快速补液对烧伤延迟复苏并发心肌损害的防治

目的　探讨快速补液对烧伤延迟复苏血液流变学特性和心肌局部血流量的改善作用。方法　采用大鼠 30 %TBSA烧伤模型 ,动态观察烧伤延迟复苏快速补液和均匀补液后 ,大鼠血液流变学特性和心肌局部血流量及血浆中心肌肌球蛋白轻链 - 1浓度的改变。结果　伤后 1h ,全血粘度即显著升高 ,6h达高峰 ,补液后 ,全血粘度均降低 ,快速补液组的降低幅度显著大于均匀补液组 ,血浆粘度、红细胞比积、血浆纤维蛋白原含量和红细胞膜带电性质等血液流变学参数也发生改变 ;心肌局部血流量和血浆中心肌肌球蛋白轻链 - 1的浓度也相应发生改变 ,其变化趋势与全血粘度改变密切相关。结论　烧伤延迟复苏快速补液能够改善血液流变学特性 ,提高心肌局部血液灌注量 ,使心肌损害程度减轻 ,因此 ,对烧伤延迟复苏是有益的     

快速补液对大鼠烧伤延迟复苏心肌血管内皮细胞的保护作用

目的　探讨快速补液对烧伤延迟复苏大鼠心肌微血管通透性、心肌局部内皮素 1(ET 1)和一氧化氮等细胞因子产生和分泌的改善及其心肌损害的保护作用。方法　采用大鼠 3 0 %TBSAⅢ度烧伤模型 ,动态观察烧伤延迟复苏快速补液和均匀补液后 ,大鼠心肌微血管通透性和心肌局部内皮素 1和一氧化氮等细胞因子含量及血浆中心肌肌球蛋白轻链 1浓度的改变。结果　伤后 1h ,心肌微血管通透性、心肌局部内皮素 1和一氧化氮含量即显著升高 ,6h达高峰。补液后 ,微血管通透性、心肌局部内皮素 1和一氧化氮含量均明显降低 ,快速补液组的心肌微血管通透性和心肌局部内皮素 1含量的降低幅度显著大于均匀补液组。而一氧化氮含量则两组间无明显差异。血浆中心肌肌球蛋白轻链 1的浓度变化与心肌局部内皮素 1含量改变呈正相关。结论　烧伤延迟复苏快速补液能够改善心肌血管内皮细胞功能 ,减轻心肌受损程度 ,因此 ,对烧伤延迟复苏是有益的。     

快速补液对烧伤延迟复苏的心肌保护作用

目的 :探讨快速补液对大鼠烧伤延迟复苏心肌局部肾素—血管紧张素系统的影响及其心肌保护作用。方法 :采用大鼠 30 %TBSAⅢ度烧伤模型 ,分为快速补液组和均匀补液组 ,测定伤前和伤后1、3、6、1 2、2 4、4 8h心肌组织中血管紧张素转换酶 (ACE)的活性 ,血管紧张素 -Ⅱ (AⅡ )的含量及其血浆中心肌肌球蛋白轻链 -1 (CMLC -1 )的浓度。结果 :伤后 1h ,两组鼠心肌ACE活性由 ( 1 .2 1± 0 .54)nmol·mgpro- 1·min- 1升高至 ( 1 .91± 0 .71 )nmol·mgpro- 1·min- 1,同时 ,AⅡ含量及CMLC -1浓度也显著升高 ,伤后 6h均达高峰。补液复苏后三者均逐渐下降。快速补液组的下降幅度显著大于均匀补液组。三者变化趋势一致 ,呈明显正相关。结论 :烧伤延迟复苏快速补液能够降低心肌组织肾素—血管紧张素系统活性 ,减少心肌局部AⅡ的生成 ,从而对心肌损害有一定的保护作用     

