Severe cardiovascular changes associated with pancuronium after cardiopulmonary resuscitation and after brain injury

Severe hypertension, tachycardia or ECG changes have been reported following i.v. administration of pancuronium to patients with pheochromocytoma or bronchial asthma. These cardiovascular changes were explained by an interaction between autonomic effects of pancuronium and elevated serum catecholamines or aminophylline. We noted similar cardiovascular changes associated with i.v. administration of pancuronium in two patients after successful cardiopulmonary resuscitation and in two with midbrain hemorrhage and epidural hematoma. In these patients, pancuronium produced no abnormal cardiovascular changes when given during elective surgery or before the occurrence of midbrain hemorrhage. Thus, ischemic brain damage may play a role in producing the severe cardiovascular changes associated with pancuronium.     

Lung injury after cardiopulmonary bypass

Pulmonary injury during cardiopulmonary bypass is common as patient factors (smoking, pain, pneumonia) and the effects of cardiopulmonary bypass combine to compromise lung function after cardiac surgery. Lung injury follows the propagation of an inflammatory response involving cytokines, complement, neutrophils, monocytes, activated endothelial cells and platelets. Neutrophils sequester in the lung in response to chemotactic agents and release injurious oxygen free radicals and specific enzymes resulting in widespread pulmonary injury. To alleviate this lung injury a number of possible interventions exist. Off pump surgery may reduce the degree of systemic inflammation but respiratory impairment still occurs and the clinical advantage is uncertain. The use of leukocyte filtration can attenuate the acute inflammatory response with encouraging though variable results. Aprotinin, Pentoxyfilline, Nitric oxide, Aspirin and other agents have shown benefits in lung function after cardiopulmonary bypass induced lung injury. Given the magnitude and diversity of the inflammatory response to cardiopulmonary bypass many possible interventions exist to attenuate lung injury resulting from extracorporeal circulation. Immediate clinical benefits are likely to result from successful amelioration of the processes involved.     

复方药物支气管肺泡灌洗对蒸气吸入伤犬呼吸循环功能的影响

目的探讨吸入性损伤的治疗方法,研究小剂量复方药物支气管肺泡灌洗（BAL）对蒸气吸入伤犬呼吸、循环功能的影响。方法犬蒸气吸入致伤4小时后,将纤维支气管镜楔入3～4级肺叶支气管管口进行小剂量药物BAL。结果BAL后30、60和90分钟的吸气时间（T     

复苏后心功能不全与炎症因子关系的实验研究

目的:观察犬心跳骤停复苏后血流动力学和细胞因子的变化及其关系。方法:体外电击诱发犬室颤,3min后复苏,12只犬随机分为2组,常规治疗组(CPR组)和正常对照组,每组6只,采用Swan-Ganz漂浮导管监测复苏前和复苏后6h的心输出量(CO)和肺动脉楔压(PAWP),同时抽血检测血清肿瘤坏死因子-α(TNF-α),白介素-6(IL-6)和白介素-10(IL-10)水平(放免法)。结果:两组各血流动力学指标在心跳骤停前差异无统计学意义,CPR组的MAP在复苏成功即时高于正常对照组,随后开始下降,在复苏后4、6h低于正常对照组。CPR组的PAWP从心跳骤停前的(5.0±1.26)mmHg一直上升,到复苏后达高峰(28.83±4.79)mmHg,各观察点均高于正常对照组,CO在复苏成功后随时间延长而下降,6h降至最低,复苏后各观察点均低于正常对照组和电击前。TNF-α、IL-6浓度在复苏后即时和2h开始出现明显的升高,并随时间的延长而增高,与本组电击前及同时间的正常对照组比较差异有统计学意义。在整个实验过程均未能检测到IL-10的浓度。细胞因子TNF-α和IL-6与CO之间呈负相关。结论:电击诱发室颤犬复苏成功后存...     

