Treatment of uncontrolled hemorrhagic shock with hypertonic saline solution

Hypertonic saline solution (HTS) treatment of uncontrolled hemorrhagic shock (UCHS) induced by incision of three major branches of the ileocolic artery, leading to free intra-abdominal bleeding, was studied in rats. The rats were divided into two groups. In group 1, the abdominal wall was closed immediately after induction of hemorrhage and the rats were divided into six subgroups--1a, five untreated; 1b, 14 treated with 5 milliliters per kilogram of sodium chloride 7.5 per cent (HTS) after five minutes; 1c, eight had HTS infused after 15 minutes; 1d, nine had HTS infused after 30 minutes; 1e, nine had HTS infused after 60 minutes, and 1f, nine had HTS infused after 120 minutes. In rats in group 2, the abdominal wall was kept open during HTS therapy and bleeding was estimated by the amount of sponges used to absorb shed blood. These rats were also divided into six subgroups--2a, five untreated; 2b, nine had HTS infused after five minutes; 2c, six had HTS infused after 15 minutes; 2d, six had HTS infused after 30 minutes; 2e, eight had HTS infused after 60 minutes, and 2f, six had HTS infused after 120 minutes. UCHS in group 1 was followed by a fall in the mean arterial pressure (MAP) from 99 to 46 torr (p less than 0.001) in five minutes and a gradual rise to 63 torr (p less than 0.01) after 30 minutes, with a survival rate of 80 per cent. HTS infusion five minutes after hemorrhage was followed by a further fall in MAP to 37 torr (p less than 0.01) after 30 minutes and a mortality rate of 85.7 per cent (p less than 0.01). HTS treatment after 15, 30, 60 and 120 minutes also led to a further fall in MAP and increased mortality. In group 2, the hemodynamic response to intra-abdominal vessel injury in untreated rats was similar to that of those in group 1 and the amount of sponges used to absorb shed blood was 2.4. After five, 60 and 120 minutes of HTS treatment, the hemodynamic response was similar to that in group 1. Five and one-half (p less than 0.01), 3.5 and 3.0 sponges, respectively, were used to absorb shed blood.(ABSTRACT TRUNCATED AT 400 WORDS)     

限制性液体复苏孕兔失血性休克对代谢产物变化的影响

目的探讨限制性输液复苏孕兔失血性休克对机体代谢终产物的变化的影响。方法建立孕兔失血性休克模型,采取限制性输液(LVR)和传统输液方法(AFR)分别复苏失血性休克孕兔,比较不同组别和不同时间点乳酸(LA)、碱缺失(BD)的变化规律和孕兔的生存情况。结果①急性失血后血浆LA水平成倍增加,非控出血期继续升高,止血控制期逐步下降,LVR组与AFR组比较,第90分钟,P0.05;第4小时,P0.01;第8小时LVR组血浆LA水平已完全恢复正常,而AFR组仍高于正常值;②急性失血后血浆BD水平成倍增加,非控出血期继续升高,止血控制期逐步下降,LVR组与AFR组比较,第180分钟,P0.05;第4小时,P0.05;第8小时LVR组血浆BD水平已完全恢复正常,而AFR组仍高于正常值;③复苏后24h,AFR组有1例孕兔死亡,LVR组无孕兔死亡;复苏后48h及72h,AFR组有2例孕兔死亡,LVR组有1例孕兔死亡。结论休克发生后,机体代谢产物LA、BD血浆水平均明显升高,限制性输液能增强机体有氧代谢,利于体内LA等代谢产物的清除,同时还改善失血性休克孕兔BD状况,减轻酸中毒反应,增强复苏效果,减少SIRS的发生,提高孕兔生存率。     

