正常淋巴液对大鼠血液流变性异常的干预作用

目的观察外源性正常淋巴液对高分子右旋糖酐(Dextran500)致大鼠血液流变性异常的干预作用。方法Wistar雄性大鼠30只,随机分为淋巴液组、模型组和对照组,静注10%Dextran500(10ml/kg·bw)复制急性血液流变性异常模型(对照组以等量生理盐水代替)。6min后,淋巴液组自颈静脉缓慢推注肠淋巴液(全血量的1/15),其它两组以等量生理盐水代替。40min后,观察血液流变学指标及红细胞流变学指标的变化。结果模型组全血黏度、全血相对黏度、血浆黏度、Hct、ESR、红细胞电泳时间显著高于对照组(P<0.05~0.01);模型组和淋巴液组红细胞电泳率、细胞迁移率显著低于对照组(P<0.01);淋巴液组全血相对黏度、Hct、ESR、红细胞电泳时间、红细胞变形指数显著高于对照组(P<0.05~0.01),且全血黏度、全血相对黏度、全血还原黏度显著低于模型组,红细胞变形指数均显著高于模型组和对照组(P<0.05~0.01)。结论外源性正常淋巴液能明显改善Dextran500所致的急性血液流变性异常。     

淋巴液干预休克时肠系膜微循环的变化

目的探讨不同部位淋巴液(胸导管淋巴液和肠淋巴液)对重症失血性休克大鼠的治疗作用。方法30只Wistar大鼠分为肠淋巴液治疗组和生理盐水对照组(n=15);另30只分为胸导管淋巴液治疗组和白蛋白对照组(n=15)。引流正常犬的肠淋巴液和胸导管淋巴液 ,常规处理后 ,冷冻备用。实验均按Lamson法自颈总动脉放血至血压为5.32kPa ,维持1h ,复制重症失血性休克模型。治疗组经自动抽注机从颈静脉输入肠淋巴液或胸导管淋巴液(量为失血量1/5 ,失血量按丢失全血量的1/3计算)并以等量的生理盐水稀释 ;对照组分别以等量生理盐水代替肠淋巴液或等量的3.8 %白蛋白溶液代替胸导管淋巴液。应用显微电视录像设备 ,对比观察肠系膜微血管口径和流态的变化 ,以及肠系膜微淋巴管收缩性指数的变化 ,并记录存活时间。结果休克时各组均出现显著的血液和淋巴微循环障碍 ,输入肠淋巴液或胸导管淋巴液治疗 ,均有良好的抗休克效果。肠淋巴液治疗组的存活时间显著长于生理盐水对照组(P<0.05)。治疗组输入肠淋巴液后 ,血压显著回升 ,肠系膜微动脉、微静脉和微淋巴管的痉挛解除 ,口径均恢复正常 ,血液流态明显改善 ,微淋巴管收缩性指数恢复正常 ,而生理盐水对照组的上述指数仍处于休克时的低水平 ,除微淋巴管收缩频率未见统计学差异外 ,治疗组的     

输入肠淋巴液治疗休克的作用及其微循环机制

目的探讨输入小量肠淋巴液或胸导管淋巴液对重症失血性休克的治疗效果及其改善微循环障碍的作用.方法Wistar雄性大鼠60只,均分为肠淋巴液治疗组、胸导管淋巴液治疗组、白蛋白组及生理盐水对照组(均n=l5).Lamson法自颈总动脉放血至血压5.3kPa,维持1h,复制重症失血性休克.立即以自动抽注机分别静脉输入无细胞肠淋巴液或胸导管淋巴液(量为失血量的l/5,失血量按全血量的1/3计算),并以等量生理盐水稀释;对照组分别输入等量3.8%白蛋白或生理盐水.通过显微电视录相对比观察休克及治疗过程中各组动物回肠下段肠系膜的血液和淋巴微循环变化,并连续记录颈总动脉血压,观察存活时间.结果休克时各组大鼠均出现显著的血液和淋巴微循环障碍,且随着低血压时间的延长而逐渐加重.不论输入肠淋巴液或胸导管淋巴液后,肠系膜一、二级细动脉、细静脉和微淋巴管的痉挛解除,口径均恢复正常;血液流态由休克时的粒缓流、泥流、停流,改善为粒流、粒线流、线粒流;休克时降低的微淋巴管收缩分数、总收缩活性指数和淋巴管动力学指数均恢复正常;而白蛋白与生理盐水对照组的血液及淋巴微循环障碍未见明显改善,与两个淋巴液治疗组形成了鲜明的对比(P＜0.05,P＜0.01)、但各组的微淋巴管收缩频率均未见显著改善,且组间无明显差异.此外,输入肠淋巴液或胸导管淋巴液后,血压均显著回升,且明显高于白蛋白及生理盐水对照组(P＜0.05,P＜0.01),两个淋巴液治疗组的存活时间也显著长于应用白蛋白及生理盐水者(P＜0.01).在两种淋巴液治疗组之间、白蛋白与生理盐水对照组之间,未见组间差异(P＞0.05).讨论肠淋巴液和胸导管淋巴液均能改善失血性休克大鼠的血液和淋巴微循环障碍、提升血压和延长存活时间,这种对休克良好的治疗作用是不同部位淋巴液的共性,由于其用量小,结合对照组的观察表明,其治疗作用难以用补充血容量及恢复渗透压解释,而改善微循环的作用,可能是一个重要的治疗机理.结论不同部位淋巴液均有良好的治疗休克作用,其治疗机理与改善血液及淋巴微循环障碍有关.     

