 of DOB are necessary.     

Kappa-opioid receptor antagonism improves recovery from myocardial stunning in chronically instrumented dogs

We tested the hypothesis that the selective kappa-opioid receptor antagonist nor-binaltorphimine (nor-BNI) improves recovery from myocardial stunning. Ten dogs were chronically instrumented for measurement of heart rate, left atrial, aortic and left ventricular pressure (LVP), and the maximum rate of LVP increase (LV dP/dt(max)) and decrease (LV dP/dt(max)), coronary blood flow velocity and myocardial wall-thickening fraction. Regional myocardial blood flow was determined with fluorescent microspheres. Catecholamine plasma levels were measured by high-performance liquid chromatography, and beta-endorphin and dynorphin plasma levels by radioimmunoassay. An occluder around the left anterior descending artery (LAD) allowed induction of a reversible LAD-ischemia. Animals underwent two experiments in a randomized crossover fashion on separate days: (a) 10 min LAD-occlusion (control experiment), (b) second ischemic episode 24 h after nor-BNI (2.5 mg/kg IV) (intervention). Dogs receiving nor-BNI showed an increase in wall-thickening fraction, LV dP/dt(max) and LV dP/dt(min) before ischemia and during the whole reperfusion (P < 0.05 versus control experiment). After nor-BNI pretreatment, dynorphin levels increased after induction of ischemia to a peak level of 15.1 +/- 3.6 pg/mL (P < 0.05 versus control experiment). The increase in plasma beta-endorphin during ischemia and early reperfusion was attenuated after nor-BNI. Compared with the control experiment, nor-BNI left global hemodynamics, regional myocardial blood flow, and catecholamine levels unchanged. In conclusion, nor-BNI improves recovery from myocardial stunning after regional myocardial ischemia in chronically instrumented dogs.     

大鼠烧伤后早期心肌组织核因子κB活化对细胞因子表达及心肌功能的影响

目的观察核因子(NF)κB活化在大鼠烧伤后早期心肌组织表达肿瘤坏死因子(TNF)α及心肌功能损害中的作用,进一步阐明烧伤后早期心肌功能损害的发生机制。方法将170只Wistar大鼠随机分为对照组(20只)、烧伤组(90只)、吡咯烷二硫代氨基甲酸盐(PDTC)组(60只)。后两组大鼠均于背部造成35％TBSAⅢ度烧伤后,立即腹腔注射等渗盐水,且PDTC组同时皮下注射PDTC 250 mg／kg。对照组除不烧伤外,其余处理同烧伤组。伤后3、6、12、24 h采用八导生理记录仪记录左心室收缩压(LVSP),左心室舒张末期压(LVEDP),室内压最大上升、下降速率( dp／dtmax、-dp／dtmax);逆转录聚合酶链反应和原位杂交法观察心肌组织TNF-αmRNA的表达。伤后1、3、6、12、24 h采用凝胶电泳迁移率变动分析法检测心肌组织NF-κB活性,以积分吸光度(A)值表示。对照组作相同检测。结果伤后3～24 h烧伤组大鼠LVSP、±dp／dtmax低于对照组(P<0．01),而LVEDP高于对照组(P<0．01)。伤后3 h烧伤组大鼠心肌组织TNF-αmRNA表达明显高于对照组, 6 h达峰值(P<0．01),它在心肌细胞中表达尤为明显。伤后1 h烧伤组大鼠心肌组织NF-κB活性迅速升高[积分A值为(20．3±3．4)×104],明显高于对照组积分A值(2．2±0．4)×104,3 h时达峰值,24 h时仍高于对照组(P<0．01)。与烧伤组比较,PDTC组上述指标有较明显的改善(P< 0．01)。结论大鼠严重烧伤后心肌组织NF-κB被活化,使其表达和释放促炎细胞因子,在心肌功能损害发生过程中起重要作用。