快速补液对烧伤延迟复苏并发心肌损害的保护作用

制作大鼠30%TBSAⅢ度烧伤模型,动态观察了烧伤延迟复苏快速补液和均匀补液前后血浆中CMLC-1浓度变化及伤后24h的病死率。结果,伤后大鼠血浆中CMLC-1浓度为(924±315)μg/L,伤后1h即显著升高至(18198±6692)μg/L(P<005),6h达最高峰(35941±13219)μg/L。补液后,伤后12、24、48h,快速补液组的血浆中CMLC-1浓度下降幅度显著大于均匀补液组(P<005)。24h的病死率,快速补液组为1466%,明显低于均匀补组的4666%。结果提示,烧伤延迟复苏快速补液能迅速补充循环血容量,在一定程度上遏制心肌继续缺血缺氧性损害,减轻心肌受损程度,对于临床延迟复苏的大面积烧伤病人救治具有重要意义。     

切痂对烧伤延迟复苏大鼠血液动力学的影响

目的探讨切痂结合快速补液对烧伤延迟复苏大鼠血液动力学的影响。方法30%TBSAⅢ度烧伤大鼠于伤后6h开始快速补液2h后,行切痂植皮术。测定其LVSP、LVEDP、AOSP、AODP、MAP、±dp/dtmaxt等血液动力学指标,并观察其伤后48h内的病死率。结果伤后1h,各项血液动力学指标即明显下降,于伤后6h,降至最低点。快速补液后,各项指标均有明显回升。伤后12h,切痂手术对血液动力学指标影响不明显(P≥0.05)。至伤后24h,切痂手术对各项血液动力学指标有明显的改善作用(P≤0.05)。于伤后48h,两组差异不明显(P≥0.05)。同时,切痂组的大鼠48h内病死率高于非切痂组。结论切痂对烧伤延迟复苏大鼠血液动力学有一定的改善作用,但其临床可行性有待于进一步探讨。     

严重烧伤大鼠中性粒细胞L-选择素mRNA的表达

目的 研究严重烧伤后大鼠中性粒细胞(PMN)L-选择素mRNA的表达。方法 30％Ⅲ度烧伤大鼠,伤后随机分为早期复苏(BE)组和延迟复苏(BD)组。伤前、伤后1、3、6、9h用持续灌注法收集血细胞,分离PMN,抽提总RNA,用RT-PCR法测定PMNL-选择素mRNA表达。结果BE组在烧伤后1h L-选择素mRNA表达增高,两组在伤后6h、9h的表达均再次增高。结论 烧伤后L-选择素mRNA的表达存在动态变化,早期增高可能与烧伤后的休克状态有关,后期增高则与L-选择素参与烧伤后细胞的信号传导有关。     

烧伤延迟快速复苏补液治疗

目的:探讨烧伤延迟快速复苏补液治疗的作用。方法:通过82例烧伤面积20%～80%,程度Ⅱ～Ⅲ度,因延迟复苏导致休克的患者,进行快速补液复苏。观察休克期补液量、尿量、脉搏、呼吸等指标的变化。结果:快速补液后,各观测指标均获改善,休克得到快速纠正。结论:快速补液可以迅速纠正休克。     

中西医结合抢救烧伤休克

大面积烧伤病人延迟复苏 ,给机体留下了许多隐患 ,已被许多学者证实。怎样快速抢救休克病人 ,分秒必争的纠正由于灌注不良给组织选成缺血缺氧 ,是救治大面积烧伤病人成功的重要起始与基础。现尚无有效的抗渗治疗措施 ,西医是以补液为治疗休克的主要手段。本文用中医辅助西医抢救延迟复苏病人 6 0例 ,现报告如下。1　临床资料　　 6 0例休克烧伤病人均为我科住院重度 ,特重度病人。本组男 4 9人 ,女 11人 ,年龄 16～ 2 4岁 ,平均 2 6岁。伤后 2ｈ以上入院 ,呈休克状态 ,最晚入院的是伤后 16ｈ ,入院后立即抗休克治疗。按西医抢救休克常规治疗…     