正常淋巴液对大鼠血小板功能及肝、肾、肺组织形态的影响

目的观察外源性正常淋巴液对高分子右旋糖苷(Dextran 500)致血液流变性异常时,大鼠血小板功能以及肝、肾、肺形态的影响。方法W istar雄性大鼠30只,随机分为淋巴液治疗组、生理盐水治疗组和正常对照组,静注10%Dextran 500(10 m l/kg.BW)复制急性血液流变性异常模型(正常对照组以等量生理盐水代替)。6 m in后,淋巴液治疗组自颈静脉缓慢注射小量肠淋巴液(全血量的1/15),其它两组以等量生理盐水代替。40 m in后,观察血小板功能以及器官形态的变化。结果两治疗组血小板黏附率、解聚率明显高于正常对照组(P<0.01~0.05),且血小板聚集率、脑血流量、血栓形成长度、湿重、干重及血栓形成率均显著低于正常对照组(P<0.01),淋巴液治疗组血小板黏附率、血栓干重、血小板聚集率显著低于生理盐水治疗组(P<0.01~0.05)。病理形态学显示,正常对照组肝、肾、肺结构正常,生理盐水治疗组各器官病变较重,多见红细胞瘀滞、血栓形成及坏死,淋巴液治疗组病变较轻,未见坏死。结论外源正常淋巴液能明显改善Dextran 500所致急性血液流变性异常大鼠的血小板功能及器官形态。     

淋巴液对失血性休克大鼠肠系膜微循环变化的影响

大鼠３０只，分为肠淋巴液治疗组及生理盐水对照组，复制重度失血性休克模型后，应用显微电视录像技术观察淋巴液对肠系膜微血管及微淋巴管的作用。结果：治疗组的存活时间显著长于对照组。输入淋巴液后，血压显著回升，肠系膜一、二级细动脉、细静脉口径和微淋巴管的静态口径均恢复正常，流态改善，微淋巴管收缩性恢复正常。提示肠淋巴液可以改善休克时的血液和淋巴循环障碍，对休克具有较好的治疗作用     

Rho激酶在阻断休克肠淋巴液回流、提高大鼠血管钙敏感性中的作用

目的: 观察Rho激酶在肠淋巴管结扎或肠淋巴液引流提高失血性休克大鼠血管钙敏感性中的作用。方法: Wistar雄性大鼠随机分为假手术组(sham)、失血性休克组(shock)、休克肠淋巴管结扎组(shock+ligation,行肠淋巴管结扎)、休克肠淋巴液引流组(shock+drainage,行肠淋巴液引流),在休克3 h或sham组的相应时点,制备肠系膜上动脉(SMA)血管环,采用离体血管环张力测定技术,观察SMA血管环对梯度钙离子收缩性的变化;shock+ligation与shock+drainage组SMA血管环分别与Rho激酶激动剂血管紧张素Ⅱ(Ang Ⅱ)、抑制剂fasudil孵育后,观察钙敏感性变化。结果: Shock组SMA血管环的钙敏感性显著低于sham组;shock+ligation组与shock+drainage组SMA血管环钙敏感性显著高于shock组,但低于sham组。Shock+ligation组与shock+drainage组SMA血管环与AngⅡ或fasudil孵育后,AngⅡ不同程度地提高了shock+ligation组与shock+drainage组大鼠SMA血管环对梯度钙离子的收缩性与pD₂;fasudil显著降低了两组大鼠SMA血管环对梯度钙离子的收缩性与最大收缩力E_max,降低了shock+ligation组的pD₂。结论: Rho激酶在阻断休克肠淋巴液回流提高血管钙敏感性中发挥重要作用。     

