血必净注射液对凝血功能障碍危重病患者的临床价值研究

目的 探讨血必净注射液在有凝血功能障碍危重病患者中的临床应用价值.方法 将67例入住ICU有凝血功能障碍的危重病患者随机分为治疗组34例,对照组33例.两组患者均给予常规综合治疗,治疗组同时给予血必净注射液治疗7 d.治疗前后分别取静脉血,检测凝血功能相关指标[凝血酶原时间(PT)、凝血酶时间(TT)、活化部分凝血活酶时间(APTT)、纤维蛋白原(FIB)和血小板计数(PLT)]及血浆降钙素原(PCT)、白细胞介素-6(IL-6)、C-反应蛋白(CRP)浓度.结果 治疗组治疗前后PLT、PT、APTT、TT、FIB及CRP、IL-6、PCT、急性生理及慢性健康状况评分Ⅱ(APACHEⅡ)比较差异均有统计学意义(P<0.05);治疗后两组PLT、PT、FIB及IL-6、PCT、APACHEⅡ评分比较差异均有统计学意义(P<0.05).结论 血必净注射液可以明显改善危重病患者的凝血功能障碍,减少炎症因子的生成,具有很高的临床应用价值.     

血必净注射液通过改善严重脓毒症患者凝血功能保护肾功能的多中心随机对照临床研究

目的 探讨血必净注射液通过改善严重脓毒症患者凝血功能来保护肾功能的治疗作用和机制.方法 采用多中心、随机、对照的试验设计方法,将128例严重脓毒症患者随机分为血必净治疗组60例与对照组68例.测定血肌酐(Cr)、尿素氮(BUN)、血小板计数(PLT)、凝血酶原时间(PT)、纤维蛋白原(FIB)、活化部分凝血活酶时间(APTT),并观察患者28d生存率.结果 根据凝血功能进行分层分析,治疗组改善肾功能优于对照组,治疗组凝血功能异常亚组对肾功能改善优于治疗组凝血功能正常亚组,治疗组改善28d生存率优于对照组,治疗组凝血功能异常亚组和治疗组凝血功能正常亚组对改善28d生存率两组比较差异无统计学意义.结论 血必净注射液可通过改善严重脓毒症患者凝血功能来保护肾功能,从而降低严重脓毒症患者28d死亡率. 测定血肌酐(Cr)、尿素氮(BUN)、血小板计数(PLT)、凝血酶原时间(PT)、纤维蛋白原(FIB)、活化部分凝血活酶时间(APIrr),并观察患者28d生存率.结果 根据凝血功能进行分层分析,治疗组改善肾功能优于对照组,治疗组凝血功能异常亚组对肾功能改善优于治疗组凝血功能正常亚组,治疗组改善28d生存率优于对照组, 疗组凝血功能异常亚组和治疗组凝血功能正常亚组对改善28d生存率两组比较差异无统计学意义.结论 血必净注射液可通过改善严重脓毒症患者凝血功能来保护肾功能,从而降低严重脓毒症患者28d死亡率. 测定血肌酐(Cr)、尿素氮(BUN)、血小板计数(PLT)     

血必净对脓毒症患者凝血功能的影响

目的 探讨血必净注射液治疗脓毒血症患者时对凝血功能的影响.方法 选取符合人选标准的ICU脓毒症患者42例,分为两组,对照组给予常规综合治疗,治疗组在此基础上加用血必净注射液,分别监测两组患者治疗7d前后PT、APTT、FIB、PLT、D-二聚体.结果 治疗后治疗组较常规组PT、APTT时间均有缩短,PLT值增大,D-二聚体下降,FIB变化不大.结论 血必净注射液可以改善脓毒症患者的凝血功能,在一定程度上改善预后.     