乌司他丁对严重烧伤大鼠延迟复苏的影响

目的:探讨乌司他丁对严重烧伤延迟复苏的作用。方法:18只SD大鼠随机分成假烫组(S组)、烫伤延迟复苏组(B组)和烫伤延迟复苏+乌司他丁组(U组)。U组在烫伤后延迟复苏的同时,于伤后6h、12h分别予乌司他丁20 000 U·kg~(-1)腹腔内注射。伤后24h处死大鼠,测定伤后24h肺、肝干湿重比,测定血清白细胞介素8(IL-8)、肿瘤坏死因子α(TNF-α)、乳酸值和血浆丙二醛含量。结果:B组IL-8、TNF-α、乳酸和丙二醛含量均高于S组,肺、肝干湿重比低于S组(P<0.01),U组大鼠肺、肝干湿重比为0.229 4±s 0.001 2、0.275±0.008,血清IL-8和TNF-α值为(226±16)ng·L~(-1)、(514±24)ng·L~(-1),血清乳酸与血浆丙二醛含量分别为(4.5±0.8)mmol·L~(-1)、(2.52±0.27)nmol·L~(-1),均比B组有明显改善(P<0.05或P<0.01)。结论:乌司他丁可减轻严重烧伤延迟复苏对机体的损伤。     

牛磺酸对烫伤大鼠血浆及心肌组织肿瘤坏死因子和血管紧张素Ⅱ含量的影响

目的 :观察牛磺酸对大鼠严重烧伤后心肌损害的影响。方法 :用健康Wistar大鼠 ,随机分为对照组、烧伤组 (造成 30 %TBSAⅢ度烫伤 )和治疗组 (烧伤后腹腔注射牛磺酸 ,剂量 4 0 0mg·kg-1体重 )。于伤后 1、3、6、12和 2 4h检测血浆TNF α、AngⅡ和TnT含量与心肌中TNF α、AngⅡ含量。结果 :烧伤大鼠烧伤后 3h血浆cTnT呈显著升高 ,12h达峰值 ,2 4h显著高于对照组 ;烫伤后 6h血浆和心肌组织TNF α含量显著高于对照组 (P <0 .0 1) ,12h达峰值 ;伤后1h血浆AngⅡ含量呈显著升高 ,伤后 2 4h血浆及心肌中AngⅡ高于对照组 ;牛磺酸治疗组血浆cTnT、TNF α和AngⅡ水平较烧伤组均有显著性降低。血浆TNF α、AngⅡ含量与血浆cTnT变化密切相关。结论 :牛磺酸对严重烫伤后心肌损伤有较好的保护作用。     

Coronary collateral blood flow in acute myocardial ischemia is not increased by dihydropyridine-induced coronary vasodilatation

The effect of two dihydropyridine derivatives, nifedipine and felodipine, on myocardial blood flow distribution 1 h after ligation of the left anterior descending coronary artery (LAD) was studied in open-chest dogs by means of radioactive microspheres. The myocardium normally perfused from the LAD was first labeled with 125I-labeled microspheres injected directly into the LAD before ligation. Microspheres used for blood flow measurements were given in the left atrium. An intravenous infusion rate of 0.3 nmol/kg/min felodipine slightly depressed mean aortic blood pressure (approximately 5 mm Hg) and decreased coronary vascular resistance in normal myocardium. Nifedipine, at three times the dose of felodipine, had a comparable hypotensive effect, but the decrease in coronary vascular resistance was not statistically significant. The two dihydropyridines were also compared in a dose range that was four times higher. The mean arterial blood pressure reduction (approximately 30% for both drugs) was counterbalanced by inflation of an intraaortic balloon to avoid a drastic decrease in afterload and coronary perfusion pressure. Under these circumstances, felodipine and nifedipine decreased coronary vascular resistance and increased blood flow to nonischemic myocardium comparably. However, in severely ischemic, truly collateral-dependent myocardium without admixture of interdigitating healthy myocardium, the blood flow was unaffected after administration of both felodipine and nifedipine. Although felodipine was three times more potent than nifedipine with regard to vasodilatation in the normal myocardium, the difference in vascular selectivity between the two agents did not influence the effect on the "true" collateral blood flow in acute myocardial ischemia.     