益母草注射液对失血性休克大鼠转归时淋巴循环的干预作用

目的探讨益母草注射液（LHI）对失血性休克转归时淋巴循环的干预作用。方法采用淋巴学研究方法，对16只Wistar雄性大鼠进行研究，观察LHI对失血性休克大鼠肠淋巴循环的作用。结果失血性休克时，肠淋巴流量、淋巴细胞输出量明显降低，淋巴液中有少量单核细胞，经LHI治疗后，肠淋巴流量、淋巴细胞输出量增加，并且淋巴液中单核细胞增多，与对照组比较有显著性差异（P〈0．05）。此外，LHI可明显降低淋巴液黏度，其作用明显强于对照组（P〈0．05）。结论LHI能通过增强淋巴转运功能、降低淋巴液黏度而改善失血性休克时的淋巴循环障碍。     

肠血管活性多肽或生长抑素抑制大鼠肠CD8~+淋巴细胞归巢

为观察肠血管活性多肽 (VIP )及生长抑素 (SST )对大鼠肠淋巴细胞在肠相关淋巴组织归巢的影响 ,本实验将 18只大鼠随机分为三组 ,每组 6只 ,分别从股静脉输入生理盐水、VIP组或SST ,从肠系膜淋巴管插管引流淋巴液。结果显示 ,大鼠经静滴VIP或SST后 ,5h内肠系膜淋巴管淋巴细胞总数降低 (P <0 0 5 ) ;肠淋巴液量和对照组比较无显著改变 (P >0 0 5 ) ;每毫升淋巴液中细胞数降低 (P <0 0 5 )。VIP组和SST组肠淋巴液中CD8+ 细胞比例降低 (P <0 0 5 )。两实验组回肠粘膜CD8+ 细胞数降低 (P <0 0 5 )。VIP或SST能减少肠粘膜CD8+ 淋巴细胞与其他器官及系统免疫的沟通 ,也抑制从其他器官及系统免疫中归巢至肠粘膜的CD8+ 细胞     

休克淋巴液对肠系膜微淋巴管内皮细胞炎症介质表达的影响

目的：观察休克淋巴液对大鼠肠系膜微淋巴管内皮细胞（MMLEC）诱生型一氧化氮合酶（iNOS）、肿瘤坏死因子（TNF-α）、白细胞介素6（IL-6）表达的影响，探讨休克淋巴液损伤MMLEC的机制。方法：正常大鼠MMLEC原代培养，应用第三代MMLEC进行研究。无菌条件下复制大鼠重症失血性休克模型（血压40 mmHg，维持90 min），引流休克时肠淋巴液及门静脉血，并以正常肠淋巴液、门静脉血作为对照。以4%终浓度的休克淋巴液作用MMLEC 6 h，以休克血浆、正常淋巴液、正常血浆、胎牛血清（FBS）、DMEM培养液作为对照。提取MMLEC的cDNA，RT-PCR检测iNOS、TNF-α及IL-6 mRNA的表达；同时检测培养上清液MDA、NO、TNF-α及IL-6含量的变化。结果：4%终浓度的休克淋巴液作用6 h后，MMLEC的iNOS、TNF-α、IL-6 mRNA表达以及培养上清液MDA、NO、TNF-α和IL-6水平显著高于正常淋巴液组、休克血浆组、正常血浆组、FBS组以及DMEM组；且休克血浆作用MMLEC 6 h后的iNOS、TNF-α、IL-6 mRNA表达以及培养上清液的MDA、NO、TNF-α及IL-6水平显著高于正常淋巴液组、正常血浆组、FBS组以及DMEM组。结论：休克淋巴液可使大鼠MMLEC的 iNOS、TNF-α及IL-6 mRNA表达增强，促进自由基释放，从而诱导细胞损伤。     

