人体红细胞生存期中血液流变学的变化

研究红细胞衰老过程中变形性的变化,可以使我们对幼年红细胞与老年红细胞的循环性能有深入理解。业已证明:在整个生命进程中,红细胞的血粘度和渗透脆性逐渐增加,而新陈代谢等理化变化     

红细胞在体内生存期中的流变学变化

研究红细胞衰老过程中变形性的变化,可以使我们对“年轻”红细胞与“老化”红细胞的循环性能有深入理解。许多研究表明,在整个生命过程中,红细胞的内粘度和渗透脆性逐渐增加,而新陈代谢等理化变化确有所削弱。本文作者根据红细胞的密度随生存期而增大这一事实,采用Murphy密度分离法,将7例不同性别健     

维生素C和地塞米松增加兔血红细胞渗透抵抗性

目的研究尿素、乌拉坦、维生素 Ｃ、地塞米松对兔血红细胞渗透抵抗性的影响，为临床用药提供一定的理论依据。方法实验分对照组、维生素Ｃ组、尿素组、维生素Ｃ＋尿素组、维生素Ｃ＋乌拉坦组、尿素＋乌拉坦＋维生素Ｃ组、尿素＋乌拉坦＋地塞米松组。观察维生素Ｃ、尿素及二者同时作用，维生素Ｃ、乌拉坦及二者同时作用对红细胞渗透脆性的影响以及地塞米松和维生素Ｃ抑制尿素和乌拉坦所致的红细胞渗透脆性增加的影响。结果维生素Ｃ组与对照组红细胞渗透脆性有显著差异（Ｐ< ０．０１），尿素＋乌拉坦组与尿素＋乌拉坦＋维生素Ｃ组红细胞渗透脆性有显著差异（Ｐ<０．０１），尿素＋乌拉坦组与尿素＋乌拉坦＋地塞米松组红细胞渗透脆性有显著差异（Ｐ<０．０１）。结论维生素Ｃ单独作用增加红细胞渗透抵抗性，维生素Ｃ和地塞米松具有抑制尿素和乌拉坦所致红细胞渗透脆性增加的作用。     

糖尿病患者红细胞形态和渗透脆性的初步研究

应用扫描电镜观察了22例糖尿病人4400个红细胞形态的异常百分比，并测定红细胞的渗透脆性。结果表明随着糖尿病病程延长、糖化血红蛋白升高，口形、嵴形红细胞的百分比明显升高（2．64±1．27比4．29±1．03，P＜0.001），细胞渗透脆性明显上升（0．17±0．04比0．33±0．17，P＜0.05）。提示，糖尿病人异常形态红细胞的出现不仅与红细胞的能量代谢障碍外，还可能与红细胞所处的高血糖、高血脂、高血液粘度的环境有关。而影响红细胞的渗透脆性的因素较为复杂，红细胞的圆形隆起在降低其渗透脆性方面起了重要作用。     

红细胞衰老过程中的密度变化

作者在用抗体诱发动物急性溶血的方法建立的红细胞在体衰老模型的基础上，对红细胞衰老过程中的细胞密度变化进行了研究。其结果显示：随着红细胞年龄的增加，其平均密度增加，细胞密度与细胞年龄呈线性相关关系，但同龄红细胞的密度离散较大，不同年龄细胞间密度重叠的红细胞数量较多。提示用密度的差异对不同年龄红细胞进行分离，分辨率不高。     

轻度烧伤后红细胞流变学特性的变化

我们用轻度烧伤动物模型研究了烧伤后红细胞（RBC）变形性及渗透脆性的变化。结果发现,轻度烧伤后红细胞变形性随时间有一先抑后扬的变化趋势。烧伤后立即取血（0h）所测结果与烧伤前比较,RBC最大变形指数(DI)max、积分变形指数IDI及红细胞渗透脆性都未见显著性差异;烧伤后1、2h时(DI)max、IDI显著降低（P<0.01或P<0.05）;4、7h时(DI)max、IDI虽略低于烧伤前水平,但未见显著性差异（P>0.05）。烧伤后不同时间点（0、1、2、4、7h）所取血样的RBC渗透脆性与烧伤前比较,除在烧伤后4h时显著增加外,在其余各时间点均未见显著变化。说明在用该动物模型所得结果中,(DI)max、IDI的受损及RBC渗透脆性的增加,可能都只与体液因素的作用有关。但RBC变形性的受损与其渗透脆性的变化不是同步的,说明可能存在着不同的损伤机制。     

红细胞膜结构的改变对红细胞脆性的影响

红细胞胎性的增加会导致细胞的溶血,使红细胞寿命缩短。有研究指出随着红细胞的老化,其膜结构发生变化,导致红细胞胎性增加,使之易溶血。Kuypers等用不饱和卵磷脂置换正常人红细胞中的卵磷脂,但不改变其含量,结果发现,随着膜中卵磷脂不饱和度的增加,红细朐稳定性下降,渗透脆性增加。而红细胞结构的改变对可以认为是导致红细胞脆性（机械定性）变化的分子基础。本文通过不同浓度胰蛋白酶、戊二醛对红细胞的处理,造成红细胞膜蛋白结构的改变,用新型激光衍射法测量了这些样品的弹性模量E及变形指数;用不问渗透压的缓冲液及施加剪…     

