乌司他丁对创伤失血性休克患者TXA_2/PGI_2平衡和肾功能的影响

目的:探讨乌司他丁(UTI)对失血性休克患者血循环血栓素/前列环素(TXA2/PGI2)平衡的影响及对肾功能的保护机制。方法:将50例患者随机分为UTI组和对照组各25例,UTI组在抗休克、手术止血基础上,术中、术后(术中1次、术后8h1次)给予UTI1700U/kg10次,对照组给予同等次数的等量生理盐水。结果:术后1hUTI组TXA2/PGI2比值就明显低于对照组(P0.05),术后24h两组TXA2/PGI2比值基本一致(P0.05)。两组术后血BUN、Scr均较术前明显升高(P0.05),但升高幅度UTI组明显低于对照组(P0.05),术后恢复明显快于对照组(P0.05)。两组术后尿NAG、γ-GTP均较术前明显升高(P0.05),但升高幅度UTI组明显低于对照组(P0.05)。结论:UTI对失血性休克患者血循环TXA2/PGI2比值失衡有一定的调节作用;UTI通过调节TXA2/PGI2平衡,改善了休克患者肾单位的血流灌注,从而保护了肾脏的滤过功能和肾小管的分泌功能。     

股骨多段闭合骨折病人术前凝血功能的变化

目的 探讨股骨多段闭合骨折病人术前凝血功能的变化。方法 选择创伤股骨多段闭合骨折后当天入院的病人20例,年龄19-45岁,ASA Ⅰ级,为试验组(Ⅰ组);选择健康成年人15人,年龄21-39岁,作为对照组(Ⅱ组);Ⅱ组于清晨空腹采上肢静脉血标本,Ⅰ组病人入院后于骨折的第2天、第6天(手术当天清晨)空腹采上肢静脉血样本,检测血栓弹力图(TEG)指标[R时间、K时间、α角、血栓最大幅度(MA)、血栓硬度(G)]、D-二聚体浓度(D-Di)、血小板计数(PLC)及血小板聚集率(PAgR)的变化。结果 Ⅱ组TEG指标、D-Di、PLC及PAgR均在正常范围。与Ⅱ组比较,Ⅰ组骨折后第2天,K时间缩短(P<0.05),α角、MA、G及D-Di增高(P<0.01);骨折后第6天,R时间缩短(P<0.05),α角、MA、G、D-Di、PLC及PagR增高(P<0.01)。与骨折后第2天比较,Ⅰ组骨折后第6天MA、G、PLT及PAgR增高(P<0.05或0.01)。结论 病人创伤骨折后凝血功能24 h内增强,随时间的延长至术日呈高凝状态,应加强术中管理,并采取相应措施预防术中静脉血栓的发生。     

牵拉子宫时血流动力学变化与血浆PGI_2变化的关系

探讨硬膜外阻滞下行子宫切除术牵拉子宫时血流动力学变化和血浆前列环素变化的关系。２０例病人，ＡＳＡⅠ～Ⅱ级，采用自身对照的方法，于麻醉前、牵拉子宫前、牵拉后５ｍｉｎ、１０ｍｉｎ、１５ｍｉｎ及子宫切除后观察病人血流动力学变化。同时随机选其中１０例抽血测定血浆前列环素和血栓素的变化。结果：牵拉子宫后，ＭＡＰ、ＴＰＲ、ＰＡＷＰ均明显下降，而ＰＧＩ２明显升高，高峰出现于牵拉后１０ｍｉｎ。这提示ＰＧＩ２增加是导致子宫牵拉血流动力学变化的因素之一。     

甲泼尼松龙对体外循环肺内血小板聚集、血栓素生成的抑制作用及其意义

探讨大剂量甲泼尼松龙（ＭＰＳＳ）对肺再灌注早期血小板聚集、血栓素生成的抑制作用。方法将３０例体外循环心脏手术患者随机分成对照组与ＭＰＳＳ用药组，各１５例。用药组于体外循环前静注ＭＰＳＳ１５ｍｇ／ｋｇ体重。３０例患者分别于体外循环前、复跳后１０、４５分钟、２小时抽左右心房血，检测血小板数、ＴＸＢ２及６－ｋｅｔｏ－ＰＧＦ１αｏ。结果对照组复跳后各时相左房血血小板数明显比右房者低（Ｐ＜０．０５），左房血ＴＸＢ２含量明显比右房者高（Ｐ＜０．０１）；而用药组复跳后左、右房血血小板数、ＴＸＢ２差异无显著意义。用药组并能明显降低复跳后ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１α比值（Ｐ＜０．０５～０．０１）。结论大剂量ＭＰＳＳ对肺再灌注早期血小板聚集有明显抑制作用，减少肺内血栓素生成，降低血栓素／前列环素比值，起到预防或减少灌注肺发生的作用。     

