HYPOTHERMIC CARDIOPLEGIA TO PROTECT THE MYOCARDIXJM IN HEART SURGERY

The cffect of hypothermic cardioplegia in protecting myocardial function durLng cardiac surgery under extracorporeal circulation was clinjcally investigated in 525 cases. The lowest myocardial temperature after coronary perfu- sion With the cardloplegic solution precooled to about 4 C was about 15 C. Supplemented with other local cooling methods to keep the heart in a deep hypothermic state, complete cardio- plegia and excellent myocardial protection were obtained as shown by the spontaneous return of sinus cardiac beat without need for electric dc. [i:orillatlon occurrecl in about hvo thirds of the cases and much less vaSOPresors were needed after the operation. Extract of a Chinese medi- cinal herb, Radiz' astragali黄芪 was tried in part of the cases and it's pharmacology is briefly presented. Compared .with other myocardial protection methotls, it was found to be a sjmple and very efficacious tcchnic. Even better re- sults mjght be aehieved if the serum potassium level and acid-base balance were well regulated throughout anesthesia and perfusion and the body temperature rewarmed to nearly normal at the end of surgery.     

PROTECTIVE EFFECTS ON RIGHT VENTRICLE BY RETROGRADE CORONARY SINUS PERFUSION OF CARDIOPLEGIA

The myocardial protective effects on right and left ventricles by retrog-rade coronary sinus perfusion(RCSP)of cardioplegia was Compared to that by aortic rootperfusion(ARP)in16 dogs which were divided into two groups at random.The criteriainclude:(1)intramyocardial temperature,(2)electrical activity of ventricles,(3)semiqu-antitative evaluation of myocardial ATPase and succinic dehydrogenase(SDH)in Niles’scale,(4)semiquantitative evaluation of myocardial mitochondria by Flameng′s method.All results showed no significant difference between the two groups.It is indicated thatthe results from RCSP cardioPlegia with toPical hyPothermia and from ARP cardioPlegiaWith topical cooling for myocardial protection in right and left ventricles are closelysimilar.     

Enhanced myocardial protection with Ginsenosides in St.Thomas'''' Hospital cardioplegic solution

Several studies suggest that Ginsenosides have a protective effect on myocardialischemia and reperfusion injury.Using the isolated working rat heart model the effect ofthe St.Thomas' Hospital cardioplegic solution containing different concentrations ofGinsenosides on the enhancement of myocardial protection following hypothennic ischemicarrest(20 ℃,120min)was evaluated.The concentrations of Ginsenosides in thecardioplegic solutions were 0(control),50,100,and 150μg/ml,respectively.Recoveries ofaortic flow,cardiac output,and minute work markedly improved by adding Ginsenosidesto cardioplegia.Dose-response tests indicated the best protective effect in the group using100 μg/ml,where the generation of thiobarbituric acid reactive materials(malondialdehyde,MDA)markedly reduced.These results showed that Ginsenosides may enhance themyocardial protection of the St.Thomas′ Hospital cardioplegic solution,and that additionof Ginsenosides to cardioplegia may protect the ischemic myocardium from free-radical in-jury.     

Myocardial protection of cold crystalloid and warm blood cardioplegia. A comparative study.

Twenty patienta adergoing open-heart valvular operations were divided randomly into two groups. Intermittent perfusion of cold crystaHoid (St. Thomas Hospital solution) with hypothermic cardiopuimonary bypass (CPB) in the hypothermic group and continuous administration of warm blood cardioplegia with normothermic CPB in the normothermic group were used respectively. The results of warm blood cardioplegia were superior to those of cold crystalloid. 70% of patients treated with the warm technique had spontaneous return of normal sinus rhythm shortly after removal of the aortic cross-clamp, compared with only 10% of the hypothermic group (P<0.05). The extracorporeal support time from releasing of aortic clamp to the weaning of CPB was significantly shorter in the normothermic group (33.50±3.78 min vs. 25.00±4.64 min, P<0.05). The postoperative ventilation support time was also much shorter than that of the hypothermic group (19.84± 1.11 h vs. 38.98± 16.55 h, P<0.05). More atrial beating occurred in the     

Ischemic preconditioning in immature hearts： mechanism and compatibility with cardioplegia