限制性输液复苏孕兔失血性休克对体液因子变化的影响

目的:探讨限制性输液复苏孕兔失血性休克时,机体内皮素(ET)、血管活性肠肽(VIP)的变化规律及对全身炎症反应综合征(SIRS)发生、发展的影响。方法:建立孕兔失血性休克模型,分别用限制性输液和传统输液方法复苏失血性休克孕兔,比较了两组于不同时间点ET、VIP的含量。结果:(1)急性失血后VIP血清浓度明显升高,经输液处理后血清VIP浓度开始下降,限制性输液组下降明显,与传统输液组比较,第3h,4h和8h,差异有统计学意义(P<0.05);(2)急性失血后ET血清浓度明显升高,经输液处理后血清ET浓度开始下降,限制性输液组下降明显,与传统输液组比较,第3h,4h和8h,差异有统计学意义(P<0.05)。结论:休克发生后,参与或加剧机体发病的体液因子ET、VIP循环水平均明显升高,限制性输液能降低循环ET、VIP水平,减少组织损伤和休克恶化程度,有利于机体促炎-抗炎介质平衡,有效阻断了SIRS的发生和发展。     

Infusion of small volume of 7.5 per cent sodium chloride in 6.0 per cent dextran 70 for the treatment of uncontrolled hemorrhagic shock

The effect of a solution of 7.5 per cent sodium chloride in 6.0 percent dextran 70 was studied in a rat model of uncontrolled hemorrhagic shock induced by partial resection of the tail of the rat. Fifty rats were randomly assorted into five groups of ten rats each. In group 1, uncontrolled hemorrhagic shock was induced by sharp resection of 10 per cent of the terminal portion of the tail of the rat. In group 2, uncontrolled hemorrhagic shock was treated with 5 milliliters per kilogram of 0.9 per cent sodium chloride. In group 3, uncontrolled hemorrhagic shock was treated with 5 milliliters per kilogram of 6 per cent dextran 70. In group 4, rats were treated with 5 milliliters per kilogram of 7.5 per cent sodium chloride, and in group 5, 5 milliliters per kilogram of 7.5 per cent sodium chloride in 6.0 per cent dextran 70 were infused. During the first five minutes, bleeding in rats in group 1 was 3.0 +/- 0.4 milliliters and the mean arterial pressure fell from 105 +/- 5 to 73 +/- 7 torr (p less than 0.001). In group 4, bleeding at 15, 30 and 60 minutes was 1.9 +/- 0.3 milliliters (p less than 0.02), 2.0 +/- 0.7 milliliters (p less than 0.04) and 2.4 +/- 1.1 milliliters (p less than 0.02), and in group 5, 2.5 +/- 0.6 milliliters (p less than 0.02), 2.2 +/- 0.6 milliliters (p less than 0.04) and 3.1 +/- 0.8 milliliters (p less than 0.04), respectively, compared with bleeding in group 1. Increased bleeding was followed by a fall in mean arterial pressure in groups 4 and 5 with a 60 per cent mortality rate (p less than 0.01) in both groups and respective, mean survival times of 135 +/- 29 and 144 +/- 26 minutes, which were significantly increased compared with group 1 (p less than 0.01 for both). The intravenous infusion of 6 per cent dextran 70 alone in group 3 resulted in delayed bleeding of 1.23 +/- 0.6 milliliters (p less than 0.04) after 180 minutes. It is concluded that infusions of small volume of 7.5 per cent sodium chloride or 7.5 per cent sodium chloride in 6.0 per cent dextran 70 solutions in rats in a state of uncontrolled hemorrhagic shock led to increased bleeding, decrease in mean arterial pressure and increased mortality.     

The normal electron histochemistry and the effect of hemorrhagic shock on the pulmonary surfactant system.

An electron histochemical study was carried out on eight baboons to localize the phospholipid constituent of pulmonary surfactant in the normal state and after hemorrhagic shock. In the normal state, phospholipid was seen as a continuous layer lining the alveolar spaces. Phospholipid also was seen in the inclusion bodies of the granular pneumocytes, suggesting these cells as the site of production of surfactant. After hemorrhagic shock, the previously continuous phospholipid layer lining the alveolar spaces became totally fragmented. In addition, increased numbers of phospholipid particles were seen within the pulmonary interstitium. The results of this study suggest that the pulmonary surfactant system may be impaired after hemorrhagic shock.     