血必净注射液对重症监护病房严重脓毒症患者器官功能保护作用的临床研究

目的 观察血必净注射液对重症监护病房(ICU)严重脓毒症患者器官功能的保护作用.方法 142例严重脓毒症患者按随机数字表法分为血必净治疗组(72例)和对照组(70例).两组均给予常规西医治疗;治疗组在此基础上同时加用血必净注射液50 ml静脉滴注,12 h 1次,连用7 d.观察治疗前后两组患者的生命体征、动脉血气、血常规、肝肾功能、凝血时间等器官功能指标及格拉斯哥昏迷评分(GCS)、Marshall评分、胃肠功能评分、中医体征评分、急性生理学与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分、血清炎症因子水平、血管外肺水指数(EVLWI)及28 d病死率.结果 142例脓毒症患者治疗前有不同程度的肝肾功能损伤、血清促炎因子浓度升高、凝血时间延长、血小板计数(PLT)降低等凝血异常状态,合并肺损伤者EVLWI增高.治疗后治疗组患者氧合指数、PLT较对照组升高显著,白细胞计数、体温、凝血时间[凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、凝血酶时间(TT)]、总胆红素(TBil)、EVLWI、APACHEⅡ评分、中医体征评分、血清促炎因子[肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、IL-8]及28 d病死率均较对照组显著降低(P<0.05或P<0.01).结论 在常规治疗基础上加用血必净注射液能降低严重脓毒症患者升高的血清促炎因子水平,改善临床症状,保护器官功能,改善预后,降低28 d病死率.     

肝硬化患者凝血功能和血小板检测分析

目的探讨肝硬化患者凝血指标-凝血酶原时间(PT)、活化部分凝血酶原时间(APTT)、凝血酶时间(TT)、纤维蛋白原(FIB)和血小板(PLT)检测的临床意义。方法采用ACL-ADVANCE全自动血凝仪检测94例肝硬化患者PT、APTT、TT、FIB,采用ABX-120全自动血细胞分析仪检测PLT,并与健康对照组相比较。结果肝硬化组PT、APTT、TT均较健康对照组显著延长,FIB及PLT明显低于健康对照组(P<0.05);且肝硬化合并出血组PT、APTT、TT高于无出血组,FIB及PLT低于无出血组(P<0.05)。结论及时对肝硬化患者检测凝血功能及血小板有利于了解其肝功能损害程度,预防继发性出血,指导临床诊断。     

血必净注射液联合乌司他丁治疗创伤性脓毒症临床效果及对炎性因子、肝功能影响

目的探讨血必净注射液联合乌司他丁治疗创伤性脓毒症临床效果及对炎性因子、肝功能影响。方法选取2017年1月—2019年12月收治的确诊创伤性脓毒症134例,根据治疗方法不同将其分为观察组和对照组两组各67例。观察组给予血必净注射液联合乌司他丁治疗,对照组给予血必净注射液治疗。两组均连续治疗7 d。观察比较两组治疗前及治疗后3、7 d急性生理与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分,治疗前及治疗后7 d血常规、凝血功能、炎性因子和肝功能情况,以及治疗过程中不良反应发生情况。结果治疗后3和7 d, APACHEⅡ评分两组均低于治疗前,且观察组低于对照组,差异有统计学意义(P0.05)。治疗后7 d,两组血白细胞、中性粒细胞、D-二聚体(D-D)、纤维蛋白原(FIB)、凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、C反应蛋白(CRP)、降钙素原(PCT)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、总胆红素(TBIL)和天冬氨酸转氨酶(AST)均较治疗前降低或缩短,血小板均较治疗前升高;且观察组血中性粒细胞、D-D、FIB、PT、APTT、CRP、PCT、IL-6、TNF-α、TBIL和AST低于或短于对照组,血小板高于对照组,差异有统计学意义(P0.05)。治疗过程中,两组不良反应总发生率比较差异无统计学意义(P0.05)。结论血必净注射液联合乌司他丁治疗创伤性脓毒症患者效果良好,可改善凝血功能,降低炎性因子水平,保护肝功能,且安全性较好。     

ICU脓毒症患者凝血相关参数的变化与预后关系的研究

目的 探讨ICU脓毒症患者凝血相关参数的变化与预后的关系。方法 选取2016年8月至2019年8月收入首都医科大学附属北京朝阳医院京西院区ICU脓毒症患者100例,依据sepsis3.0标准分为脓毒症组50例和脓毒症休克组50例,监测入院24 h和72 h血小板计数（PLT）、血小板压积（PCT）、血小板平均体积（MPV）、凝血酶原时间（PT）、部分凝血酶原时间（APTT）、凝血酶时间（TT）。记录患者入院时年龄、性别、急性生理与慢性健康状况评估（APACHEⅡ）评分、28 d生存情况等。比较脓毒症与脓毒症休克患者入院24 h和72 h凝血相关参数变化的差异,采用受试者工作特征（ROC）曲线分析凝血相关参数对脓毒症患者死亡的预测能力。结果 入院24 h、72 h,脓毒症组PLT、PCT高于脓毒症休克组,MPV、PT、APTT、TT均低于脓毒症休克组,差异均有统计学意义（P<0.05）。入院24 h,APACHEⅡ≤22分组PLT、PCT高于APACHEⅡ> 22分组,MPV、PT、APTT、TT均低于APACHEⅡ> 22分组,差异均有统计学意义（P<0.05）...     