休克淋巴液对大鼠内皮细胞VEGF表达的影响

目的观察休克淋巴液对大鼠肺微血管内皮细胞(PMVEC)、肠系膜微淋巴管内皮细胞(MMLEC)、血管内皮生长因子(VEGF)表达的影响。方法无菌条件下复制大鼠重症失血性休克模型,引流休克时肠系膜淋巴液或收集门静脉血,同时收集正常淋巴液及门静脉血作为对照。以4%终浓度的处理因素与第3代PMVEC及MMLEC共同孵育6h,RT-PCR测定VEGF mRNA表达。结果不同处理因素与PMVEC及MMLEC孵育6h后,休克淋巴液组两种内皮细胞的VEGF mRNA表达均显著低于休克血浆组、正常淋巴液组、正常血浆组、胎牛血清(FBS)组、DMEM组;休克血浆组显著低于正常淋巴液组、正常血浆组、FBS组和DMEM组;其它组间无统计学差异。结论休克淋巴液可抑制内皮细胞的VEGF mRNA表达,且作用强于休克血浆。     

Exogenous normal lymph alleviates microcirculation disturbances and abnormal hemorheological properties in rats with disseminated intravascular coagulation

Disturbances of the microcirculation and abnormal hemorheological properties are important factors that play an important role in disseminated intravascular coagulation (DIC) and result in organ dysfunction or failure. In the present study, we established an animal model of DIC using intravenous Dextran 500 in rats, and used exogenous normal lymph corresponding to 1/15 of whole blood volume for injection through the left jugular vein. We found that normal lymph could improve the blood pressure and survival time of rats with DIC. The results regarding the mesenteric microcirculation showed that the abnormality of the diameter of mesenteric microvessels and micro-blood flow speed in the DIC+lymph group was significantly less than in the DIC+saline group. Whole blood viscosity, relative viscosity, plasma viscosity, hematocrit (Hct), erythrocyte sedimentation rate (ESR), and electrophoresis time of erythrocytes were significantly increased in the DIC+saline group compared to the control group. The electrophoretic length and migration of erythrocytes from the DIC+saline and DIC+lymph groups were significantly slower than the control group. Blood relative viscosity, Hct, ESR, and electrophoretic time of erythrocytes were significantly increased in the DIC+lymph group compared to the control group. Whole blood viscosity, relative viscosity and reduced viscosity were significantly lower in the DIC+lymph group than in the DIC+saline group, and erythrocyte deformability index was also significantly higher than in the DIC+saline and control groups. These results suggest that exogenous normal lymph could markedly improve the acute microcirculation disturbance and the abnormal hemorheological properties in rats with DIC induced by Dextran 500.     

Physiologic effects of normal-or low-oxygen-affinity red cells in hypoxic baboons.

Baboons were bled one-third their red cell mass and were given homologous transfusions of red blood cells to restore the red cell volume. One group of baboons received red blood cells with a normal 2,3-diphosphoglycerate 2,3-DPG) level and normal affinity for oxygen, and in this group the 2,3-DPG level after transfusion was normal. The other group received red blood cells with a 160% of normal 2,3-DPG level and decreased affinity for oxygen, and in this group the 2,3-DPG level after transfusion was 125% of normal. In both groups of baboons, the inspired oxygen concentration was lowered and arterial PO2 tension was maintained at 55-60 mmHg for 2 h after transfusion. During the hypoxic state, systemic oxygen extraction was similar in the two groups, whereas oxygen saturation was lower in the high 2,3-DPG group than in the control animals. Cardiac output was significantly reduced 30 min after the arterial PO2 was restored to normal. These data indicate that red blood cells with decreased affinity for oxygen maintained satisfactory oxygen delivery to tissue during hypoxia.     

雌激素增强失血性休克大鼠肠系膜淋巴管的收缩功能

目的:观察17β-雌二醇(E2)对失血性休克大鼠肠系膜淋巴微循环和离体肠系膜淋巴管收缩性的作用及其与淋巴管平滑肌细胞(LSMCs)内外钙离子浓度([Ca2+])差的关系.方法:雄性Wistar大鼠随机均分为假手术组、休克组和休克+E2组,建立失血性休克模型[(40±2)mmHg维持1.5 h,液体复苏],休克+E2组在...     