The bacterial factor in hemorrhagic shock.

After a century of research on hemorrhagic shock, traumatic shock, septic shock and burn shock, it is known that all of the states lead to cellular injury and death through the same common pathways. Methods for blocking these pathways may ameliorate all of these conditions.     

Hemodynamic, hematologic and eicosanoid mediated mechanisms in 7.5 percent sodium chloride treatment of uncontrolled hemorrhagic shock.

Hypertonic saline solution (HTS) (7.5 percent sodium chloride [NaCl]) treatment (5 milliliters per kilogram) of rats subjected to uncontrolled hemorrhagic shock (n = 7) caused an initial partial recovery of blood pressure (+38 +/- 5 percent, p<0.05) and cardiac index (+48 +/- 6 percent, p<0.01) followed by increased bleeding (+53 +/- 5 percent versus rats treated with 0.9 percent NaCl, p<0.05), secondary shock (mean arterial pressure [MAP] 23 +/- 7 millimeters of mercury, p<0.01) and decreased survival (-54 +/- 15 minutes versus control, p<0.05). The increased blood loss resulted from: 1, increased vascular pressure and vasodilatation (total peripheral resistance index -27 +/- 5 percent, p<0.05), as initial bleeding occurred when MAP and cardiac index are increased compared with the control group (+88 +/- 10 percent, p<0.05 and +82 +/- 7 percent, p<0.01, respectively) and as the concomitant infusion of angiotensin II, a potent vasoconstrictor, delayed the HTS-induced bleeding (resumed at 60 minutes), and 2, a defect in platelet aggregation reflected by decreased adenosine diphosphate (ADP)-induced maximal aggregation (-79 percent versus rats treated with 0.9 percent NaCl, p<0.05) and increased EC50 of ADP (+159 percent, p<0.05). These hemodynamic and hematologic responses might be mediated at least in part by prostacyclin, a vasodilator and antiplatelet aggregator, as HTS-treated rats markedly elevated the 6-keto-PGF1 alpha per thromboxane B2 ratio (+140 +/- 12 percent, p<0.01) and pretreatment with indomethacin decreased blood loss and improved MAP and survival. These data point out potential untoward hemodynamic and hematologic consequences of HTS treatment in traumatic injury in which control of bleeding cannot be confirmed.     