The calcium antagonist nisoldipine improves the functional recovery of reperfused myocardium only when given before ischemia.

It is unclear whether the protective effects of calcium antagonists on reperfused myocardium are secondary to increased blood flow during ischemia (anti-ischemic action) or reperfusion (Gregg phenomenon), or are mediated through altered calcium kinetics in ischemic or reperfused myocardium. To study the effect of the calcium antagonist nisoldipine on the functional recovery of stunned myocardium, 32 enflurane-anesthetized dogs were subjected to 15 min of occlusion of the left circumflex coronary artery and subsequent 4 h of reperfusion. Eight dogs served as placebo controls (group I), and eight dogs received nisoldipine (5 micrograms/kg i.v.) before occlusion (group II), eight dogs at 10 min of occlusion (group III), and eight dogs at 4 min of reperfusion (group IV). The mean aortic pressure was kept constant with an intra-aortic balloon, and the heart rate did not change. In group I, posterior systolic wall thickening (WT, sonomicrometry) decreased from 18.3 +/- 2.4% (mean +/- SD) during control conditions to -3.0 +/- 2.0% at 13 min of occlusion. At 10 min of reperfusion, WT was 1.7 +/- 3.9% and did not recover further (-1.2 +/- 3.7% at 4 h of reperfusion). Posterior transmural blood flow (BF, colored microspheres) decreased from 1.42 +/- 0.43 ml/min/g during control conditions to 0.26 +/- 0.08 ml/min/g at 13 min of occlusion. BF was 2.07 +/- 0.93 ml/min/g at 10 min and 0.95 +/- 0.31 ml/min/g at 4 h of reperfusion. In groups III and IV, the WT and BF were not different from those in group I throughout the experimental protocol. In group II, however, the WT, although similar to the WT of group I before and during ischemia, recovered from 2.7 +/- 4.3% at 10 min to 11.8 +/- 6.0% at 4 h of reperfusion (p less than 0.05 vs. groups I, III, and IV). The BF in group II decreased from 2.52 +/- 0.66 ml/min/g after administration of nisoldipine to 0.22 +/- 0.14 ml/min g at 13 min of occlusion. The BF was 1.31 +/- 0.51 ml/min/g at 10 min and 1.33 +/- 0.43 ml/min/g at 4 h of reperfusion. Nisoldipine exerts no beneficial effect when given immediately before or after the onset of reperfusion. The improved functional recovery of reperfused myocardium in dogs pretreated with nisoldipine cannot be attributed to an increased regional myocardial blood flow during ischemia or reperfusion. The better myocardial recovery, therefore, appears to be related to an attenuated myocardial calcium overload during the first few minutes of ischemia.     

Calcium antagonist protects the myocardium from reperfusion injury by interfering with mechanisms directly related to reperfusion: an experimental study with the ultrashort-acting calcium antagonist clevidipine