慢性肾脏病各期ET、TXA_2、PGI_2的临床观察及与血瘀证关系的探讨

目的：探讨内皮素（ET）、血栓素A2（TXA2）、前列腺素I2（PGI2）在慢性肾脏病进展中的作用,及与血瘀证的关系。方法：测定135例来我院门诊和住院的2～4期慢性肾脏病（MDRD公式计算GFR以确定分期）患者的血清肌酐（Scr）、尿素氮（BUN）、血清白蛋白（Alb）、内皮素（ET）、6-酮-前列腺素F1α（6-Keto-PGF1α）、血栓素B2（TXB2）,并与正常对照组相比,观察不同慢性肾脏病分期患者ET、TXB2、6-Keto-PGF1α的变化;并将这些患者分为血瘀证和非血瘀证,观察各期患者血瘀证的检出率,各期血瘀证和非血瘀证患者ET、TXB2、6-Keto-PGF1α的差异。结果：从CKD2期到4期,ET逐渐增高,2期、3期、4期均与正常对照组差异有统计学意义（P〈0.05）,2期和3期之间差异无统计学意义,4期分别与正常对照组、2期、3期相比差异有统计学意义（P〈0.05）;从CKD2期到4期,TXB2逐渐增高,6-Keto-PGF1α逐渐降低,2期、3期、正常对照组之间差异均无统计学意义,4期分别与正常对照组、2期、3期差异有统计学意义（P〈0.05）。从2期到4期,血瘀证检出率逐步增加（2期21.4%,3期49.0%,4期68.2%）,CKD2期和3期的血瘀证均较非血瘀证ET、TXB2为高,6-Keto-PGF1α为低,差异有统计学意义（P〈0.05）,而CKD4期的血瘀证较非血瘀证ET、TXB2为高,6-Keto-PGF1α为低,差异无统计学意义（P〉0.05）。结论：慢性肾脏病患者凝血机制的紊乱随着CKD的进展逐步增加,在进入CKD4期后尤为明显,TXA2/PGI2的代谢异常,血小板活化,内皮细胞受损是慢性肾脏病进展的重要因素。凝血机制紊乱在临床上可表现为血瘀证,随着CKD进展,血瘀证患者逐步增多,在CKD4期血瘀证虽然较非血瘀证患者的凝血机制有异常,但无明显差异,提示CKD4期非血瘀证患者虽然没有宏观的血瘀表现,仍可能存在肾脏的微型癥积,即肾脏局部的瘀血阻络是慢性肾脏病进展的重要因素之一。     

非体外循环冠状动脉旁路移植术后的阿司匹林抵抗

目的 通过检测非体外循环冠状动脉旁路移植术(OPCAB)后患者血小板聚集率以及尿11-脱氢-血栓烷B2(11-DH-TXB2)指标，动态观察术后阿司匹林抵抗(AR)的发生情况，探索术后AR的危险因素。方法 冠心病患者290例，首次行OPCAB患者145例(手术组)，接受内科药物治疗患者145例(非手术组)。手术组患者于术前及术后服用阿司匹林后第1、4、10天及6个月，检测血小板聚集率以及尿11-DH-TXB2。非手术组患者于服药前及服药后第1、4、10天检测上述指标。同时记录患者各项临床资料。结果 手术组患者服用阿司匹林后第1天的AR发生46例(32％)(抵抗组)，其余为非抵抗组。用药后第4天和第10天AR患者下降至19例(13％)和5例(3％)。半年随访中未发现有AR患者存在。非手术组患者，服药后第1天，血小板聚集率均下降至20％以下，平均(8.8±6.8)％，未见AR现象出现。手术组患者术后血小板计数显著高于术前(P＜0.05)。Logistic回归分析发现，OPCAB患者中，体重大于75 kg(OR =0.38，95％CI:0.18～0.79)和术后引流量超过500 ml(OR=3.12，95％CI:1.29～7.53)为术后出现AR的危险因素。结论 OPCAB术后早期，阿司匹林的抗血小板作用受到不同程度抑制，部分患者出现AR现象，予以更为积极有效的抗血小板治疗有重要临床意义。     