氟碳化合物用于烧伤治疗

严重烧伤后出现进行性红细胞缺失,血中多种循环寿命很短的异常型红细胞不断增加。热烧伤所致红细胞损伤为细胞膜损伤,表现为渗透和机械脆性改变,对于氧合性血细胞溶解的抵抗力降低。所以烧伤之初被损坏的红细胞数量不断增加,而红细     

模拟高原不同时间缺氧暴露对大鼠红细胞结构与功能的影响

目的:初步探讨模拟高原不同时间缺氧暴露对大鼠红细胞结构与功能的影响及机制。方法:40只雄性SD大鼠随机分成5组(每组8只):常氧组、缺氧1周组、缺氧2周组、缺氧3周组和缺氧4周组。各缺氧组大鼠置于模拟海拔5 800 m的低压舱内,连续暴露相应时间后,采集全血,测定血常规、红细胞变形指数和红细胞渗透脆性,绘制血红蛋白氧解离曲线,分析计算红细胞凋亡率,观察骨髓切片病理学变化。结果:与常氧组相比,各缺氧组红细胞计数、血红蛋白含量、红细胞平均体积、红细胞平均血红蛋白含量和磷脂酰丝氨酸外翻率均显著增加(P0.01),血红蛋白氧饱和度为50%时的氧分压显著增大(P0.05),骨髓红系增生增加,红细胞变形指数及渗透脆性显著降低(P0.01),血红蛋白氧离曲线右移。结论:在模拟高原缺氧初期,外周血中红细胞的结构与功能发生代偿性改变以利于高原习服;但是,随着缺氧时间的延长,血管内滞留过多的异常红细胞容易导致血栓形成及微循环障碍,并加重机体的组织细胞缺氧。     

网织红细胞膜生物物理特性的研究

用苯肼使动物造成急性溶血性贫血的方法，诱发动物体内新生网织红细胞大量增多，通过对新生网织红细胞的电泳率、渗透脆性、膜的流动性等生物物理指标连续72h的测量，发现网织红细胞在由网织红细胞转变为成熟红细胞的过程中．其生物物理特性有明显改变。这对研究由于贫血等原因造成的网织红细胞增多情况下，全血的微观流变学特性具有重要的临床意义，同时对新生网织红细胞膜的生物物理特性加以系统研究，具有重要的基础理论研究价值。     

Effect of Intramuscular or Intrahepatic Injections of Clostridium perfringens on Rabbit Serum Lactate Dehydrogenase

Serum lactate dehydrogenase (LDH) activity, LDH isoenzyme pattern, phospholipase C activity, phosphorous level, hemoglobin, and erythrocyte osmotic fragility were followed in rabbits after intramuscular (IM) or intrahepatic (IH) injections of Clostridium perfringens. On the first day after IM injection, there was a drop in LDH activity; this was followed by an increase of LDH activity on the third and sixth day. On the seventh day, LDH activity began to decline, and by the ninth day it had almost returned to normal. On the sixth day after IM injection, there was an increase in serum LDH isoenzyme 5, hemoglobin, and erythrocyte osmotic fragility, but the increase of erythrocyte osmotic fragility and serum hemoglobin could not be attributed to phospholipase C activity since that enzyme was not detected nor was there an increase in serum phosphorus. C. perfringens was recovered by culturing the wound of IM-injected rabbits but not recovered from IH-injected rabbits. Rabbits injected IH showed no change from normal values in any of the tests performed.     

Altered red cell osmotic fragility in Huntington disease (HD)

We have studied in fresh and 24-hour incubated samples the osmotic fragility of erythrocytes from 13 individuals with Huntington disease (HD) and 22 at-risk, asymptomatic individuals. Five older at-risk, asymptomatic individuals and six Alzheimer disease individuals were also studied. Results suggest that osmotic fragility of red cells from HD individuals in significantly decreased in fresh (P less than 0.0001) and incubated (P less than 0.0001) samples. At-risk individuals appear to fall into two groups: 1) those with normal osmotic fragility (n =10), and 2) those with decreased osmotic fragility (n = 12). Fragility in older at-risk persons and those with Alzheimer disease were within normal limits. These data suggest that red cell osmotic fragility measurement may be useful to identify at-risk persons with an HD gene; however, longitudinal follow-up will be required to confirm the predictive power of this observation. These data suggest additional support for focusing on the erythrocyte in investigating the molecular pathogenesis of HD.     

