体外循环对紫绀型先天性心脏病病人血小板的影响

检测１８例体外循环紫绀型先天性心脏病手术病人术前，术中及术后３，８天外周血血小数量和 附，聚集功能，探讨体外循环对血小板质和量的影响。结果显示，血小板数量和聚集功能在术后显著下降并持续至术后８天，血小板粘附功能显著下降，术后３天恢复。提示体外循环气血界面，人工材料非内皮表面可导致血小板激活，粘附，聚集面在量消耗，数量和功能显著下降。     

温血高钾间断灌注心肌保护的临床应用

目的　探讨浅低温体外循环 (CPB)温血间断灌注心肌保护的临床效果。方法　全组随机分为对照组 (A组 )6 8例 ,采用浅低温CPB温血高钾持续灌注心肌保护。实验组 (B组 ) 91例 ,采用浅低温CPB温血高钾间断灌注心肌保护。观察两组术中心肌保护效果的差别。结果　CPB时间、主动脉阻断时间B组明显小于A组 (P <0 .0 5 ) ;库血用量和 2 4h胸腔引流量B组明显少于A组 (P <0 .0 5 ) ;主动脉开放前血钾浓度B组明显低于A组 (P <0 .0 5 ) ;主动脉开放后心脏自动复跳率B组明显高于A组 (P <0 .0 5 ) ;术后心功能临床观察两组无显著差异。结论　浅低温CPB温血高钾间断灌注保护心肌效果良好。     

抑肽酶对瓣膜置换术患者心肌粘附分子表达及细胞凋亡的影响

目的探讨抑肽酶对二尖瓣置换术患者围体外循环（CPB）期心肌细胞及心肌血管内皮细胞上细胞间粘附分子-1（ICAM-1）、血管细胞粘附分子-1（VCAM-1）表达及心肌细胞凋亡的影响。方法择期二尖瓣置换术患者30例,年龄24～59岁,体重46～73 kg,心功能分级Ⅱ级或Ⅲ级,随机分为2组（n=15）：对照组和抑肽酶组,抑肽酶组于CPB转机前,预充液中加入抑肽酶300万KIU,对照组则给予等容量生理盐水,分别于CPB前和CPB停止时取右心房心肌组织标本,采用免疫组织化学SP法染色,检测心肌细胞和心肌血管内皮细胞上ICAM-1、VCAM-1的表达,采用病理图像分析系统对ICAM-1、VCAM-1表达的灰度值作定量分析,采用TUNEL法检测凋亡心肌细胞。结果抑肽酶组CPB停止时ICAM-1、VCAM-1的表达低于对照组（P〈0.01）;2组CPB停止时心肌细胞凋亡指数较CPB前增高（P〈0.05）,抑肽酶组CPB停止时心肌细胞凋亡指数低于对照组（P〈0.05）。结论预充液中加入抑肽酶300万KIU可抑制二尖瓣置换术患者CPB期间心肌细胞和心肌血管内皮细胞ICAM-1、VCAM-1的表达及心肌细胞的凋亡。     

七氟醚预处理对体外循环冠状动脉旁路移植术病人围术期心肌的保护作用

目的探讨七氟醚预处理对体外循环(CPB)下冠状动脉旁路移植术(CABG)病人心肌的保护作用。方法择期CPB下CABG病人40例,ASAⅡ级或Ⅲ级,随机分为2组(n=20):七氟醚组(S组)或异丙酚组(P组)。麻醉维持:P组靶控输注异丙酚,血浆靶浓度2～3μg/L,静脉输注芬太尼2～3μg·kg~(-1)·h~(-1);S组夹闭主动脉前,吸入0.5%～2%七氟醚,静脉输注芬太尼2～3μg·kg~(-1)·h~(-1),夹闭主动脉后靶控输注异丙酚,血浆靶浓度2～3μg/L,静脉输注芬太尼2～3μg·kg~(-1)·h~(-1)。于切皮前即刻、CPB前即刻、CPB后即刻、回ICU后即刻、6、12h记录心率(HR)、平均动脉压(MAP)、肺动脉楔压(PCWP)、中心静脉压(CVP)、心脏指数(CI)、体循环血管阻力指数(SVRI)。于麻醉诱导前、回ICU后即刻、6、12、24h采集静脉血,测定血清心肌肌钙蛋白I(cTnI)浓度。记录术后不良事件的发生情况。结果2组各时点MAP、PCWP、CVP、HR和SVRI比较差异无统计学意义(P>0.05);与切皮前即刻和P组比较,S组回ICU后各时点CI升高(P<0.05)。与P组比较,S组回ICU后各时点cTnI浓度降低(P<0.05)。2组病人术后均无死亡;2组心肌梗塞、房颤和心肌缺血的发生率差异无统计学意义(P>0.05);S组cTnI浓度>2ng/ml的发生率低于P组(P<0.05)。结论七氟醚预处理对体外循环下冠状动脉旁路移植术病人围术期心肌具有一定的保护作用。     

