A study of erythrocyte deformability using an ektacytometer in normal adults and in patients with acute cerebral infarction

We studied the erythrocytes deformability with an ektacytometer made in China in 55 normal adults and in 22 patients with acute cerebral infarction (ACI). The results showed that sex has no influence upon the deformability of RBC in normal adults. The deformability of RBC decreases with the age, but there is no significant difference between different age groups. The deformability of RBC in ACI decreases obviously. It may be one of the factors that increase the whole blood viscosity in ACI. The measurement of RBC deformability with ektacytometer is simple, fast and only 20u mu whole blood needed. The ektacytometer is a valuable tool in experimental and clinical researches.     

肾性高血压动物红细胞变形性及内皮素的研究

目的研究高血压对脑动脉的病理影响及实验性高血压时红细胞变形性的改变。方法 肾性高血压兔及正常对照兔各１０只，进行脑病理观察，测定红细胞变形指数，测定血浆及脑组织内皮素（ＥＴ）含量。结果 发现肾性高血压兔脑动脉普遍性管壁增厚，管腔缩小，脑组织有缺血和出血性病变，红细胞变形能力下降，血浆及下丘脑和颞叶皮层脑组织ＥＴ含量增高，且正常兔和高血压兔下丘脑ＥＴ浓度均高于相应的颞叶皮层。结论 高血压小动脉病变是     

Red blood cell lipid alterations in type II diabetes mellitus

Alterations in blood rheological properties have been reported in diabetes mellitus. Changes in lipid composition of red blood cell (RBC) membranes resulting in an impairement of RBC deformability may play a role in the altered blood rheological pattern. The aim of this study was to investigate the lipid composition of RBC membrane in a group of patients affected by type II diabetes (age 21–45 years), selected on the basis of the absence of complications and good metabolic control, and in a group of suitable control subjects. Saturated fatty acid amounts in the different phospholipid fractions were significantly higher in diabetics than in controls (p<0.05), whereas polyunsaturated fatty acids were decreased (p<0.05). Cholesterol/phospholipid molar ratio was not altered. On the contrary, sphingomyelin/phosphatidylcholine ratio was higher in diabetics than in controls (1.10±0.08 vs 0.96±0.10, p相似文献   

急性脑梗塞患者红细胞免疫功能变化对红细胞变形性的影响

本文测定了４１例急性脑梗塞患者红细胞滤过指数（ＲＢＣ－ＩＦ）。红细胞Ｃ３ｂ花环率（ＲＢＣ－Ｃ３ｂＲＲ）和红细胞免疫复合物花环率（ＲＢＣ－ＩＣＲ）观察红细胞免疫粘附（ＲＣＩＡ）功能变化对红细胞变形性（ＲＣＩ）的影响，结果显示脑梗塞患者ＲＢＣ－ＩＦ增高，ＲＢＣ－Ｃ３ｂＲＲ下降，ＲＢＣ－ＩＣＲ上升，表明脑梗塞患者ＲＣＤ和红细胞免疫粘附功能下降，且ＲＢＣ随着ＲＣＩＡ功能下降其变形能力也有所降低。提示脑梗塞     

大豆磷脂对脑梗死患者红细胞脂质成分的作用

目的　寻求脑梗死患者红细胞 (RBC)膜脂质成分正常化、流动性增加的措施。方法　给 30名急性期脑梗死者在脑梗死常规治疗基础上加服大豆磷脂 10g·tid .服用 30d。观察服用大豆磷脂前后RBC和血浆脂质成分的变化 ,并与不服用大豆磷脂常规治疗的急性期脑梗死患者和正常组对比。结果　脑梗死患者服用大豆磷脂 30天 ,血浆总胆固醇下降 0 .72mmol/L ,总磷脂上升 1.4 5mmol/L ,RBC中胆固醇下降 0 .11mg/10 10 RBC、磷脂酰胆碱上升 0 .10mg/10 10 RBC、总磷脂上升 0 .14mg/10 10 RBC ,胆固醇 /总磷脂比值下降0 .0 6 ,饱和脂肪酸 /双键不饱和脂肪酸比值下降 0 .12 ,红细胞滤过指数下降 0 .0 9,RBC的脂质成分与流动性均与正常组无显著差异 (P >0 .0 5 )。结论　大豆磷脂可使脑梗死患者RBC脂质成分正常化和膜流动性增加     