To test the hypothesis that calcium antagonists protect the myocardium from reperfusion-induced damage by local myocardial mechanisms just at the time of reperfusion, the myocardioprotective effects of the dihydropyridine clevidipine were investigated, taking advantage of its ultrashort-acting effect. Pigs were subjected to 45 min of myocardial ischemia by occlusion of the left anterior descending coronary artery followed by 4 h of reperfusion. Either clevidipine (0.3 nmol/kg/min, n = 6) or the corresponding amount of vehicle (n = 6) was administered to the ischemic myocardium by retrograde coronary venous infusion over a 30-min period starting 10 min before reperfusion. Hemodynamic variables (heart rate, left ventricular systolic and end-diastolic pressure, max dP/dt, and mean arterial blood pressure) as well as coronary blood flow were measured throughout the experiment. At the end of reperfusion, the area at risk (percentage of left ventricle) was determined by infusion of Evans blue into the left atrium, and the infarct size, by triphenyl tetrazolium chloride (TTC) staining. The plasma level of endothelin-like immunoreactivity (ET-LI) was analyzed in blood from the aorta and the anterior coronary vein before ischemia and at different times during reperfusion. The area at risk was similar in the vehicle and the clevidipine groups. The infarct size, expressed as a percentage of the area at risk, was 80 +/- 9.2 in the vehicle group, whereas it was significantly reduced to 51 +/- 9.2% in the clevidipine group (p < 0.01). Clevidipine did not influence any of the hemodynamic variables measured throughout the study. A nonsignificant trend toward decreased total ET-LI overflow during 4-h reperfusion was observed in the clevidipine-treated pigs compared with vehicle-treated ones (5.3 +/- 1.4 vs. 7.1 +/- 3.4 pmol). These results demonstrate that, in this model of ischemia/reperfusion-induced myocardial infarction, clevidipine reduced the damage to the myocardium when given in association with reperfusion. The local administration of the compound together with its short blood half-life shows that clevidipine reduces reperfusion-induced damage by local mechanisms within the ischemic tissue rather than by peripheral mechanisms.     

Effects of intracoronary nifedipine on blood flow and segment shortening in normal and ischemic myocardium: potentiation by ischemia of the negative inotropic effect

The effects of intracoronary nifedipine on myocardial blood flow (flow probe or microspheres) and regional function (ultrasonic crystals in subendocardium) were examined both in the normal myocardium and in myocardium made ischemic by a partial coronary occlusion in the open-chest anesthetized dog. In a first group of experiments (n = 7), without ischemia, nifedipine infused into the left anterior descending coronary artery (LAD) during a 1-min period (doses 0.75-8 nmol/kg body weight) decreased coronary vascular resistance with a maximal effect at 4 nmol/kg. Systolic segment shortening was decreased from 10.7 to 7.4% (p less than 0.05) by 6 nmol/kg, whereas lower doses had no effect. In a second experimental group (n = 7), a partial LAD occlusion was applied to decrease subendocardial segment shortening by about 50%. Nifedipine (2 nmol/kg) injected into the partially occluded LAD induced a marked segmental bulging during early systole and systolic segment shortening was eliminated (from 4.2 to -3.1%, p less than 0.02) in the LAD-dependent myocardium. Concomitant with the decreased regional function, nifedipine caused a transmural redistribution of myocardial blood flow in the ischemic area, the endocardial/epicardial blood flow ratio increasing from 0.49 to 0.61 (p less than 0.02). It is concluded that ischemia potentiates the direct depressant effect of nifedipine on myocardial regional function.     

生脉输液对麻醉犬血流动力学及心肌耗氧量的影响

目的研究生脉输液对麻醉犬血流动力学及心肌耗氧量的影响。方法将杂种犬36只,随机分为6组(每组6只):对照组、阳性药组(硝酸甘油注射液组和生脉注射液组)、生脉输液高、中、低三个剂量组。人工呼吸下开胸,观察用药前后不同时间点麻醉犬的冠脉流量(CBF)、心输出量(CO)、冠脉阻力(CAVR)、总外周阻力(TPVR)、心搏出量(SV)、心搏指数(SI)、心脏指数(CI)、左室作功(LVSW)、心肌血流量(MBF)、心肌耗氧指数(MOCI)、耗氧量(VO2)、心肌氧利用率(MOUR)等指标的变化。结果与对照组比较,生脉输液(200,100 mg生药.kg-1)能显著增加麻醉犬冠状动脉和主动脉的血流量、增加心肌血流量,降低总外周血管阻力和冠状动脉阻力,提高心搏出量和心肌氧利用率。结论生脉输液对麻醉犬血流动力学参数有改善作用,具有良好的抗心肌缺血作用。