实验性胰腺炎大鼠血浆ET和PGI_2水平的改变及川芎嗪治疗的影响

目的 :探讨内皮素 (ET)与前列环素 (PGI2 )在急性出血坏死性胰腺炎 (AHNP)病理生理中的作用及川芎嗪 (TMP)治疗意义。 方法 :动态测定AHNP大鼠血浆ET和PGI2 水平 ,观察胰腺组织形态及大鼠的存活率 ,并观察TMP对它们的影响。结果 :AHNP大鼠术后随时间延长 ,血浆ET含量及ET/PGI2 比值递增 ,胰腺组织病理形态损害加重 ,均较假手术组有显著性差异 (P <0 .0 5 ) ;腹腔注射TMP组血浆ET含量及ET/PGI2 比值较之降低 ,且ET/PGI2 比值接近正常 ,胰腺出血坏死程度及腺泡细胞超微结构破坏减轻 ,大鼠存活率提高 ,均较AHNP对照组有显著性差异 (P <0 .0 5 )。 结论 :AHNP大鼠早期存在着ET与PGI2 平衡失调 ,此平衡失调可通过胰腺血循环障碍而在AHNP大鼠病理生理中起重要作用。TMP对AHNP大鼠有一定治疗作用 ,可能与纠正ET、PGI2 失衡从而改善胰腺微循环、降低血清淀粉酶有关。     

CT灌注成像早期诊断犬急性脑梗死的实验研究

目的探讨CT灌注成像技术(CTP)对脑梗死超急性期诊断的应用价值。方法成年比格犬10只,介入技术建立犬急性脑栓塞动物模型,分别在栓塞前及栓塞后2 h行脑血管造影,观察所栓塞血管的血流情况,同时在栓塞后2 h行CT平扫及CTP检查。24 h处死动物后取脑组织进行病理检查。结果10只犬全部成功栓塞左侧大脑中动脉,其中4只合并其他脑血管栓塞,至栓塞后2 h造影所有被栓血管没有发生再通。CT平扫没有发现明确异常,CTP检查显示9只局部脑血流量减少为对侧的33.7%~69.2%(平均0.483±0.132),1只无明显的变化,与数字减影血管造影诊断比较没有明显的统计学差异(P>0.05)。24 h后动物均存活,没有出现严重并发症,病理检查证实在深部脑组织皆出现脑梗死病灶。结论CTP检查可快速、准确、无创地评价犬急性局部脑梗死动物模型的脑血流动力学变化。     

连续腰麻下子宫牵拉对血液动力学及血浆TXA2、PGI2水平的影响

目的观察在连续腰麻下牵拉子宫对血液动力学及血浆TXA2、PGI2水平的影响.方法子宫切除术病人30例,选L2-3间隙行蛛网膜下腔穿刺,置入Spinocath导管,通过留置的导管注入的重比重0.5%布比卡因进行连续腰麻,观察子宫牵拉前后血液动力学的变化,并于麻醉前、手术前、牵拉子宫前、牵拉子宫10min及手术后15min抽静脉血测定血浆TXB2、6-keto-PGF1α的浓度.结果连续腰麻下,镇痛肌松效果均满意,下肢运动均达完全阻滞.在子宫切除术中牵拉子宫后血压下降明显,心率减慢(P＜0.05);子宫牵拉10min时血浆TXB2、6-keto-PGF1α的水平明显增高(P＜0.01),TXB2/6-keto-PGF1α(T/K)比值显著降低(P＜0.01);子宫牵拉所致的低血压与6-keto-PGF1α、T/K比值的变化有相关性(P＜0.05).结论在连续腰麻下,牵拉子宫可造成血液动力学的改变,与牵拉子宫引起PGI2的释放,T/K的比值降低有关.     