Objective To investigate (1) whether ischemic preconditioning (IPC) could protect immature rabbit hearts against ischemia-reperfusion injury and (2) the role of K(ATP) channel in the mechanism of myocardial protection. Since cardioplegia is a traditional and effective cardioprotective measure in clinic, our study is also designed to probe the compatibility between IPC and cardioplegia. Methods New Zealand rabbits aged 14-21 days weighing 220-280 g were used. The animals were anesthetized and heparinized. The chest was opened and the heart was quickly removed for connection of the aorta via Langendorff’s method within 30 s after excision. All hearts were perfused with Krebs-Henseleit buffer balanced with gas mixture (O［２］∶CO(2)=95%∶5%) at 60 cm H［2O］ (perfusion pressure). IPC consisted of 5 min global ischemia plus 10 min reperfusion. Glibenclamide was used as the K(ATP) channel blocker at a concentration of 10 μmol/L before IPC. Cardiac arrest was induced with 4℃ St. Thomas cardioplegic solution, at which point the heart was made globally ischemic by withholding perfusion for 45 min followed by 40 min reperfusion. Thirty immature rabbit hearts were randomly divided into four groups: CON (n=9) was subjected to ischemia-reperfusion only; IPC (n=9) underwent IPC and ischemia-reperfusion; Gli (n=6) was given glibenclamide and ischemia-reperfusion; and Gli+IPC (n=6) underwent glibenclamide, IPC and ischemia-reperfusion. Coronary flow (CF), HR, left ventricle developed pressure (LVDP), and ±dp/dt(max) were monitored at equilibration (baseline value) and 5, 10, 20, 30 and 40 min after reperfusion. The values resulting from reperfusion were expressed as a percentage of their baseline values. Arrhythmia quantification, myocardial enzyme in the coronary effluent and myocardial energy metabolism were also determined. Results The recovery of CF, HR, LVDP and ±dp/dt(max) in preconditioned hearts was best among the four groups. The incidence of arrhythmia was low and less CK-MB leaked out in the IPC group. Myocardial ATP content was better preserved by IPC. Pretreatment with glibenclamide completely abolished the myocardial protection provided by IPC, but did not affect ischemia-reperfusion injury. Conclusions While applying cardioplegia, IPC provides significant cardioprotective effects. Activation of K(ATP) channels is involved in the mechanism of IPC-produced cardioprotection.     

Myocardial protection during heart surgery in China

Myocardial protection （MP） is the key for cardiopulmonary bypass （CPB） heart surgery. MP during cardiac surgery （CS） aims to preserve myocardial function while providing a bloodless and motionless operating field. Strategies on how to attenuate or prevent post-ischemic myocardial dysfunction that occurs intra-operatively during CS have been discussed for more than half a century. In 1950, Bigelow et al, first reported to decrease myocardial oxygen demand by means of hypothermia. Moreover, Melrose and coworkers2 described the use of electromechanical cardiac arrest induced by potassium infusion, permitting CS to be performed on a non-beating flaccid heart and clear surgical field. The combination of both of these techniques has been the golden standard in MP during surgery until now, allowing surgery with excellent clinical outcome. In 1975, Braimbridge et al introduced a crystalloid solution into clinical practice at St. Thomas Hospital. By the 1980s, blood-based potassium solutions were advocated to further improve MP and to reduce myocardial enzymes release based on the theory that blood would be a superior delivery vehicle for its oxygenating and buffering capacity.Fortunately, the majority of MP strategies now available do allow patients to undergo conventional and complex CS with an operative mortality rate ranging from less than 2% to 4%.     

Cardioprotective effects of mitochondrial KATP channels activated at different time

Backgroud Recent studies in adult hearts have indicated that KATP channels in the inner mitochondrial membrance are responsible for the protection. And we investigated whether opening of mitochondrial KATP channels (mKATP) could provide myocardial protection for immature rabbits and determined its role in cardioprotection.Methods Thirty-four 3-4-week-old rabbits, weighing 300-350 g, were divided randomly into five groups: Group Ⅰ (control group, n=8); Group Ⅱ ［diazoxide preconditioning group; n=8; the hearts were pretreated with 100 μmol/L diazoxide for 5 minutes followed by 10-minute wash out with Krebs-Henseleit buffer (KHB)］; Group Ⅲ ［diazoxide+5-hydroxydeconate (5-HD) preconditioning group; n=5; the hearts were pretreated with 100 μmol/L diazoxide and 100 μmol/L 5-HD); Group Ⅳ (diazoxide+cardioplegia group; n=8; cardioplegia containing 100 μmol/L diazoxide perfused the hearts for 5 minutes before ischemia); Group Ⅴ (diazoxide+5-HD+cardioplegia group; n=5; the cardioplegia contained 100 μmol/L diazoxide and 100 μmol/L 5-HD). All hearts were excised and connected to langendrff perfusion system and passively perfused with KHB at 38℃ under a pressure of 70 cmH2O. After reperfusion, the recovery rate of left ventricular diastolic pressure (LVDP), ±dp/dtmax, coronary flow (CF), the creatinine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST) in coronary sinus venous effluent and the tissue ATP were measured. Mitochondria were evaluated semiquantitatively by morphology.Results After ischemia and reperfusion (I/R), the two groups that were treated by diazoxide only (Groups Ⅱ and Ⅳ) had a significant improvement in LVDP, ±dp/dtmax, and CF recovery. AST, LDH, and CK were decreased, and the levels of tissue ATP in the two groups were higher. Mitochondria was protected better in Group Ⅳ than in other groups. Conclusions Activating mKATP channels before and during ischemia can similarly protect immature rabbit hearts, and the mechanism is related to the direct protective effect on mitochondria. Opening of mKATP channel during ischemia provides a better protection for mitochondria than it does before ischemia.     