老年人脑白质疏松症血液流变性及血液成分的改变

对３８例老年脑白质疏松症（ＬＡ）患者进行了部分血液流变性和血液成分指标的测定。结果：与健康者比较，ＬＡ患者全血粘度、血浆粘度、ＲＢＣ刚性指数和聚集指数、纤维蛋白原显著增高，ＲＢＣ变形能力明显降低，血Ｈｂ、ＭＣＶ、ＭＣＨ、ＭＣＨＣ、ＲＤＷ－ＣＶ显著增高。提示：血液流变性异常和红细胞老化参与了ＬＡ的发生。设法纠正患者高粘和高凝状态、提高红细胞变形能力有益于阻止该病的进展     

Effect of short-term strenuous exercise on erythrocyte 2,3-diphosphoglycerate in untrained men: a time-course study

The literature on the response of erythrocyte 2,3-diphosphoglycerate (2,3-DPG) following exercise is replete with inconsistencies, and recent studies have shown that the time of blood sampling during and following exercise, as well as the duration of exercise, are important in evaluating the response of 2,3-DPG. Experiments were designed to measure the response of 2,3-DPG following short-term strenuous exercise in two groups of untrained men. Twelve men, 19–22 years old (study 1), exercised on a bicycle ergometer at 122.5 W for 10 min and red blood cell (RBC) 2,3-DPG was measured at 0 and 50 min following exercise. The level of 2,3-DPG (mol · ml^–1 RBC) increased after exercise (P < 0.05), but this increase was not significant when 2,3-DPG was expressed as mol · mol^–1 hemoglobin (Hb). However, following 50min of rest, 2,3-DPG (mol · mol^–1 Hb) decreased significantly. In a second group (study 2), nine other men, aged 18–19 years, exercised at the same workload for 15 min and 2,3-DPG was measured at 0, 30, 60, 180, and 330 min respectively after exercise, and no significant mean changes in the level of the phosphate were observed. Findings from these studies suggest that 2,3-DPG does not provide a compensatory adjustment to facilitate oxygen delivery in the hypoxia of short-term strenuous exercise in untrained males immediately following exercise and when recovery intervals of up to 330min are also examined. It is suggested that 2,3-DPG be reported as mol · mol^–1 Hb, since the phosphate exists on Hb in an equimolar ratio in normal physiological states.     

新生SD大鼠血常规各项与发育时间的相关性分析及其与血清铁浓度变化的机制

 目的：探讨经心脏穿刺和剪尾2种采血方式对新生SD大鼠血常规的影响;建立其血常规正常参考值范围;研究发育过程中血常规各项、血细胞形态和血清铁（SI）的消长变化及其相互关系,揭示SI变化的可能机理。方法：新生鼠出生后1、2、3、7和14 d,经全自动血液分析仪检测心脏血和鼠尾血中红细胞(RBC)计数、血红蛋白(HGB)含量、血小板(PLT)计数和白细胞(WBC)计数的改变;通过瑞氏-姬姆萨染色观察2种血液中血细胞形态的差别,及其在不同发育阶段的变化情况;选择心脏穿刺采血建立血常规正常值参考范围;经血液生化分析仪检测各时点心脏血SI含量变化;统计学分析发育时间、血常规各项及SI含量三者间的动态关系。结果：鼠尾血中RBC计数、HGB含量和WBC计数均高于心脏血,且RBC碎片较多;RBC形态随发育逐渐成熟稳定,其碎片亦明显减少;发育时间与心脏血中RBC和PLT计数呈正相关(P<0.01),与HGB含量、红细胞压积(HCT)、红细胞平均体积(MCV)、平均血红蛋白量(MCH)、平均血红蛋白浓度(MCHC)、WBC计数和SI含量呈负相关(P<0.01)。SI含量与RBC计数呈负相关(P<0.05),与MCV(P<0.01)和MCH(P<0.05)则呈显著正相关。结论：经心脏采血能建立相对完善的正常新生SD大鼠血常规参考值范围;新生鼠血常规各项与发育时间存在显著相关性;发育早期RBC的不稳定性可能是导致SI含量在发育早期较高的原因。     

On the mechanisms of the hypoxia-induced increase of 2,3-diphosphoglycerate in erythrocytes