烧伤早期血清CRP、C_3、T_f、PA变化及临床意义

为探索烧伤早期血清急性期蛋白的变化规律及其临床意义，将３２例烧伤病人按烧伤总面积大小分为小于２０％，２０％～５０％和大于５０％三组。于伤后８，２４，４８，７２小时采血，组３加测伤后７，１４，２１天三个时相点以观察与感染的关系。以免疫速率散射浊度法测定ＣＲＰ，Ｃ３，Ｔｆ用琼脂扩散法，ＰＡ用火箭免疫电泳法测定。结果表明：伤后４８～７２小时血清ＣＲＰ达到高峰（Ｐ＜０．０１）；伤后８小时Ｃ３显著下降（Ｐ＜０．０５），２４小时达最低值，Ｃ３下降与ＣＲＰ升高无相关性（ｒ＝０．０８８５，Ｐ＞０．０５）；４８小时Ｔｆ显著下降（Ｐ＜０．０１），ＰＡ与Ｔｆ变化相似。感染及脓毒症发生时各监测指标变化不显著。提示：①ＣＲＰ的变化主要反映组织损伤的程度而不能预示脓毒症的易感性；②Ｃ３下降并非ＣＲＰ升高引起。Ｔｆ下降有利于细菌生长。     

麻醉药对TxA_2-PGl_2平衡及血小板聚集性影响的临床观察

本文用放射免疫方法测定了胆囊切除术患者在麻醉期间血浆TXB_2、PGF_(lu)水平,同时观察了血小板聚集功能。结果发现以利多卡因和地卡因施行硬膜外麻醉对上述花生四烯酸代谢产物无明显影响,而异氟醚吸入麻醉则使TXB_2和PGF_(lα)。增加,并抑制由ADP诱导的血小板聚集。这些发现的具体临床意义及实际净效应有待进一步探讨。     

实验性脊髓损伤早期三七总皂甙对PGI2和TXA2的影响

将４８只Ｗｉｓｔａｒ大鼠随机分为两组，Ａｌｌｅｎ’ｓ脊髓损伤模型２５０ｇ．ｃｍ致致伤Ｔ１３－Ｌ１脊髓节段，实验组伤后３０ｍｉｎ，２ｈ及４ｈ，腹腔注射三七总皂甙，对照组伤后不做任何处理。１ｈ及４ｈ时伤区脊髓组织放射免疫测定前列腺素Ｉ２和血小板血栓素Ａ２的稳定分解产物６ｋｅｔｏ－ＰＧＦ１α和ＴＸＢ２，同时作病理检查。     

地氟醚维持麻醉对SjvO2和CSFP的影响

研究地氟醚维持麻醉时ＰａＣＯ２对ＳｊｖＯ２和ＣＳＦＰ的影响。方法：４３例脑肿瘤病人用地氟醚维持麻醉,术中持续监测颅内压和动脉压。当人为改变ＰＥＴＣＯ２时,取颈内静脉血和同步采集动脉血作血气分析和测定两者乳酸含量。     

Correlation Between Jugular Bulb Oxygen Saturation and Partial Pressure of Brain Tissue Oxygen During CO2 and O2 Reactivity Tests in Severely Head-Injured Patients

Summary  Purpose. To correlate the jugular bulb oxygen saturation (SjvO₂) and brain tissue oxygen pressure (PbtO₂) during carbon dioxide (CO₂) and oxygen (O₂) reactivity tests in severely head-injured patients.  Methods and Results. In nine patients (7 men, 2 women, age: 26±6.5 years, GCS of 6.5±2.9), a polarographic microcatheter (Clark-type) was inserted into nonlesioned white matter (frontal lobe). PbtO₂ and SjvO₂ were monitored simultaneously and cerebral vasoreactivity to CO₂ and O₂ was tested on days three, five and seven after injury. Simultaneous measurements of vasoreactivity by transcranial Doppler (TCD) were undertaken. A total of twenty-one CO₂ and O₂ reactivity tests were performed. Critical values of PbtO₂ (<15 mm Hg) during induced hyperventilation could be observed four times in two patients. High PbtO₂ values up to 80 mm Hg were observed during hyperoxygenation (FiO₂ 100%). CO₂ vasoreactivity by means of PbtO₂ was absent in four tests in which measurements by TCD showed intact responses. A stronger correlation between SjvO₂ and PbtO₂ during the O₂ reactivity tests was observed (r=0.6, p<0.001), in comparison to values obtained during the CO₂ reactivity tests (r=0.33, p<0.001). In addition, there was no statistically significant correlation (r=0.22, p=0.26) between CO₂ reactivity values measured by TCD (4.5±5.7%) and PbtO₂ (3±2.8%).  Conclusions. Correlation between SjvO₂ and PbtO₂ during CO₂ reactivity test is low, even if significant differences between normo- and hyperventilation values are present. In comparison to SjvO₂, monitoring of PbtO₂ might more accurately detect possible focal ischaemic events during rapidly induced hyperventilation in severely head-injured patients. The CO₂ vasoreactivity by means of changes in Vm MCA seems to be higher in comparison to changes of PbtO₂. These observations lead to the hypothesis that vasoreactivity measured by TCD overestimates the cerebrovascular response to CO₂.     