Aortic and mitral valve replacement with retrograde perfusion in the beating heart

Objective To estimate the value of aortic valves and combined mitral valve replacement wit h retrograde perfusion in beating hearts.Methods Continuous retrograde coronary sinus perfusion with beating hearts was used in 8 3 patients undergoing aortic valve or aortic valve combined with mitral valve re placement, without application of cardioplegia. After aortic valve replacement, the retrograde perfusion was changed to antegrade perfusion for mitral valve re placement or correction of the other deformities (group A). Cold blood cardiopl egia solution (15℃) was infused at intervals in 20 cases (group B). The follow ing parameters were tested: lactate, ET, CTn-T and MDA in blood; myocardial ult ra-structure; and cardiac rhythm and cardiac output (CO).Results All biochemical values increased after cardiopulmonary bypass (P&lt;0.05-0.01 ). Empty and beating heart sinus rhythm was maintained in group A. Myocardial ultrastructure did not change significantly. The pump was stopped smoothly as t he surgical procedure finished. No postoperative low cardiac output syndrome or arrhythmia was observed. Eight-one patients recovered smoothly, two died from renal failure or infective shock. When the pump stopped, all patients in group B were supported by 5-10 μg·kg(-1)·min(-1) dopamine. Transie nt pacing was used in 9 patients. One patient died from low cardiac output synd rome. Conclusion This method is a good myocardial protection which simulates physiologic status. It is applicable to aortic valve and combined mitral valve replacement of patie nts with large heart or heart failure and long time aortic cross-clamping. Ide al clinical effect can be achieved.     

WHO西太区与世界中医药学会联合会中医名词术语国际标准比较研究：卫气营血辨证（一）（英文）

Syndrome differentiation of defense,qi,nutrient and blood aspects is a method developed by Ye Tian-shi,a celebrated traditional Chinese medicine （TCM）physician in the Qing Dynasty,for the treatment of warm disease of external contraction,which is a further development of syndrome differentiation of the six meridians.According to the theory of TCM,     

温血停跳液间断灌注在心内直视手术的应用65例报道

目的探讨温血停跳液间断灌注心肌保护方法在心内直视手术中的应用效果。方法在65例心内直视手术中应用温血停跳液间断灌注的心肌保护方法，观察其临床效果。结果全组病人无死亡，无低心排综合症，无严重的心律失常，脑、肺，肾等器官并发症，均痊愈出院。结论温血停跳液间断灌注的心肌保护方法临床应用效果好。     

温血心肌停搏液微流量连续灌注法在老年心脏病患者中的应用

目的 :探讨温血心肌停搏液微流量连续灌注法在老年心脏直视手术中的应用效果。方法 :本组 3 4例 ,年龄 60～ 71岁。病种包括先天性房间隔缺损 5例 ,心脏瓣膜病 2 8例 ,左心房粘液瘤 1例。阻断升主动脉 ,先用含钾 2 3～ 2 8mmol/L的温血停搏液诱导心脏停搏 ,再用含钾 6～ 8mmol/L温血停搏液以 0 5～ 1 0ml/kg·min速度连续灌注至开放主动脉阻断钳前 ,心肌温度维持在 3 2℃～ 3 6℃。心脏病变给予矫治。结果 :阻断升主动脉灌注含钾温血停搏液后 ,心脏停搏迅速 ,且不经心室颤动阶段。开放升主动脉后 3 3例( 97 1% )自动恢复为窦性心律 ,血管活性药物用量小 ,无低心排及严重心律失常发生。死亡 1例。结论 :温血心肌停搏液微流量连续灌注法对老年心脏病手术患者效果较好 ,是一种安全、可靠的心肌保护方法。     