急性脑血管病患者红细胞流变学研究

对３５例急性脑血管病（ＡＣＶＤ）患者，分脑出血（ＣＨ）组及脑梗塞（ＣＩ）组，分别检测红细胞各实验参数、红细胞变形能力（ＲＣＤ）及红细胞聚集（ＥＡＧ），并设立３２例对照。结果显示红细胞各实验参数有不同程度改变，部分具统计学意义。脑出血组ＲＣＤ及ＥＡＧ与对照组比较无统计学意义，而脑梗塞组ＲＣＤ各切应力下均低于对照组（Ｐ＜０．０１），ＥＡＧ高于正常对照（Ｐ＜０．００１）。ＣＩ组红细胞各参数间有一定相关性，ＣＨ组相关不明显。对ＲＣＤ改变机理及临床意义进行了初探。     

New functional aspects of the L-arginine-nitric oxide metabolism within the circulating blood

Nitric oxide (NO) is a signaling molecule of major importance modulating not only the function of the vascular wall but also that of blood cells, such as platelets and leukocytes. The synthesis of NO in the circulation has been attributed mainly to the vascular endothelium. Red blood cells (RBC) have been demonstrated to carry a non-functional NOS and--due to their huge haemoglobin content--have been assumed to metabolize large quantities of NO. More recently, however, RBC have been identified to reversibly bind, transport, and release NO within the cardiovascular system. We provide evidence that RBC from humans express an active and functional endothelial type NOS. RBC NOS activity may regulate deformability of RBC, and inhibits activation of platelets. This review aims to discuss the potential role of RBC NOS in the circulation and new concepts of NO research in the microcirculation.     

脑梗死患者血浆及RBC铜、锌、铁、钙元素的观察

目的：为了研究铜、锌、铁、钙元素在脑梗死时的变化及其相关性。方法;对48例脑梗死患者血浆和红细胞内上述元素进行了检测,并与28例正常老年人进行了比较。结果：急性期和恢复期RBC钙均明显升高,血浆及RBC锌明显减低,血浆及RBC铜则明显升高。恢复期血浆铁明显降低。结论：RBC钙超载、铜／锌比值升高可能发生在脑梗死之前,也可能是患者红细胞行为异常的原因之一。     

普遍脑萎缩与血液流变学关系的探讨

采用Ｈｕｃｋｍａｎｎ氏方法对１４２例颅脑ＣＴ平片进行脑室、脑沟测量，并逐一测定有关血液流变学指标：ＲＢＣ变形性、全血粘度、ＲＢＣ压积、血小板聚集率、纤维蛋白原含量，结果表明：（１）有随年龄增长逐渐出现普遍性脑萎缩的趋向，但大都在进入老年期后才日益明显；（２）普遍脑萎缩病人存在某些显著的血液流变学异常，如ＲＢＣ变形能力下降、全血粘度升高等；（３）显著皮层萎缩组与显著脑白质萎缩组血液流变学指标变化不尽相同，前者ＲＢＣ压积、全血粘度、纤维蛋白原含量，ＲＢＣ变形性明显高于后者，而后者的血小板聚集率高于前者。     

Platelet-activating factor acetylhydrolase activity in red blood cell-stroma from patients with cerebral thrombosis

Platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine, PAF) is a bioactive phospholipid and inactivated by a specific enzyme, PAF acetylhydrolase (PAF-AH). We have measured PAF-AH activity in red blood cells (RBCs) from patients with a history of cerebral thrombosis and age-matched healthy controls. The activities in 34 patients and 34 controls were 1.29 +/- 0.28 and 1.64 +/- 0.26 nmol/10(9) RBCs/min (or, 30.0 +/- 5.8 and 35.1 +/- 4.7 nmol/g protein/min) (mean +/- SD), respectively, and the difference was significant (p less than 0.001). In patients, RBC PAF-AH activity correlated positively with RBC filterability, an index of RBC deformability (r = +0.501, p less than 0.05). The RBC activity may play a role in scavenging oxidation products of membrane phospholipids. Lower RBC PAF-AH activity may predispose to ischemic diseases by disturbing microcirculatory behavior of the RBCs.     

Erythrocyte membrane studies in familial hypokalemic periodic paralysis.

A study of RBC membrane functions was performed in four patients suffering from familial hypokalemic periodic paralysis who had permanent muscular weakness. Electrophoretograms of membrane proteins, cell deformability, calcium-promoted potassium efflux, calcium-ATPase activity, and endogeneous phosphorylation of membrane proteins were all within the normal range. These results are compared with similar studies performed in myotonic and Duchenne-type dystrophies, in which abnormalities in the RBC membrane have been described. The results do not support the theory of RBC involvement in hypokalemic periodic paralysis. However, this does not imply that the muscle cell membrane is not involved in the underlying pathological processes in this disorder.     