Effects of Prostaglandin F2α and Cisapride on Small Intestinal Activity During the Early Postoperative Period in Humans

2 α (PGF) and cisapride were investigated during the early postoperative period in 26 patients who underwent abdominal surgery. Records of intestinal motility were made using an infusion catheter. PGF, 0.4 μg/kg per minute, given intravenously over 60 min, and cisapride, 5 mg, given intraintestinally, were administered to 13 patients each, first immediately after the operation, and then after the migrating motor complexes (MMCs) had reappeared following a period of intestinal quiescence. The MMCs were reestablished within the first postoperative day. Both PGF and cisapride stimulated irregular, high-amplitude contractions; however, the MMCs reappeared following these induced contractions only if the drugs were administered just after the postoperative MMCs became evident. These prokinetic drugs did not affect gastrointestinal hormone concentrations, but induced contractile activity even in the early postoperative period. Although the findings of this study demonstrate that these drugs may be useful as prokinetic agents to promote recovery from postoperative ileus just after the reappearance of MMCs in the early postoperative period, their precise mode of action has not been established. (Received for publication on May 7, 1997; accepted on Nov. 6, 1997)     

地氟醚维持麻醉对S_(jv)O_2和CSFP的影响

目的 :研究地氟醚维持麻醉时PaCO2 对SjvO2 和CSFP的影响。方法 :43例脑肿瘤病人用地氟醚维持麻醉 ,术中持续监测颅内压和动脉压。当人为改变PETCO2 时 ,取颈内静脉血和同步采集动脉血作血气分析和测定两者乳酸含量。结果 :地氟醚浓度 <1MAC时 ,ICP随PaCO2 变化而变化 ,SjvO2 与PaCO2 呈显著正相关 ,低PaCO2 可能增加脑静脉血乳酸含量。地氟醚 >1MAC时 ,SjvO2 与PaCO2 相关性差 ,静脉乳酸含量变化小。正常CPP条件下进行过度通气时 ,SjvO2 值仅与地氟醚浓度呈显著正相关。结论 :神经外科病人用地氟醚维持麻醉时 ,浓度为≤ 1MAC维持脑静脉血氧饱和度对二氧化碳反应性 ,可能具有剂量依赖性脑血管扩张效应。     

后腹腔镜CO2气腹对机体免疫功能的影响

目的：探讨后腹腔镜CO2气腹对机体免疫功能的影响。方法：前瞻性研究患者在后腹腔镜CO2气腹手术前后静脉血中IL-2和IL-6值的变化,以了解后腹腔镜CO2气腹对机体免疫功能的影响。以腹膜后开放手术作为对照。结果：腹腔镜组患者术前、手术开始45min、手术后第1天和手术后第3天IL-2值为先下降后回升,但此变化差异无统计学意义（P〉0．05）;IL-6值为先升高后下降,但此变化亦无统计学意义。而开放手术上述4时间段IL-2值为先下降后升高,此变化规律与腹腔镜手术相仿;IL-6值为先升高后下降,此变化规律亦与腹腔镜手术相仿,但上述变化均无统计学意义（P〉0．05）。结论：后腹腔镜CO2气腹对机体免疫功能的影响小,可能与后腹腔镜气腹空间小、对机体尤其是内脏功能干扰小有关。     

BMP2 Regulation of CXCL12 Cellular,Temporal, and Spatial Expression Is Essential During Fracture Repair