Summary Hypoxia induces in rats a rather rapid increase of the concentration of 2,3-DPG in red blood cells. This increase is reversed when the animals are returned to normal conditions. Pigeons do not respond to hypoxia with an increase of inositol hexaphosphate concentration in their erythrocytes.In rats exposed for 24 h to gas mixtures containing low oxygen and in addition 5% CO₂ the hypoxia induced rise of 2,3-DPG concentration is abolished. The hemoglobin concentration in whole blood is negatively correlated to red cell 2,3-DPG levels in normal as well as in anemic or polycythemic rats.The rate of 2,3-DPG decomposition in human erythrocytes incubated without glucose is the same in the presence and in the absence of oxygen. The incorporation of³²P into 2,3-DPG proceeds faster in deoxygenated than in oxygenated human red blood cells and exceeds considerably the concomitant acceleration of the glycolytic flux rate. These findings indicate that the rate of 2,3-DPG synthesis becomes enhanced in deoxygenated cells. This is mainly due to an elevation of the intracellular pH; the relief of product inhibition of DPG mutase brought about by a greater binding of 2,3-DPG to deoxyhemoglobin seems to be of minor importance.The regulation of 2,3-DPG concentration by the intraerythrocytic pH as well as by the oxygenation state of hemoglobin and the significance of these regulatory mechanisms in inducing and limiting the changes of red cell 2,3-DPG during hypoxia and anemia are discussed.Preliminary reports of parts of this work were presented at the 36th Meeting of the German Physiological Society, Mainz, September 1969 [11] and at the First International Conference on Red Cell Metabolism and Function, Ann Arbor, October 1969 [23].     

The effects of pentoxifylline treatment on bacterial translocation after hemorrhagic shock in rats

Bacterial translocation is thought to be responsible for infectious complications after hemorrhagic shock. The aim of this study was to investigate the effects of pentoxifylline treatment on bacterial translocation in animals subjected to hemorrhagic shock. Thirty-one Wistar albino rats (280–360 g) were divided into three groups: sham (n=10), shock (n=11), and shock-pentoxifylline (n=10). Blood was not withdrawn from sham rats. Shock rats were subjected to 30 min of shock followed by reinfusion of shed blood. Shock/pentoxifylline rats received pentoxifylline after reinfusion of shed blood. After hemorrhage and reinfusion (24 h), the mesenteric lymph nodes, liver, spleen, and blood samples were evaluated using quantitative microbiological techniques, and the numbers of colony-forming units were compared between groups. Cecum was removed to evaluate the bacterial population. Ileum and cecum were examined histologically. The incidence of bacterial translocation was higher in the shocked rats (63%) than in the sham shock rats (10%). Pentoxifylline reduced the incidence of shock-induced bacterial translocation to 0%. Cecal bacterial levels were significantly higher in the shock rats than in the sham and shock/pentoxifylline rats. The histological damage caused by hemorrhagic shock was prevented by pentoxifylline treatment. In conclusion, the hemorrhagic shock triggered translocation of bacteria to the mesenteric lymph nodes, spleen, liver, and blood of rats. Pentoxifylline treatment just after shed blood transfusion significantly attenuated this phenomenon. Received: 21 October 2000 / Accepted: 10 December 2000     

益母草对失血性休克大鼠器官血流量和血液流变的影响

目的:探讨益母草注射液(LHS)对失血性休克大鼠血液动力学的影响。方法:通过从颈总动脉放全复制大鼠失血性休克模型,采用观察器官微循环观察、微血流量和血液流变学测定方法,观察LHS对失血性休克转归时血液动力学的调节作用。结果:失血性休克时,器官血流量降低,血粘度增高;LHS和NS组均能改善胃、肠、肝的微区血流量,但前者效果优于NS组(p<0．05);AHL治疗后,血粘度、血小板粘附率和聚集率明显低于NS治疗组,且红细胞变形能力明显增强 (p<0．05)。结论:LHS能明显改善失血性休克时的血液动力学异常。     

Red cell 2,3-DPG,ATP, and mean cell volume in highly trained athletes

Summary 20 male elite long distance runners were compared to a control group of blood donors to determine the effect of training on red blood cells. The acute effects of exercise on red cells were investigated in 11 of the runners following a race of 15–30 km. The runners had elevated resting values of red cell 2,3-DPG (P<0.05) and mean cell volume (P<0.01); blood Hb and ATP were not different from concentrations in the control group. The red cell status of the athletes may be explained by an increased proportion of young erythrocytes in runners. No statistically significant changes in red cell 2,3-DPG, ATP, mean cell volume or blood Hb were found post exercise.