限制性输液对失血性休克孕兔微循环灌注的影响

目的 探讨限制性输液对失血性休克孕兔微循环灌注的影响.方法 选择妊娠15～25 d的新西兰孕兔30只分为3组:(1)传统复苏组(NS组):院前复苏期开始接受大量的生理盐水及复方氯化钠液快速输注,以维持平均动脉压在80 mm Hg(1 mm Hg=0.133 kPa)左右;(2)限制性输液复苏组(NH组):院前复苏期开始接受小量生理盐水及复方氯化钠液输注,以维持平均动脉压在60 mm Hg左右;(3)高渗高胶限制性输液复苏组(HHH组):院前复苏期开始输注10%羟乙基淀粉注射液±7.5%氯化钠+生理盐水及复方氯化钠液,以维持平均动脉压在60 mm Hg左右.制作各组孕兔失血性休克模型,实验开始后分为基础期(0 min)、休克期(0～30 min)、院前复苏期(30～90 min)及院内复苏期(90～180 min).监测指标:(1)应用微循环检测仪连续监测耳窗微动脉和微静脉直径;(2)检测各期功能性毛细血管密度(FCD),FCD为开放的毛细血管相对于基础期百分比;(3)应用全自动血气分析仪检测孕兔氧分压(PO2)、二氧化碳分压(PCO2)、pH值、剩余碱(BE)的水平.结果(1)微动脉和微静脉直径:各组孕兔基础期微动脉直径分别比较,差异有统计学意义(P＞0.05).NS组、NH组及HHH组休克期微动脉直径分别为(50.8±5.6)、(47.6±3.7)及(51.3±2.4)μm,各组间比较差异无统计学意义(P＞0.05),NS组、NH组及HHH组院前复苏期及院内复苏期微动脉直径分别为(52.8±4.9)及(56.0±3.8)、(61.3±2.9)及(65.4±3.2)、(67.0±4.1)及(74.1 ±4.8)μm,各组间比较,差异均有统计学意义(P＜0.05);NS组、NH组及HHH组休克期微静脉直径分别为(79.6±7.0)、(75.3±5.3)及(76.2±5.8)μm,各组间比较差异无统计学意义(P＞0.05),NS组、NH组及HHH组院前复苏期及院内复苏期微静脉直径分别为(81.1 ±6.7)及(84.4±6.0)、(82.8±3.3)及(85.4±4.3)、(86.9±5.8)及(89.4±6.8)μm,各组间比较,差异均无统计学意义(P＞0.05).(2)FCD检测:各组孕兔基础期FCD均为100%.NS组、NH组及HHH组休克期FCD分别为(39.8±6.8)%、(43.9±4.0)%及(44.0±4.8)%,各组间比较,差异均无统计学意义(P＞0.05);NS组、NH组及HHH组院前复苏期及院内复苏期FCD分别为(54.5±7.3)%及(59.7±4.8)%、(63.1±5.8)%及(70.3±5.6)%、(80.5±6.9)%及(91.7±4.7)%,组间比较,差异均有统计学意义(P＜0.05).(3)血气分析结果:各组孕兔基础期血气分析结果均在正常范围.各组孕兔休克期均出现代偿性过度呼吸,表现为血PCO2水平下降和血PO2水平上升;NH组及HHH组孕兔院内复苏期血PCO2与NS组比较,差异无统计学意义(P＞0.05);NH组及HHH组孕兔院内复苏期血PO2水平与NS组比较,差异有统计学意义(P＜0.05).各组孕兔休克期均出现了代谢性酸中毒,表现为血pH及BE水平下降;各组孕兔在院前复苏期pH及BE水平逐渐回升,但在院内复苏期仍未达到基础期水平;NH组及HHH组孕兔院内复苏期血pH及BE水平与NS组比较,差异有统计学意义(P＜0.05).(4)各组孕兔生存时间分别是HHH组(3.6±0.3)d、NH组(3.0±0.3)d、NS组(2.1±0.2)d,NH组及HHH组孕兔生存时间长于NS组,两者比较,差异有统计学意义(P＜0.05).各组孕兔院内复苏期FCD水平与生存时间呈明显正相关(r=0.655,P=0.000).结论 (1)限制性输液较之传统性输液,对失血性休克孕兔微循环有良好的改善作用,并能增加FCD数目,减轻代谢性酸中毒,提高孕兔生存率.(2)高张高胶复苏液较之等渗晶体复苏液能较明显地改善失血性休克孕兔微循环,但未能明显提高孕兔生存率,因此,院前复苏液体的应用种类尚需进一步深入研究.     

Plasma volume, electrolyte, and coagulation factor changes following intra-amniotic hypertonic saline infusion

To determine the relationship of coagulapathy to saline infusions for abortion, plasma volume, electrolyte, and coagulation factors were studied in 6 patients of a gestational average of 18 weeks undergoing intraamniotic hypertonic saline infusion for therapeutic abortion. Blood samples were taken before the operation and afterwards at 3-hour intervals for 30 hours. Mean plasma volume increased by 8.9% of the base-line values by 15 hours. The direct correlation found between fluid intake, weight, and plasma volume indicates that unlimited fluid intake may be allowed following saline infusion. Serum electrolytes showed no significant change. Urine sodium and chloride increased at 3 hours, reaching a peak of 60 meg at 27 hours, and returning to base-line values at 36 hours. Urine potassium decreased at 3 hours and remained slightly below base-line values for the remainder of the test period. Disperse variations in the coagulation factor studies might suggest mild diffuse intravascular coagulation, but further research is required.     