温血诱导及冷血停搏液持续灌注对婴幼儿的心肌保护作用

目的:探讨温血诱导心停搏加冷血停搏液持续灌注对婴幼儿心脏手术的心肌保护作用。方法:选择体外循环心内直视手术的婴幼儿20例,随机分为两组:冷血停跳液间断灌注组;温血诱导心停搏加冷血停搏液持续灌注组(观察组)。检测于手术前后白细胞β2整合素(CD11b)表达,TNF-α和心肌钙蛋白I(cTnT)含量。观察自动复跳率(例),后并行时间,术后心功能,术后正性肌力药物用量。结果:两组相比,对照组CD11b表达增强(P<0.01),TNF-α和cTnI含量增高(P<0.01)。对照组后并行时间,术后正性肌力药物用量显著高于观察组(P<0.05);自动复跳率(例),心功能指标明显低于观察组(P<0.05)。结论:温血诱导心停搏加冷血停搏液持续灌注技术对婴幼儿心脏手术比冷血停搏液间断灌注有更好的心肌保护效果。     

Effects of Warm Blood Cardioplegic Solution on Myocardial Protection

ＥｆｆｅｃｔｓｏｆＷａｒｍＢｌｏｏｄＣａｒｄｉｏｐｌｅｇｉｃＳｏｌｕｔｉｏｎｏｎ　ＭｙｏｃａｒｄｉａｌＰｒｏｔｅｃｔｉｏｎＤＵＸｉｎ－ｌｉｎｇ（杜心灵）；ＬＡＮＨｏｎｇ－ｊｕｎ（蓝鸿钧）；ＳＵＮＺｈｏｎｇ－ｑｕａｎ（孙宗全）（ＩｎｓｔｉｔｕｔｅｏｆＣ...     

温血停搏液持续逆行灌注对心肌保护作用

目的研究温血停搏液经冠状静脉窦持续灌注对心肌保护作用。方法60例心脏瓣膜病患者，随机分成两组：持续灌注组(实验组n=30)和间断灌注组(对照组n=30)。术中测定心肌酶及取心肌组织电镜观察超微结构。结果对照组与实验组相比，心肌酶峰值提前，且持续时间较长。心肌超微结构显示：对照组心肌细胞线粒体出现普遍空泡化，部分嵴溶解。结论温血心肌停搏液持续逆灌对心肌保护作用优于间断灌注组，适合重症心脏病心瓣膜置换术患者。     

氧合温血停搏液对心肌保护的临床与基础研究

目的：观察氧合温血停搏液对心脏直视手术缺血期间的心肌保护作用。方法：选取30例病人,分为3组,对照组、氧合温血组、氧合温血加1,6二磷酸果糖组（简称FDP组）各10例。观察3组术前、术后12h、术后24h心肌酶谱的动态变化;心脏停跳后10min、30min及升主动脉开放前3个时相的心肌超微结构的改变;术毕心脏自动复跳率的变化。结果：对照组心脏均经室颤停跳,其余两组均不经室颤且心脏自动复苏率明显高于对照组。心肌酶谱变趋势显示对照组释放峰值高于氧合温血组及FDP组,下降也低于其余两组。电镜观察显示氧合温血组及FDP组保存了较好的心肌超微结构。结论：氧合温血及FDP具有心肌保护作用。     

末次温血停搏液在瓣膜置换术中的应用

目的：评估末次温血停搏液灌注对瓣膜置换术患者的心肌保护作用。方法：80例择期行瓣膜置换术的患者被随机分为2组，对照组用间断冷血停搏波灌注，实验组用末次温血停搏液合并间断冷血停搏液灌注。分别于阻断前、体外循环停止后30，60，120min记录平均动脉压、中心静脉压、肺毛细血管楔压、心输出量及心率，计算心脏指数，术前、开放升主动脉后l，4，12，24，48h检测血浆肌酸激酶同工酶(CK-MB)，同时观察临床恢复情况。结果：实验组术后多巴胺或多巴酚丁胺的平均最大剂量较对照组少，使用率低，CK-MB峰值显著低于对照组(P＜0．01)，自动复跳率高(P＜0．05)，停循环2h的心脏指数显著高于对照组(P＜0.01)。结论：末次温血停搏液灌注对瓣膜置换术患者具有良好的心肌保护作用。     