小儿体外循环采用中度低温低流量灌注技术的临床研究

目的研究先天性心脏病患儿体外循环手术中采用中度低温合并低流量灌注技术的可行性。方法３０例手术患儿体外循环降温至肛温２５．６±０．８４℃，食管温度２４．１±１．３２℃，鼓膜温度２３．８±１．４１℃，维持流量１．２３±０．０９Ｌ／ｍｉｎｍ２，转流时间９５．４±３４．６分钟，主动脉阻断时间５１．４±２０．２分钟，低流量维持时间４５．７±２２．４分钟。结果低流量灌注时静脉血氧饱和度均在８０％以上，除１例外，其余均无缺氧酸中毒的血气表现，血乳酸值也未升高，术后恢复良好。结论中度低温体外循环选用低流量灌注可满足机体代谢的需要，有利于减少长时间高流量灌注的不良反应。     

Intrathoracic pressure fluctuations move blood during CPR: Comparison of hemodynamic data with predictions from a mathematical model

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. We developed a mathematical model that predicts that blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, however, the model predicts that flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. The model was validated for direct cardiac compression by studying the hemodynamics of cyclic cardiac deformation following thoracotomy in four anesthetized, 21–32-kg dogs. As predicted by the model, there was no change in myocardial or cerebral perfusion pressures when the duration of compression was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. The model was validated for intrathoracic pressure changes by studying the hemodynamics produced by a thoracic vest (vest CPR) in eight dogs. The vest contained a bladder that was inflated and deflated. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was <0.8 cm. As predicted by the model and opposite to direct cardiac compression, there was no change in perfusion pressures when the rate was increased from 60 to 150/min at a constant duration of 45% of the cycle. Manual CPR was then studied in eight dogs. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres and behaved as predicted from the model of intrathoracic pressure, not direct cardiac compression. At nearly constant peak sternal force (378–426 N), flow was significantly increased when the duration of compression was increased from short (13%–19% of the cycle) to long (40%–47%), at a rate of 60/min. Flow was unchanged, however, for an increase in rate from 60 to 150/min at constant compression duration. In addition, myocardial and cerebral flow correlated with their respective perfusion pressures. Thus vital organ perfusion pressures and flow for manual external chest compression are dependent on the duration of compression, but not on rates of compression of 60 and 150/min. These data are of course similar to those produced by vest CPR, where intrathoracic pressure is manipulated without sternal displacement, and to those predicted for movement of blood by intrathoracic pressure changes. These data are, however, opposite to those produced by cardiac deformation and to those predicted for movement blood by direct cardiac compression. We conclude that intrathoracic pressure fluctuations generate blood flow during manual CPR.     

Spontaneous arterial baroreflex control of the heart rate during head-down tilt in heat-stressed humans