乌司他丁对重症烧伤患者血小板水平及凝血功能的影响

[目的]探讨乌司他丁对重症烧伤患者血小板水平及凝血功能的影响.[方法]选择本院2013年1月至2014年1月就诊的重症烧伤患者25例,将其随机分为观察组(n=13)和对照组(n=12),对照组给予常规治疗,观察组患者在常规治疗的基础上静脉注射乌司他丁,连续用药7 d.观察治疗前及治疗后d1、d3、d7血小板计数(PLT)、血小板粘附率(PAR)、血小板分布宽度(PDW)及血小板平均容积(MPV)的变化,并检测两组患者治疗前及治疗后凝血酶原时间(PT)、凝血酶时间(TT)、部分凝血活酶时间(APTT)、血浆纤维蛋白原(FIB)及血浆-D二聚体(DD)水平.[结果]观察组治愈率显著高于对照组,创面脓毒症、创面感染、电解质紊乱、器官功能障碍发生率均低于对照组,差异均具有统计学意义(均P<0.05);与治疗前比较,两组患者治疗后d1、d3、d7血小板PLT、PAR、MPV、PDW水平显著高于治疗前,差异具有统计学意义(P<0.05);两组患者PT、APTT治疗后较治疗前均明显缩短,FIB、DD水平明显降低,差异均具有统计学意义(均P<0.05).[结论]重症烧伤患者应用乌司他丁对凝血功能具有一定的改善作用,对其病情变化、并发症、器官功能均有较好改善作用.     

乙型慢性病毒性肝炎病患者血小板及凝血功能检测及临床意义

目的 探讨血小板参数及凝血功能与慢性肝炎病患者病情进展的关系.方法 206例乙型慢性病毒性肝炎患者分为4组:A组(54例慢性肝炎患者)、B组(56例慢性肝炎中度患者)、C组(48例慢性肝炎重度患者)、D组(48例肝炎肝硬化患者),对照组为50例健康体检者.各组均用五分类血球仪和全自动血凝仪检测血小板数(PLT)、血小板平均体积(MPV)、血小板体积分布宽度(PDW)及凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、凝血酶时间(TT)、纤维蛋白原(FIB).结果 B组中的PT、APTT、PLT与对照组比较有差异(P<0.05).C组、D组中的PT、APTT、TT及PLT与对照组比较有显著差异(P<0.01).C组中的FIB和D组中的MPV与对照组比较有差异(P<0.05).D组中的FIB与对照组比较有显著差异(P<0.01).结论 血小板参数及凝血指标检测可对临床慢性肝炎诊治提供部分依据,有利于临床对症治疗.     

脑梗死和脑出血患者凝血和血小板状态的研究

目的　探讨脑梗死 ,脑出血患者凝血及血小板方面的变化情况。方法　脑梗死患者 4 0例 ,脑出血患者30例 ,正常对照组 35例 ,患者在发病后 72小时内抽肘静脉血抗凝。患者和对照组均未接受任何止血、凝血药物。分析脑梗死患者与健康人 ,脑出血患者与健康人 ,脑梗死患者与脑出血患者 ,大面积脑梗死患者与腔隙性脑梗死患者在凝血酶原时间 (PT)、活化部分凝血酶原时间 (APTT)、凝血酶时间 (TT)、纤维蛋白原 (FIB)、血小板计数 (PLT)、血小板平均体积 (MPV) 6项指标上有无统计学意义。结果　急性脑梗死组与健康人比较 ,FIB和MPV均明显高于对照组(P <0 .0 1)。高血压性脑出血组与健康人比较 ,FIB和MPV均明显高于对照组 (P <0 .0 1)。急性脑梗死组与高血压性脑出血组比较 ,PT ,APTT ,TT ,FIB ,PLT ,MPV 6项指标均无统计学意义 (P >0 .0 5 )。大面积脑梗死组与腔隙性脑梗死组比较 ,PT ,APTT ,TT ,FIB ,PLT ,MPV 6项指标均无统计学意义 (P >0 .0 5 )。结论　血浆纤维蛋白原升高和血小板体积增大是脑梗死的重要危险因素 ,也是脑出血的重要危险因素。脑梗死与脑出血有共同的发病基础。较大血管闭塞引起的脑梗死与腔隙性脑梗死在凝血与血小板状态方面无统计学意义。     