Erythrocyte (Ca2+ + Mg2+)-ATPase activity and calcium homeostasis in Duchenne muscular dystrophy

Because the erythrocyte (RBC) in Duchenne's muscular dystrophy (DMD) is thought to be a suitable experimental paradigm for the sarcolemma, the RBC membrane-bound enzyme (Ca2+ + Mg2+)-ATPase has been investigated as to its relevance to abnormalities of calcium metabolism in DMD muscle. In this study, RBC (Ca2+ + Mg2+)-ATPase activity, intracellular calcium and potassium contents and complete hemogram were examined in 10 DMD patients and 16 age-matched controls. (Ca2+ + Mg2+)-ATPase activity was found elevated in the DMD RBC, consistent with reports from previous studies, but no abnormalities in intracellular calcium, potassium or hemograms were detected. It seems that although the (Ca2+ + Mg2+)-ATPase activity is changed, it bears no relevance to calcium homeostasis in DMD RBC. It is inferred that the increase in intramuscular calcium in DMD muscle, which is also found in other neuromuscular diseases, may be a non-specific finding in the diseased muscle and part of the final common pathway leading toward cellular degeneration and death.     

Prostaglandin E1 and dibutyryl cyclic AMP enhance platelet resistance to deformation.

The effect of prostaglandin E₁ (PGE₁) on platelets is mediated through the PGE₁ receptor and the consequent maintenance of the platelet's discoid shape. The effects of PGE₁ and dibutyryl cAMP (dbcAMP) on the deformability of human platelets were studied. Deformability tests based upon the micropipette aspiration on the platelets were performed by using pipettes with radii (Rp) of 0.26-0.36 gm. The time course of the extension length (Dp, in μg) of the platelets in response to aspiration with a negative pressure (ΔP) of 5 cm H₂ O (ΔP × Rp = 0.15 dynes/cm) was analyzed. PGE₁ treatment (0.1 μM) resulted in a decrease of platelet deformability as compared with results obtained for apparently non-activated, control platelets. The deformation index, i.e., Dp/Rp (PGE₁ -treated) / Dp/Rp (control), was significantly reduced to 0.90 ± 0.04. DbcAMP treatment also significantly decreased the deformability of platelets and this decrease was dbcAMP dose dependent. In contrast, colchicine- or cytochalasin D-treated platelets increased deformability. PGE₁ -treated platelets had a higher [cAMP]_i than controls. Platelets treated with PGE₁ or dbcAMP showed a reduced [Ca²⁺]i increment induced by thrombin as compared to non-treated controls. These results indicate that PGE₁ and dbcAMP treatment of platelets is accompanied by an enhancement of platelet resistance to deformation. The increased [cAMP]_i and low [Ca²⁺]_i after PGE₁ treatment may limit the rearrangement of cytoskeleton and thus enhance platelet resistance to deformation.     

UBIO疗法对脑梗塞病人红细胞变形性的影响

用ＵＢＩＯ疗法治疗脑梗塞患者５０例，治疗前后分别测定红细胞变形性以及血中脂质过氧化物（ＭＤＡ）和超氧化物歧化酶（ＳＯＤ）的含量，并与正常对照组比较。结果显示脑梗塞后红细胞变形性降低，脂质过氧化物含量增加，超氧化物歧化酶含量降低，与正常对照组比较均有显著差异。经ＵＢＩＯ疗法治疗后，红细胞变形能力明显改善，ＭＤＡ下降，ＳＯＤ增加，提示ＵＢＩＯ疗法治疗脑梗塞是有理论基础的。     

帕金森病猴模型红细胞内钙镁离子含量的测定及意义

目的：研究帕金森病猴模型红细胞内钙、镁离子浓度的改变与病情严重程度间的相互联系。方法：采用逐日肌注MPTP法(0．1mg/kg/d)制造帕金森病猴模型,运用行为学评分量表进行评分,对病情严重程度进行量化,并划分病期。抽取不同病期的血样,用火焰原子吸收光谱法检测红细胞内的钙镁离子含量。结果：红细胞内钙离子含量在亚临床期即表现为明显的增高(P＜0．05)。临床早中晚期与正常对照相比有极显著的增高(分别为P＜0．01,P＜0．01和P＜0．001)。而红细胞内镁离子含量在亚临床期及临床早期明显低于对照(均为P＜0．05),临床中晚期与对照相比有极显著的降低(均为P＜0．01)。结论：帕金森病猴模型红细胞内钙、镁离子浓度随着病情的发展呈现规律性的改变。     