The predisposition to infection following hemorrhagic shock.

Subsequent life threatening gram-negative infection in patients successfully resuscitated from hemorrhagic shock is becoming increasingly common. Following hemorrhagic shock and resuscitation, Sprague-Dawley rats were given Escherichia coli intraperitoneally to simulate the clinical setting in which peritoneal contamination and hypovolemic shock occur concurrently. A sublethal dosage of bacteria resulted in a 100 per cent mortality. This suggests that hemorrhagic shock, even when treated promptly and effectively, predisposes to infection.     

Amniotic fluid index before and after amnioinfusion of a fixed volume of normal saline.

Twenty-one women at term, with an amniotic fluid index (AFI) less than or equal to 5.0 cm and intact membranes, underwent an artificial amniotomy and transcervical amnioinfusion of 250 mL of normal saline at room temperature. The mean (+/- SD) cervical dilation at the time of the transcervical amnioinfusion was 2.6 +/- 1.3 cm (range, 1-6). The mean AFI prior to the amnioinfusion was 3.0 +/- 1.49 cm (range, 0-4.7). The mean AFI after the amnioinfusion was 8.9 +/- 2.9 cm (range, 5.1-14.3). A mean change in the AFI of 5.8 +/- 2.6 cm (range, 0.9-10.6) was noted. Among patients with AFI less than or equal to 5.0 cm and intact membranes, amnioinfusion of 250 mL of normal saline seems to be a safe and simple way to increase the AFI to greater than 5.0 cm.     

高渗盐水激发试验和运动激发试验用于诊断儿童哮喘的对比观察

目的　研究高渗盐水激发试验及运动激发试验在哮喘儿童的临床应用,旨在寻求更适合哮喘儿童的气道反应性检测的方法。方法　收集中国医科大学附属 盛京医院2007年5月至2008年6月符合儿童支气管哮喘防治常规诊断　标准的哮喘缓解期患儿34例,年龄5～13岁,在规定时间内先后做气道高渗盐水激发试验和运 动激发试验。结果　同一哮喘患儿高渗盐水激发试验的敏感性显著高于运动激发试验（P < 0.01）。结论　高渗盐水激发试验的敏感性和特异性高于运动激发试 验,而且设备低廉,方法简单、易配合,安全,副反应少,尤其适用于在哮喘治疗期间动态观察儿童气道的反应性,对指导药物治疗有重要价值。     

Ventricular function in experimental hemorrhagic shock.

Hemorrhagic shock was induced in 20 spontaneously breathing adult greyhounds by lowering the mean arterial pressure to 40 millimeters of mercury. In the first group of six dogs, reinfusion was carried out without delay; in a second group of six dogs, hypovolemia was continued for two hours, during which time the arterial pressure was permitted to rise in response to intact cardiovascular reflexes; in a third group of eight dogs, the mean arterial pressure was artificially maintained at 40 millimeters of mercury for two hours, initially by further bleeding. In all dogs in the latter group, take-up of blood from the reservoir was required during the second hour to maintain the arterial pressure, this being indicative of irreversible shock. In two of this group, fatal arrhythmias developed during reinfusion. All three groups showed evidence of ventricular dysfunction during and immediately after reinfusion, as indicated by disproportion between left ventricular stroke work and left ventricular end diastolic pressure, these data being used to construct ventricular function curves. Measurement of dP/dt maximum suggested that this dysfunction was due to impairment of myocardial contractility. The first two groups recovered normal function within one hour; the third group failed to have such a recovery. Evidence indicates that generalized tissue hypoxia, in addition to myocardial hypoxia, is important in the cause of cardiac dysfunction in irreversible shock.