Venous and arterial blood gases during and after cardiopulmonary resuscitation in dogs

This study was undertaken to characterize blood gas, pH, and lactate changes during and after cardiopulmonary resuscitation (CPR) in arterial and venous samples. Blood samples were withdrawn from the brachial artery, aortic arch, pulmonary artery, coronary sinus, and either the right or left cardiac ventricle of 24 anesthetized dogs. Ventricular fibrillation (VF) was induced electrically, and mechanical CPR was begun. Blood samples were withdrawn before CPR, at 2, 5, 7, and 9 minutes during CPR, and at 1, 3, 10, 30, and 60 minutes after defibrillation. Control arterial and venous samples indicated mild metabolic acidosis. During CPR, there was a significant arteriovenous difference in pH, PCO2, and PO2. With ventilation onset, arterial pH increased 0.25 units, PCO2 decreased 22 mm Hg, and PO2 increased 200 mm Hg. Venous blood gases exhibited gradual changes during the CPR period. With the re-establishment of circulation and spontaneous respirations, both the arterial and venous pH levels decreased to nearly 7.1, and PCO2 approached 40 mm Hg. Lactate increased to 32 mg/dl during 9 minutes of CPR and did not significantly differ after defibrillation. Blood gases and pH returned to control values within an hour. This study suggests that arterial blood gases are sensitive to rapid changes occurring in the pulmonary capillary bed, while venous blood gases reflect changes occurring in the systemic capillary bed.     

低温闭胸心肺转流对狗心肺复苏后脑损伤的保护作用

目的　观察闭胸低温心肺转流 (CPB)对狗心肺复苏后脑损伤的保护作用。方法制作狗心搏骤停模型 ,停搏 15min后行浅低温 (33～ 34℃ ) (n =5 )和深低温 (2 6～ 2 7℃ ) (n=5 )闭胸CPB复苏。于停搏前、停搏后 15min、CPB开始后 1h、 3h抽血 ,于 3h取大脑皮层 ,测定血浆和脑组织肌酸磷酸激酶 BB (CK BB)浓度。另设 5只为缺血对照组。结果　CPB开始后3h ,浅低温组和深低温组血浆CK BB浓度明显高于停搏前 (P <0 0 5 ) ,深低温组大脑皮层中CK BB浓度明显低于浅低温组 (P <0 0 5 )。结论　狗心脏停搏 15min后行深低温闭胸CPB复苏对大脑皮层的损伤较轻 ,有一定保护作用     

Mild hypothermic cardiopulmonary resuscitation improves outcome after prolonged cardiac arrest in dogs

BACKGROUND AND METHODS: This study was designed to explore the effect of mild cerebral and systemic hypothermia (34 degrees C) on outcome after prolonged cardiac arrest in dogs. After ventricular fibrillation with no flow of 10 min, and standard external CPR with epinephrine (low flow) from ventricular fibrillation time of 10 to 15 min, defibrillation and restoration of spontaneous normotension were between ventricular fibrillation time of 16 and 20 min. This procedure was followed by controlled ventilation to 20 hr postarrest and intensive care to 72 hr postarrest. In control group 1 (n = 10), core temperature was 37.5 degrees C; in control group 2 (n = 10), cooling was started immediately after restoration of spontaneous normotension; and in group 3 (n = 10), cooling was initiated with start of CPR. Cooling was by clinically feasible methods. RESULTS: Best overall performance categories achieved (1 = normal; 5 = brain death) were better in group 2 (p = .012) and group 3 (p = .005) than in group 1. Best neurologic deficit scores were 36 +/- 14% in group 1, 22 +/- 15% in group 2 (p = .02), and 19 +/- 18% in group 3 (p = .01). Brain histopathologic damage scores were also lower (better) in groups 2 (p = .05) and 3 (p = .03). Myocardial damage was the same in all three groups. CONCLUSION: Mild cerebral hypothermia started during or immediately after external CPR improves neurologic recovery.     

Lung injury after cardiopulmonary bypass: Alternative treatment prospects

Although the lung injury caused by cardiopulmonary bypass (CPB) has been extensively investigated, the incidence and mortality of lung injury after CPB remain a prominent clinical problem. The poor outcome has been attributed to multifactorial etiology, including the systemic inflammatory response and ischemia reperfusion (I/R) injury during CPB. Lung injury after CPB is a complex pathophysiological process and has many clinical manifestations of mild to severe disease. Which is associated with prognosis. To alleviate this lung injury, interventions that address the pathogenesis are particularly important. This review summarizes the pathogenesis, mechanism and treatment options of lung injury after CPB, such as lung protection with intralipid.     