Blood platelet kinetics and platelet transfusion

The discovery of citrate anticoagulant in the 1920s and the development of plastic packs for blood collection in the 1960s laid the groundwork for platelet transfusion therapy on a scale not previously possible. A major limitation, however, was the finding that platelet concentrates prepared from blood anticoagulated with citrate were unsuitable for transfusion because of platelet clumping. We found that this could be prevented by simply reducing the pH of platelet-rich plasma to about 6.5 prior to centrifugation. We used this approach to characterize platelet kinetics and sites of platelet sequestration in normal and pathologic states and to define the influence of variables such as anticoagulant and ABO incompatibility on post-transfusion platelet recovery. The “acidification” approach enabled much wider use of platelet transfusion therapy until alternative means of producing concentrates suitable for transfusion became available.The identification of platelets as a distinct cellular element of blood with a critical role in hemostasis in the late 1800s (1) inevitably led to speculation about platelet transfusion as a treatment for bleeding in patients with thrombocytopenia. The realization of this goal was delayed for many years by technical barriers. Development of citrate-based anticoagulants in the 1920s and flexible plastic blood containers in the 1950s–1960s made it feasible to collect blood in a plastic pack containing standard acid-citrate-dextrose (ACD) anticoagulant, centrifuge it slowly, and express the supernatant platelet-rich plasma (PRP) into a plastic side-pack for convenient transfusion. Early studies showed that platelets from multiple units of blood were needed to achieve a therapeutic effect in a bleeding patient. To prevent volume overload, this required that platelets be concentrated before being transfused. The obvious way to accomplish this was to centrifuge PRP at high speed, remove the supernatant plasma, and suspend the pelleted platelets in a small volume by gently massaging the plastic pack. It soon became apparent that concentrates prepared in this way almost invariably contained large and small platelet aggregates and few single platelets. Not surprisingly, clinicians were reluctant to transfuse these preparations. It was known at this time that platelets isolated from blood that had been anticoagulated with EDTA could be pelleted from PRP by centrifugation and dispersed without difficulty. To meet the growing demand for platelet transfusions, the Fenwal Company developed the “EDTA Platelet Pack,” consisting of a plastic collection bag containing EDTA and an attached satellite bag into which PRP could be expressed, concentrated by centrifugation into a pellet, and suspended in a small volume of plasma. Red cells were returned to the donor to enable repeated platelet donations. Despite the obvious limitations of this approach, thousands of pooled EDTA platelet concentrates were transfused in the late 1950s and the 1960s. This procedure was labor intensive, and its application was restricted to relatively few, critically ill patients.In 1961, Gardner and associates conducted seminal studies to define the pathophysiology of various thrombocytopenic disorders (2, 3). They labeled EDTA platelets with NaCr⁵¹O₄ to follow the cells after transfusion. In these studies, very few labeled platelets were detected in the peripheral blood during the first few hours after transfusion. After this time, a variable number of cells reentered circulation. The immediate sequestration of a large fraction of the transfused cells, possibly in the liver and lung (4), followed by the eventual return of some platelets into circulation was considered to be a consequence of the labeling procedure. At this time, working at the Thorndike Memorial Laboratory of the Boston City Hospital, we were similarly interested in studying platelet kinetics, and we confirmed the findings of Gardner and coworkers about the circulation kinetics of EDTA platelets. We examined PRP prepared from EDTA and ACD whole blood under phase microscopy and noted that platelet morphology was quite different in the two preparations. In ACD preparations, platelets were discoid in shape, but in EDTA preparations, they assumed an irregular, almost spherical configuration. Another striking difference was the appearance of PRP examined in a light beam while being gently agitated: ACD platelets shimmered and swirled, whereas an EDTA platelet suspension was uniform in appearance throughout. We wondered whether structural changes induced in platelets by EDTA explained the failure of most of these platelets to circulate after transfusion and carried out studies to determine whether platelet clumping in concentrates from ACD-prepared PRP could be prevented. Evaluation of several variables revealed that when the pH of ACD PRP was reduced from its starting value of about 7.2 to about 6.5 before centrifugation, the pelleted platelets could readily be dispersed, yet retained their normal discoid shape. In whole blood or in PRP, this degree of “acidification” could be achieved by simply adding an extra quantity of ACD, the anticoagulant then used routinely for blood collection. The apparent benefit of acidification persisted through repeated centrifugations and made it possible to characterize recovery and survival of ACD platelets in normal subjects (5). Our studies revealed that about 75% of the labeled ACD platelets were recovered in the recipient immediately after transfusion (Figure ​(Figure1).1). After the initial transfusion, the presence of labeled platelets in the blood steadily declined over nine days. In contrast, labeled EDTA platelets peaked in the blood around one day after transfusion and steadily declined afterward (Figure ​(Figure1).1). Scanning of body organs with a directional scintillation counter revealed that most of the radioactivity from ACD platelets not recovered in the blood was initially present in the spleen; however, transfused EDTA platelets mainly concentrated in the liver. As ACD platelets were cleared from the circulation, Cr⁵¹ accumulated in the liver and spleen, indicating that these organs are the major sites of platelet deposition. The linear clearance pattern suggested that under normal circumstances, platelets die as a consequence of “senescence,” rather than being randomly utilized (5). Open in a separate windowFigure 1Survival of autologous “citrate platelets” after transfusion to a normal subject.Approximately 75% of labeled platelets were recovered in the circulation immediately after being transfused. The red area denotes the range of blood platelet radioactivity after the injection of Cr⁵¹-labeled “EDTA platelets” on 10 occasions in 7 normal subjects. Adapted from ref. 5. Freireich and his colleagues at the National Cancer Institute soon confirmed the superiority of platelet concentrates prepared from acidified ACD blood in producing sustained platelet increases in thrombocytopenic patients (6). Over the next few years, this simple maneuver facilitated much wider use of platelet transfusions, especially in patients being treated for hematologic malignancies. We used the new methodology to characterize platelet clearance and sites of sequestration in normal individuals (5, 7) and in patients with platelet destruction mediated by alloantibodies (8) and autoantibodies (9), as well as to more fully define the role of anticoagulants and ABO incompatibility on recovery and survival of transfused platelets (10). We also demonstrated that “hypersplenic” thrombocytopenia is largely caused by pooling of a significant fraction of the total circulating platelet mass in an enlarged spleen, rather than being a consequence of suppressed platelet production or premature platelet destruction (11). Although acidifying citrated blood or PRP to prepare platelet concentrates for transfusion represented a significant improvement over what was previously possible, other advances soon followed. Mourad found that platelet concentrates prepared from nonacidified ACD blood could be manually suspended with little clumping, provided the platelet pellet was allowed to rest for some time at room temperature before manipulation (12). Other key developments were the finding by Murphy et al. that platelet viability is best maintained by storage at room temperature (13) and the evolution of pheresis systems for isolating large quantities of platelets from single donors. To my knowledge, reversible aggregation of platelets pelleted from citrated PRP is still not fully understood, but it seems almost certain that fibrinogen binding to partially activated α_IIbβ₃ integrin (GPIIb/IIIa) is involved, since fibrinogen-dependent platelet aggregation is markedly inhibited at pH 6.5 (6, 14). The EDTA-induced structural changes in platelets were well characterized by White (15). The “swirling” of platelets was shown to be a consequence of their normal discoid shape and to correlate fairly well with post-transfusion viability (16).     