International workshop on the fragile X and X-linked mental retardation

The erythrocyte osmotic fragility was evaluated on 19 unmedicated subjects with Huntington's disease and 42 individuals at 50% risk, 27 children at 25% risk, and a group of 60 hematologically normal control persons. Five older subjects at 50% risk for Huntington's disease as well as 6 Alzheimer's disease individuals were also evaluated for comparison. The osmotic fragility of fresh and 24-hour incubated red cells was analyzed and a fragility index calculated for each individual. The fragility index for the Huntington's disease group was statistically lower than that of the control group (P < .001) suggesting that the Huntington's disease erythrocytes had a reduced osmotic fragility. In the 50% risk group, 45% of the subjects demonstrated decreased osmotic fragility and 55% had normal fragility. For those subjects in the 25% risk group, 22.2% had decreased fragility and 77.8% had normal fragility. Twenty-seven offspring were evaluated of the 14 persons at 50% risk for Huntington's disease with children; eight of the 14 individuals at 50% risk showed normal fragility and all 16 of their children showed fragility indices with the normal range. The remaining six persons at 50% risk for Huntington's disease had increased erythrocyte fragility and out of their 11 children, five showed normal fragility and six had decreased fragility. These data support the hypothesis of reduced erythrocyte osmotic fragility in individuals affected with and at risk for Huntington disease, and demonstrate the need of further study of the erythrocyte in this complex behavioral genetic disease.     

Osmotic fragility of human erythrocytes in vitro using Vipera lebetina venom

The objective of this study was to investigate the in vitro effect of Vipera lebetina venom on human erythrocytes’ osmotic fragility with respect to different venom concentrations, time of incubation with the venom, initial volume of red blood cells, and presence of antivenom. In vitro osmotic fragility of human erythrocytes was determined using Dacie and Lewis method. Osmotic fragility is increased significantly after incubation with the venom at different concentrations. The maximal effect was detected at the venom concentration of 400 μg. Time of incubation with the venom was an important factor in hemolytic process while the initial cell volume has no significant effect. Incubation of envenomed erythrocytes for 120 min with antivenom did not reverse the changes in osmotic fragility induced by the venom. The study suggests that the venom could alter the susceptibility of erythrocytes to hemolysis when subjected to osmotic stress and the degree of hemolysis depends on venom concentration and time of intubation with the venom.     

Erythrocyte osmotic resistance during acute hypothermia in awake unrestrained rats

Summary Erythrocyte osmotic fragility and plasma ionic composition were studied in rats subjected to acute hypothermia. A decrease in osmotic fragility and a significant increase in plasma magnesium and total phosphorus were observed in blood from hypothermic rats in relation to control. A decrease in erythrocyte osmotic fragility from hypothermic animals was observed when the test was performed at 37°C, whereas osmotic fragility was unaltered if the test was carried out at body temperature. This could be interpreted as an adaptative response to counteract the opposite effect on erythrocyte osmotic fragility observed at low temperature in vitro.     

Osmotic fragility test in heterozygotes for alpha and beta thalassaemia.

This study shows that the combination of heterozygous beta thalassaemia and deletion heterozygous (-alpha/alpha alpha) or homozygous (-alpha/-alpha) alpha+ thalassaemia may result in the production of erythrocytes which have normal mean volume and haemoglobinisation but decreased osmotic fragility. Based on this finding and previous studies, which have shown that beta thalassaemia screening by the osmotic fragility test may miss a significant proportion of beta thalassaemia heterozygotes, we conclude that beta thalassaemia screening in a population in which both alpha and beta thalassaemia are prevalent should combine the one tube osmotic fragility test with electronic measurement of red blood cell indices in the initial screening process.     

Diphenylhydantoin and fragility of erythrocytes in normal subjects and in patients with hereditary spherocytic anemia.

To study the effects of diphenylhydantoin (Dilantin, DPH) on membrane function, DPH was incubated with erythrocytes from normal individuals and from patients with congenital spherocytic hemolytic anemia and osmotic fragility measured. The resulting curves show that DPH reduces the osmotic fragility of normal and spherocytic erythrocytes. In the presence of ouabain, DPH still had a protective effect on erythrocytes even though ouabain alone increases hemolysis of erythrocytes at certain saline concentrations. This study shows that erythrocyte fragility can be manipulated in vitro and provides a basis for studies in vivo.     

Effects of the phospholipase inhibitor mepacrine on injury in ischemic and metabolically inhibited adult isolated myocytes.

The phospholipase inhibitor mepacrine has been shown to delay cell death of metabolically inhibited cultured cardiomyocytes. The present study was initiated to determine if mepacrine also delays cell death and development of osmotic fragility of both metabolically inhibited and ischemic adult rat cardiomyocytes. Isolated myocyte suspensions were incubated with 3 mmol/l (millimolar) iodoacetic acid and 6 mmol/l amytal (inhibited) or were pelleted into a slurry and layered with oil (ischemic) in the presence and absence of 10 or 50 mumol/l (micromolar) mepacrine. Rates of contracture, cell viability as determined by trypan blue permeability, cell viability after osmotic swelling in 170 mOsm media (osmotic fragility), and cell morphology were monitored. Mepacrine had no effects on rates of contracture, but was found to significantly delay cell death during isotonic incubations of both metabolically inhibited and ischemic cells. In contrast, mepacrine had no effect on the development of osmotic fragility. Incubation of metabolically inhibited myocytes in calcium-free media did not delay contracture or cell injury, but did attenuate the protective effects of mepacrine. This study confirms previous reports that mepacrine protects cells from injury, extends the observations of protection to ischemic isolated adult myocytes, but shows that development of osmotic fragility is not inhibited by mepacrine.