心肺复苏后脑损害昏迷转归的早期观察与评价

目的：探讨准确、客观评估与判定心肺复苏（CPR）后脑损害昏迷的方法。方法：对27例心肺复苏12h后脑损伤仍处于昏迷状态的患者进行连续的观察和评估,评估的项目包括对神经系统的各项临床观察。结果：27例患者中19例（70．4％）在心肺复苏后1个月内死亡,其余8例存活患者从昏迷成为睁眼昏迷,存活患者中2例（25．0％）分别在第5d、第43d清醒。结论：临床综合评定心肺复苏后昏迷客观、可靠,对临床医疗决策和提高脑复苏成功率具有重要的指导意义。     

External cardiopulmonary resuscitation preserves brain viability after prolonged cardiac arrest in dogs.

Standard external cardiopulmonary resuscitation (CPR) steps A-B-C produce a low blood flow that may or may not preserve brain viability during prolonged cardiac arrest. A dog model was used with ventricular fibrillation (VF) of 20 minutes, reperfusion with brief cardiopulmonary bypass, controlled ventilation to 20 hours, and intensive care to 96 hours. A retrospective comparison was made of the results of one series, now called "group I" (n = 10)--which received CPR basic life support interposed from VF 10 to 15 minutes, and CPR advanced life support with epinephrine (without defibrillation) from VF 15 to 20 minutes--to the results of another series, now "control group II" (n = 10)--which received VF no flow (no CPR) for 20 minutes. All 20 dogs within protocol were resuscitated. All 10 of group I and 7 of 10 of group II survived to 96 hours. Pupillary light reflex returned after the start of cardiopulmonary bypass at 7.7 +/- 3.7 minutes in CPR group I, versus 16.3 +/- 7.4 minutes in control group II (P = .032). At 96 hours postarrest, final overall performance categories (1, normal; 5, brain death) were better in group I. Six of 10 dogs achieved normality (overall performance category 1) in group I, as compared with none of 10 in group II (P = .004). Final neurologic deficit score (0%, best; 100% worst) was lower (better) in group I (15% +/- 20%) than in group II (51% +/- 6%; P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)     

脊髓受压时间与损伤程度的相关性研究

目的探讨脊髓受压时间与脊髓病理改变、灰质血流量、体感诱发电位及运动功能的关系。方法将24只犬随机分为两组,应用水囊分别压迫30min和180min造成脊髓损伤。在受压期间和去除压迫后不同时间监测体感诱发电位(SEP)和脊髓灰质血流量。去除压迫后不同时间进行后肢运动功能评价,去除压迫后28d处死动物进行组织学评价。结果脊髓加压后两组血流量迅速下降,去除压迫即刻及去除压迫后28d两组血流量差异有统计学意义(P<0.05)。受压期间SEP波幅迅速下降并消失,30min组去除压迫后SEP波幅缓慢恢复,180min组始终无恢复(P<0.05)。30min组后肢运动功能恢复较快,180min组恢复较慢(P<0.05)。180min组较30min组的组织损伤重(P<0.05)。结论脊髓受压后尽早行减压术是提高局部血流量、促进神经功能恢复的关键因素。     

心肺旁路后急性肾损伤的防治

心肺旁路术后急性肾损伤(acute kidney injury,AKI)有较高的发病率,增加患者住院时间和死亡风险.判断心肺旁路AKI的危险因素和早期诊断可能给心肺旁路手术患者带来益处,一旦患者发生AKI应该尽早实施干预,目前对该类患者进行肾替代治疗的方式、剂量尚没有统一,应该遵从个体化原则.     

Distant-organ changes after acute kidney injury

Acute kidney injury (AKI) contributes significantly to morbidity and mortality in both adults and children. While clinical data suggest that AKI contributes to and exacerbates multiorgan failure, the physiologic and molecular mechanisms responsible for these interactions were previously unknown. New data linking AKI with distant-organ dysfunction includes evidence that inflammatory cascades are abnormal after organ injury. Leukocyte trafficking, cytokine expression, cell adhesion-molecule expression and membrane ion and water-channel expression in distant organs are deranged after kidney injury. The responses to oxidative stress after AKI are also altered, suggesting complex mechanisms of crosstalk between the injured kidney and distant organs. Novel methodologies, including genomics and proteomics, are now being employed to unravel interorgan communication to accelerate clinically meaningful discovery for this serious disease.     