The purpose of this study was to elucidate the effect of raised body temperature per se during acute heat stress on the spontaneous arterial baroreflex control of heart rate (f _c) in humans. To investigate whether unloading of cardiopulmonary baroreceptors during whole-body heating would alter the arterial baroreflex control of f _c, we controlled loading of the cardiopulmonary baroreceptors by head-down tilt (HDT) at angles of 5°, 10°, 15°, and 30° during heat stress produced by hot-water-perfused suits. The sensitivity of the arterial baroreceptor-cardiac reflex was calculated from the spontaneous changes in beat-to-beat arterial pressure and f _c. As an index of cardiopulmonary baroreceptor loading, the left atrial diameter (LAD) was measured by echocardiography. During whole-body heating, the LAD decreased with the rising body core temperature and increased with the HDT. The decreased LAD during heating almost recovered to the normothermic control level by 10° HDT. In the supine position, cardiac baroreflex sensitivity remained unchanged during heating. Arterial pressure, f _c and cardiac baroreflex sensitivity were not changed by HDT ranging from 5° to 30° during heating. These results suggest that cardiac baroreflex sensitivity remain unchanged during graded loading of the cardiopulmonary baroreceptors in heat-stressed humans. Also, we conclude that the sensitivity of the spontaneous arterial baroreflex controlling the f _c is not influenced by raised body temperature per se during acute heat stress. Electronic Publication     

Morphological inspection of 80 consecutive Gyro pumps after cardiopulmonary bypass

 We have been using the Gyro centrifugal pump C1E3 for cardiopulmonary bypass in anticipation of high efficiency, low hemolysis, and antithrombogenicity of this pump. However, the clinical evaluation of this pump remains to be clarified, because it has been a short time since the pump appeared in clinical situations. The aim of the present study is to inspect and analyze the Gyro pumps morphologically after clinical use. We examined 80 consecutive pumps after cardiopulmonary bypass for 186 ± 67 min with a mean flow rate of 2.52 ± 0.22 l/min/m² at a mean rotational speed of 2485 ± 81.1 rpm. Although no abnormal findings were present in 79 pumps, one pump was found to contain effusion at the connection between the impeller body and the shaft. The extudate was supposed to be blood, based upon the results of X-ray spectrometer analysis. The cause was determined to be the upward deviation of the shaft off the impeller body. Scanning electron microscopy showed scratches on a part of the bottom housing and a smooth surface of both the male and female pivots of the pump. Surface profile measurement revealed that the deformity of the female pivots was 0.14 mm (top) and 0.05 mm (bottom). These observations suggest that the floating force and vibration by the rotating impeller acted on the joint zone between the alumina ceramic shaft and the polycarbonate impeller body, resulting in dissection of the adhesive agent from the polycarbonate. Although this abnormality may be rare, the structural design still may need to be improved. Received: November 9, 2001 / Accepted: February 4, 2002     

深低温体外循环对犬趾蹼微循环指标的研究

本研究表明,深低温体外循环时,犬趾蹼微循环发生的变化与温度有关。平均动脉压(MAP)的变化不能反映组织灌注的优劣情况。毛细血管内的血流速度与灌注流量的高低有关。     

不同类型心脏患者心内直视手术期间呼气末CO2分压与动脉血CO2分压及其差值的变化

目的探讨不同类型心脏患者心内直视手术期间呼气末二氧化碳分压（PETCO2）与动脉血二氧化碳分压（PaCO2）的相关性及二者差值[P（a-ET）、CO2]的临床意义。方法45例患者分成3组，每组15例。A组：左向右分流组；B组：无分流组；C组：右向左分流组。3组分别于术前（T0）、插管后15min（T1）、手术开始时（T2）、转流前（T3）、转流停止后15min（T4）、术毕时（T5）共6个时点，用旁气流法监测PETCO2，同时抽动脉血测定PaCO2，应用直线回归分析3组各时点PETCO2与PaCO2的相关性，同时计算并分析各组不同时点的P（a-ET）CO2。结果（1）A组、B组各时点PETCO2与PaCO2呈正相关，A组r为0．70—0．85（P〈0．01），B组r为0．71—0．79（P〈0．01）；C组麻醉开始至转停后PETCO2与PaCO2均无相关（0．46—0．54，P〉0．05），而到术毕时则呈正相关（r=0．66，P〈0．05）。（2）3组患者转流前的P（a-ET）CO2变化不大，停转流后A组、B组P[a-ET）CO2增加，其中以A组增加较明显（P〈0．01），而C组P（a-ET）CO2显著减少（P〈0．05）。结论无分流或左向右分流心脏患者在体外循环转流前后PETCO2与PaCO2的相关性较好；右向左分流心脏患者转流前的相关性较差，心内畸形纠正后其相关性可发生变化。P（a-ET）CO2在不同的心脏患者之间差异较大，必须与PaCO2相结合，才能正确指导临床。