Oxidative status of platelets in normal and thalassemic blood

Chronic platelet activation may be involved in thromboembolic complications, a leading cause of morbidity and mortality in beta-thalassemia. Oxidative stress, with the generation of reactive oxygen species (ROS), is suspected to play a role in the patho-physiology of thalassemia and cardiovascular disorders. In the present study, we adapted flow cytometric techniques to measure oxidative state markers, ROS generation and reduced glutathione (GSH) content in platelets. Our results show that platelets obtained from beta-thalassemic patients contain higher ROS and lower GSH levels than do platelets from normal donors, indicating a state of oxidative stress. In the absence of any known inherent abnormality in thalassemia platelets, this may be attributed to continuous exposure to oxidative insults from extra-platelet sources. We found that exposure of platelets to oxidants such as hydrogen peroxide and tertbutylhydroperoxide or to the platelet activators thrombin, calcium ionophore or phorbol myristate acetate stimulated the platelets' oxidative stress. This was also increased by plasma of thalassemia patients, and decreased following treatment of the plasma with the iron-chelator Desferoxamin. Iron and hemin, the levels of which are augmented in plasma of thalassemia patients, stimulated the platelets' oxidative stress. The oxidative status of the platelets was also affected by red blood cells (RBC); it was higher in normal platelets incubated with thalassemic RBC than with normal RBC. Normal RBC stimulated with hydrogen peroxide had a greater effect on platelets than did unstimulated RBC. The platelets' oxidative stress was ameliorated by antioxidants such as N-acetyl-L-cysteine and vitamin C. Our findings indicate that in thalassemia, platelets undergo a state of oxidative stress, leading to their activation and potentially to thromboembolic consequences, and suggest that this hypercoagulable state might be treated with antioxidants.     

Prostaglandin E1 and dibutyryl cyclic AMP enhance platelet resistance to deformation

The effect of prostaglandin E₁ (PGE₁) on platelets is mediated through the PGE₁ receptor and the consequent maintenance of the platelet's discoid shape. The effects of PGE₁ and dibutyryl cAMP (dbcAMP) on the deformability of human platelets were studied. Deformability tests based upon the micropipette aspiration on the platelets were performed by using pipettes with radii (Rp) of 0.26-0.36 gm. The time course of the extension length (Dp, in μg) of the platelets in response to aspiration with a negative pressure (ΔP) of 5 cm H₂ O (ΔP × Rp = 0.15 dynes/cm) was analyzed. PGE₁ treatment (0.1 μM) resulted in a decrease of platelet deformability as compared with results obtained for apparently non-activated, control platelets. The deformation index, i.e., Dp/Rp (PGE₁ -treated) / Dp/Rp (control), was significantly reduced to 0.90 ± 0.04. DbcAMP treatment also significantly decreased the deformability of platelets and this decrease was dbcAMP dose dependent. In contrast, colchicine- or cytochalasin D-treated platelets increased deformability. PGE₁ -treated platelets had a higher [cAMP]_i than controls. Platelets treated with PGE₁ or dbcAMP showed a reduced [Ca²⁺]i increment induced by thrombin as compared to non-treated controls. These results indicate that PGE₁ and dbcAMP treatment of platelets is accompanied by an enhancement of platelet resistance to deformation. The increased [cAMP]_i and low [Ca²⁺]_i after PGE₁ treatment may limit the rearrangement of cytoskeleton and thus enhance platelet resistance to deformation.     

Calcium function in affective disorders and healthy controls

Calcium metabolism has been reported to be disturbed in some forms of affective disorder. We studied concurrently a battery of calcium measures in 29 unipolar, 14 bipolar depressed, 11 manic, and 10 healthy control subjects. In addition to measures of extracellular calcium, we studied intracellular calcium concentration in platelets and measures that reflect cellular capability to maintain a low intracellular Ca++ concentration in red blood cells (RBCs) and platelets. Plasma calcium was lower in unipolar and manic patients than in control subjects. Platelet calcium concentration was lower in unipolar than bipolar depressed patients. RBC Ca++ adenosine triphosphatase (ATPase) was lower in unipolar and control subjects than in bipolar depressed and manic patients. Platelet Ca++ ATPase and Ca++ uptake were inversely correlated with severity of illness in unipolar patients. In bipolar depressed patients, RBC Ca++ ATPase and platelet Ca++ uptake were inversely correlated with severity. In addition to indicating abnormalities in calcium activity in affective disorders, the data suggest that unipolar and bipolar patients differ in several measures and may have different pathophysiological disturbances in calcium metabolism.     