Apheresis donors and platelet function: inherent platelet responsiveness influences platelet quality

BACKGROUND: Process-induced platelet (PLT) activation occurs with all production methods, including apheresis. Recent studies have highlighted the range and consistence of interindividual variation in the PLT response, but little is known about the contribution of a donors' inherent PLT responsiveness to the activation state of the apheresis PLTs or the effect of frequent apheresis on donors' PLTs. STUDY DESIGN AND METHODS: The relationship between the donors' PLT response on the apheresis PLTs was studied in 47 individuals selected as having PLTs with inherently low, intermediate, or high responsiveness. Whole-blood flow cytometry was used to measure PLT activation (levels of bound fibrinogen) before donation and in the apheresis PLTs. The effects of regular apheresis on the activation status of donors' PLTs were studied by comparing the in vivo activation status of PLTs from apheresis (n = 349) and whole-blood donors (n = 157), before donation. The effect of apheresis per se on PLT activation was measured in 10 apheresis donors before and after donation. RESULTS: The level of PLT activation in the apheresis packs was generally higher than in the donor, and the most activated PLTs were from high-responder donors. There was no significant difference in PLT activation before donation between the apheresis and whole-blood donors (p = 0.697), and there was no consistent evidence of activation in the donors immediately after apheresis. CONCLUSION: The most activated apheresis PLTs were obtained from donors with more responsive PLTs. Regular apheresis, however, does not lead to PLT activation in the donors.     