温血停跳液再灌注对大鼠热缺血供心的心肌保护作用

 目的 研究温血停跳液再灌注对大鼠热缺血供心的心肌保护作用。方法 24只SD大鼠随机分为对照组（A组,n=8,无热缺血,冷缺血4 h,常规心肌保护）、热缺血组（B组,n=8,热缺血10 min,冷缺血4 h,常规心肌保护）、温血停跳液再灌注组（C组,n=8,热缺血10 min,冷缺血4 h,常规心肌保护后添加温血停跳液再灌注）。保存结束后建立Langendorff模型：观察复苏情况,检测冠状静脉窦溢出液（C组检测冠状静脉窦回血）内心肌酶水平,测定平均冠脉流量,描记左室内压波形,计算相应血流动力学指标,测定心肌组织含水量,行组织学检查。结果 A组、C组心脏复苏显著优于B组,前者在复灌初始即全部恢复窦性心律,后者复灌初始全部为室颤,须经历15～20 min恢复窦性心律,其中一只经反复按压至实验结束仍未复律。A组、C组心肌酶漏出水平分别如下。CK：（2191.25±1408.08）U/L,（2918.63±1194.55）U/L;CK-MB：（82.13±37.08）U/L,（472.25±133.74)U/L;AST：(71.25±27.91)U /L、(323.38±102.98) U/L;LDH：（189.50±71.34) U/L、（1548. 38 ±943.62）U/L,均显著高于A组;A组[CK：（94.00±99.42）U/L;CK-MB：（14.75±9.33）U/L;AST：（12.13±28. 59）U/L;LDH：（35.75±28.95）U/L]（P＜0.01）。A组平均冠脉流量为（8.71±1.42）mL/min显著大于B组流量（6.56±1.54）mL/min（P>0.05）,C组平均冠脉流量为（7.96±1.17）mL/min,与A组无统计学差异（P>0.05）。A组和C'组心率（HR）、左室内压上升支最大斜率（+dp/dt max）、左室内压下降支最大斜率（-dp/dt max）分别为HR：（248.22±36.56） bpm、（266.07±27.75) bpm,+dp/dt max：（144.32±32.89）kPa/s、（147. 04±27.04）kPa/s,-dp/dt max：（126.81±35.07）kPa/s,（141.96 ±31.83）kPa/s,两组之间无统计学差异（P>0.05）。B组HR、+dp/dt max、-dp/dt max分别为（177.88±83.96）bpm、（41.33±42.13）kPa/s,（31.77±31.14）kPa/s,显著低于A组（P>0.05）。B组、C组心肌含水量分别为（81.10±1.24）%和(80.52±0.90)%,均显著高于A组（78.90±1.33）%（P>0.05）。B组较A组、C,组心肌及冠脉内皮组织学损伤严重。结论 温血停跳液再灌注显著减少大鼠热缺血供心缺血再灌注损伤,改善复苏及复苏后血流动力学。     

Effects of supplemental sialyl Lewis(x) analogue during warm blood cardioplegia

Effects of supplemental Sialyl Lewisx analogue, a major ligand for all three selectin family members, during warm blood cardioplegia were assessed in the blood perfused isolated rat heart. The isolated hearts were arrested for 60 min with warm blood cardioplegia given at 20-min intervals. This was followed by 60 min of reperfusion. The hearts were divided into the following two groups according to the supplemental drugs added to the cardioplegic solution. The control group (n = 6) received standard warm blood cardioplegia. The Sialyl Lewisx analogue group (n = 6) received warm blood cardioplegia supplemented with Sialyl Lewisx analogue (60 micrograms/ml). Cardiac function, endothelial function, myocardial metabolism and myocardial myeloperoxidase activity were assessed before and after cardioplegic arrest. Left ventricular developed pressure and dp/dt were significantly (p < 0.05) greater and -dp/dt was significantly (p < 0.05) lower in the Sialyl Lewisx analogue group than the control group during reperfusion. Coronary flow at 15 min of reperfusion and NO production, when acetylcholine chloride was added were significantly (p < 0.05) greater in the Sialyl Lewisx analogue group than the control group. Myeloperoxidase activity was significantly (p < 0.05) lower in the Sialyl Lewisx analogue group than the control group. The results suggest that selectin-mediated endothelial-leukocyte interactions may play an important role in myocardial ischemia and reperfusion injury. Supplementation of Sialyl Lewisx analogue during warm blood cardioplegia may provide superior myocardial protection by suppressing leukocyte-endothelial interaction during early reperfusion period.     

心肌保护方法

体外循环心脏手术的心肌保护是心脏外科的一个重要课题。冷晶体停搏液、含血停搏液的心肌保护作用已被广泛研究证实，但该两种心肌保护方法均存在不同程度的心肌缺血性损伤和再灌注损伤。跳动中心内直视手术不阻断心肌血供，避免了心肌缺血损伤及再灌注损伤，临床使用已观察到较冷晶体停跳、含血停跳心脏手术更好的心肌保护作用。