Hypothalamic digoxin deficiency in obsessive compulsive disorder and la Tourette's syndrome

The isoprenoid pathway related cascade was assessed in 15 patients with obsessive compulsive disorder (OCD) and la Tourette's syndrome (TS). The pathway was also assessed in right hemispheric dominant, left hemispheric dominant, and bihemispheric dominant individuals to assess whether hemispheric dominance has any correlation with these disease states. The levels of serum digoxin, HMG CoA reductase activity, and dolichol were found to be decreased in OCD and la Tourette's syndrome as well as in left hemispheric dominant individuals with a corresponding increase in RBC Na(+)-K+ ATPase activity, serum ubiquinone, and magnesium levels. There was an increase in tyrosine and its catabolites, and a reduction in tryptophan and its catabolites in the serum. The total and individual glycosaminoglycan (GAG) fractions, carbohydrate residues of glycoproteins, and the concentration of glycolipids decreased in the serum. The activity of GAG degrading enzymes and glycohydrolases were decreased. The RBC membrane glycoconjugates were increased while the membrane cholesterol:phospholipid ratio was decreased. The activity of free radical scavenging enzymes increased while the concentration of free radicals decreased significantly. On the other hand, there was hyperdigoxinemia and the reverse biochemical patterns in those with right hemispheric dominance. Membrane Na(+)-K+ ATPase stimulation can result in decreased intracellular Ca2+ and increased magnesium levels. Increased levels of dopamine can lead to a tic syndrome, while reduced levels of serotonin and increased dopamine can both lead to obsessive compulsive disorder. Decrease in fucose and sialo-ligands, increased immunosuppressive morphine levels, decreased T-cell calcineurin signal transduction related to decreased intracellular calcium, reduced free radical production, and altered presentation of bacterial glycoconjugate antigens can lead to a hypoimmune response and recurrent respiratory infection in OCD patients. OCD and la Tourette's syndrome are associated with left hemispheric chemical dominance.     

HYPOTHALAMIC DIGOXIN DEFICIENCY IN OBSESSIVE COMPULSIVE DISORDER AND LA TOURETTE S SYNDROME

The isoprenoid pathway related cascade was assessed in 15 patients with obsessive compulsive disorder (OCD) and la Tourette s syndrome (TS). The pathway was also assessed in right hemispheric dominant, left hemispheric dominant, and bihemispheric dominant individuals to assess whether hemispheric dominance has any correlation with these disease states. The levels of serum digoxin, HMG CoA reductase activity, and dolichol were found to be decreased in OCD and la Tourette s syndrome as well as in left hemispheric dominant individuals with a corresponding increase in RBC Na &#180 +;-K &#180 +; ATPase activity, serum ubiquinone, and magnesium levels. There was an increase in tyrosine and its catabo lites, and a reduction in tryptophan and its catabolites in the serum. The total and individual glycosaminoglycan (GAG) fractions, carbohydrate residues of glycoproteins, and the concentration of glycolipids decreased in the serum. The activity of GAG degrading enzymes and glycohydrolases were decreased. The RBC membrane glycoconjugates were increased while the membrane cholesterol:phospholipid ratio was decreased. The activity of free radical scavenging enzymes increased while the concentration of free radicals decreased significantly. On the other hand, there was hyperdigoxinemia and the reverse biochemical patterns in those with right hemispheric dominance. Membrane Na &#180 +;-K &#180 +; ATPase stimulation can result in decreased intracellular Ca &#180 2+; and increased magnesium levels. Increased levels of dopamine can lead to a tic syndrome, while reduced levels of serotonin and increased dopamine can both lead to obsessive compulsive disorder. Decrease in fucose and sialo-ligands, increased immunosuppressive morphine levels, decreased T-cell calcineurin signal transduction related to decreased intracellular calcium, reduced free radical production, and altered presentation of bacterial glycoconjugate antigens can lead to a hypoimmune response and recurrent respiratory infection in OCD patients. OCD and la Tourette s syndrome are associated with left hemispheric chemical dominance.