Respiratory changes after major burn injury

In 32 major burn patients, routine respiratory measurements and blood gases analysis were performed. Striking differences were found between survivors and nonsurvivors in these variables. Marked increased in minute volume and respiratory rate were observed in nonsurvivors starting from the 6th day postburn, while PaCO2 increased with larger tidal and minute volumes. At the same time, PaO2 was lower than in survivors. In survivors, the closing volume, maximum mid-expiratory flow rate, and peak rate were lower than the predicted normal values. This may indicate that after major burn injury, ventilatory power decreased and some pathological changes occurred in small airways and alveoli without apparent pulmonary complications. Marked differences in the changes of respiratory rate and min volume between survivors and nonsurvivors may indicate the value of simple respiratory measurements for prediction of outcome in burn patients.     

心肺复苏后大鼠肾脏损伤的实验研究

目的 观察心肺复苏（CPR）后大鼠肾小管上皮细胞损伤情况并研究其可能机制。方法 采用窒息（琥珀酰胆碱）并冰氧化钾停跳液致大鼠心跳骤停，5min后开始CPR的动物模型．健康Sprague Dawley雄性大鼠48只，随机分为6组：对照组（假手术组）及复苏后3,6、12、24、48h组，每组8只。采用酶法测定对照组及复苏后3、6、12、24、48h大鼠血清中BUN、Cr的浓度；采用透射电镜观察肾小管上皮细胞的损伤情况；采用比色法测定肾脏组织丙二醛（MDA）含量及超氧化物歧化酶（SOD）、Na^＋-K^＋-ATP酶活力。结果 复苏后3h血清中BUN、Cr浓度开始升高，随后持续升高，至24h达峰值。复苏后各组肾脏组织中MDA含量较对照组显著升高（P〈0.01），同时，SOD及Na^＋-K^＋-ATP酶活力显著降低（P〈0．01）；透射电镜下可见复苏后大鼠肾小管上皮细胞损伤表现。结论 心跳骤停及CPR后大鼠存在急性肾小管上皮细胞损伤；氧自由基（OFR）介导的脂质过氧化损伤、细胞能量代谢障碍在复苏后肾小管上皮细胞损伤中起着重要作用，肾小管上皮细胞损伤是CPR后大鼠急性肾功能衰竭的重要机制之一。     

生长激素对心肺复苏大鼠心肌损伤的保护作用

目的　研究生长激素对心肺复苏后大鼠心肌细胞的保护作用。方法　本实验采用窒息合并冰氯化钾停跳液致大鼠心跳骤停 5min后开始心肺复苏的动物模型。Sprague -Dawley大鼠随机分为 3组 :对照组 (假手术组 )、常规复苏组、生长激素治疗组 (每组 6只 )。复苏后 2 4h采用酶生化法测定血浆中CK -MB的含量 ;采用放射免疫法测定血浆中肿瘤坏死因子α(TNF -α)的含量。采用透射电镜和TUNEL法观察心肌细胞的损伤及凋亡情况 ;采用免疫组化法观察心肌细胞Bcl- 2、Bax蛋白的表达情况。结果　心肺复苏后常规组大鼠血浆CK -MB、TNF -α分别为 (2 5 9± 37 93)U/L、(1 2 0 0± 0 199)ng/mL ,TUNEL阳性细胞率为 4 70 % ,Bcl- 2表达率 2 5 39% ;生长激素治疗组血浆CK -MB、TNF -α较常规组明显降低 ,而Bcl- 2的表达明显增加 (45 6 0 % ) ,降低了心肌细胞凋亡的比例 (TUNEL阳性细胞率为 2 5 8% )。结论　生长激素可通过促进Bcl- 2的表达抑制心肌细胞凋亡 ,从而起到复苏后心肌保护作用。     

Severe endothelial injury and subsequent repair in patients after successful cardiopulmonary resuscitation

Introduction  

Ischemia and reperfusion after cardiopulmonary resuscitation (CPR) induce endothelial activation and systemic inflammatory response, resulting in post-resuscitation disease. In this study we analyzed direct markers of endothelial injury, circulating endothelial cells (CECs) and endothelial microparticles (EMPs), and endothelial progenitor cells (EPCs) as a marker of endothelial repair in patients after CPR.