Status of platelet collection and platelet transfusion.

Platelet product derived from single donor plateletpheresis is required to reduce the risks of adverse reactions by blood transfusion. The objectives of this study are to evaluate the status of platelet collection and its efficacy by various kinds of plateletpheresis equipment and to assess the achievement of platelet transfusion by platelet product derived from a single donor. Since the blood centers have introduced some kinds of efficient plateletpheresis equipment, large units of platelet products have been supplied mainly for the patients. Amicus and CCS might be preferable plateletpheresis machines because of their collection efficiencies and wider indication for donors. The average number of donors of platelet product per patient has recently reached nearly 1.0, and around 90% of patients have received platelet product derived from a single donor in the recent several years. However, platelet transfusion derived from a single donor has not yet been completely achieved. Each regional blood center should seriously consider the efficacy of each plateletpheresis equipment and arrange the equipment to collect platelets more effectively to achieve platelet transfusion from a single donor.     

血小板抗体检测及配型对血小板输注无效的临床意义

目的 通过对比血小板配型前后血小板的输注效果,评估血小板抗体检测及配型对血小板输注无效的临床意义.方法 以出血症状改善情况、血小板计数增高指数(CCI)、血小板恢复百分率(PPR)为标准,对比配型前后血小板的输注效果.结果 25例血小板输注无效患者的血小板抗体筛查阳性9例; 9例血小板抗体阳性患者血小板交叉配型前后血小板输注有效率差异有统计学意义(P<0.01),配型后输注的 1 h和24 h CCI、PPR数值明显高于配型前输注的.结论 血小板抗体检测及血小板配型输注可以为患者选择适用的血小板,提高单采血小板的输注有效率,避免滥用血小板.     

Comparison of platelet count and platelet protein methods for determination of platelet MAO activity.

Platelet monoamine oxidase (MAO) activity in 10 normal volunteers was studied as a function of platelet protein or electronically-determined platelet counts. Comparisons of the two methods were made for samples assayed on the same day as well as one week later. The MAO activities resulting from both methods were significantly correlated and reproducible but the results of the platelet count method were, in most instances, slightly but significantly more reliable than the platelet protein method. The relevance of these results to the controversy concerning platelet MAO activity in schizophrenia is discussed.     

Endogenous glutathione and platelet function in platelet concentrates stored in plasma or platelet additive solution

Platelet function was studied in platelet concentrates by assay of the thrombin-induced release of endogenous serotonin and presence of the swirling phenomenon in relation to endogenous glutathione (GSH) and cysteine. In platelets stored in plasma, addition of cysteamine resulted in only a moderate fall in GSH after 5 days of storage, from an average of 14.91 to 11.46 nmol per 109 platelets. Exogenously added GSH had no effect, and addition of buthionine sulfoximine (BSO) resulted in almost complete depletion of GSH, to an average of 0.65 nmol per 109 platelets. Addition of cysteamine or GSH resulted in increased endogenous cysteine whereas BSO had no effect. In platelets stored in a platelet additive solution (T-sol), complete depletion of GSH was found in the presence of cysteamine, GSH and BSO. Endogenous serotonin was unchanged during storage both in plasma and in additive solution (2.8 nmol per 109 platelets). Despite almost total depletion of endogenous GSH, the thrombin-induced release of serotonin after 5 days' storage was significantly affected only in the presence of BSO in platelets stored in additive solution (mean values 72.3% vs. 63.3% of endogeneous serotonin, P < 0.05). Similarly, addition of cysteamine or GSH had no significant effect on swirling but BSO reduced the swirling score after 5 days' storage in platelet additive solution compared with plasma. After 10 days' storage, there was a significant reduction in swirling in the concentrates where BSO was added (P < 0.05).