The cellular and humoral responses that orchestrate fracture healing are still elusive. Here we report that bone morphogenic protein 2 (BMP2)‐dependent fracture healing occurs through a tight control of chemokine C‐X‐C motif‐ligand‐12 (CXCL12) cellular, spatial, and temporal expression. We found that the fracture repair process elicited an early site‐specific response of CXCL12⁺‐BMP2⁺ endosteal cells and osteocytes that was not present in unfractured bones and gradually decreased as healing progressed. Absence of a full complement of BMP2 in mesenchyme osteoprogenitors (BMP2^cKO/+) prevented healing and led to a dysregulated temporal and cellular upregulation of CXCL12 expression associated with a deranged angiogenic response. Healing was rescued when BMP2^cKO/+ mice were systemically treated with AMD3100, an antagonist of CXCR4 and agonist for CXCR7 both receptors for CXCL12. We further found that mesenchymal stromal cells (MSCs), capable of delivering BMP2 at the endosteal site, restored fracture healing when transplanted into BMP2^cKO/+ mice by rectifying the CXCL12 expression pattern. Our in vitro studies showed that in isolated endosteal cells, BMP2, while inducing osteoblastic differentiation, stimulated expression of pericyte markers that was coupled with a decrease in CXCL12. Furthermore, in isolated BMP2^cKO/cKO endosteal cells, high expression levels of CXCL12 inhibited osteoblastic differentiation that was restored by AMD3100 treatment or coculture with BMP2‐expressing MSCs that led to an upregulation of pericyte markers while decreasing platelet endothelial cell adhesion molecule (PECAM). Taken together, our studies show that following fracture, a CXCL12⁺‐BMP2⁺ perivascular cell population is recruited along the endosteum, then a timely increase of BMP2 leads to downregulation of CXCL12 that is essential to determine the fate of the CXCL12⁺‐BMP2⁺ to osteogenesis while departing their supportive role to angiogenesis. Our findings have far‐reaching implications for understanding mechanisms regulating the selective recruitment of distinct cells into the repairing niches and the development of novel pharmacological (by targeting BMP2/CXCL12) and cellular (MSCs, endosteal cells) interventions to promote fracture healing. © 2015 American Society for Bone and Mineral Research.     

Deletion of Rac in Mature Osteoclasts Causes Osteopetrosis,an Age‐Dependent Change in Osteoclast Number,and a Reduced Number of Osteoblasts In Vivo

Rac1 and Rac2 are thought to have important roles in osteoclasts. Therefore, mice with deletion of both Rac1 and Rac2 in mature osteoclasts (DKO) were generated by crossing Rac1^flox/flox mice with mice expressing Cre in the cathepsin K locus and then mating these animals with Rac2^‐/‐ mice. DKO mice had markedly impaired tooth eruption. Bone mineral density (BMD) was increased 21% to 33% in 4‐ to 6‐week‐old DKO mice at all sites when measured by dual‐energy X‐ray absorptiometry (DXA) and serum cross‐linked C‐telopeptide (CTx) was reduced by 52%. The amount of metaphyseal trabecular bone was markedly increased in DKO mice, but the cortices were very thin. Spinal trabecular bone mass was increased. Histomorphometry revealed significant reductions in both osteoclast and osteoblast number and function in 4‐ to 6‐week‐old DKO animals. In 14‐ to 16‐week‐old animals, osteoclast number was increased, although bone density was further increased. DKO osteoclasts had severely impaired actin ring formation, an impaired ability to generate acid, and reduced resorptive activity in vitro. In addition, their life span ex vivo was reduced. DKO osteoblasts expressed normal differentiation markers except for the expression of osterix, which was reduced. The DKO osteoblasts mineralized normally in vitro, indicating that the in vivo defect in osteoblast function was not cell autonomous. Confocal imaging demonstrated focal disruption of the osteocytic dendritic network in DKO cortical bone. Despite these changes, DKO animals had a normal response to treatment with once‐daily parathyroid hormone (PTH). We conclude that Rac1 and Rac2 have critical roles in skeletal metabolism. © 2015 American Society for Bone and Mineral Research.     

In vitro and in vivo effects of BT563, an anti-interleukin-2 receptor monoclonal antibody

Abstract BT563, a murine anti-IL-2R MoAb, was found to be more potent than anti-Tac in inhibiting proliferation in the mixed lymphocyte reaction. Results obtained with 33 B3.1 in these experiments were similar to those with BT563. The anti-IL-2R MoAb 2A3 was shown to be a suitable agent for monitoring the effect of BT563 on peripheral blood. IL-2R-positive cells were not detected in peripheral blood samples from 1 h after the first dose until 8 days after the last dose. Plasma trough levels were measured in patients receiving 5 or 10 mg daily. The administration of BT563 to allograft recipients did not lead to clinically significant side effects.