Lineation of the Osmotic Fragility Curve of Erythrocytes

Lineation of the osmotic fragility curve by the method of Detraglia et al (1974) may be performed in most samples from a hospital population. Using the lineation procedure, the osmotic fragility may be tested by only 2 solutions of known osmolarity without any great loss of precision or accuracy. The osmotic fragility curve may be described by 2 values: C₅₀ = the concentration at which 50% of the erythrocytes are haemolyzed and C₅₀ - C₈₀ = the decrease in concentration raising the fraction of haemolysis from 0.50 to 0.80.     

High Prevalence of Increased Osmotic Fragility of Red Blood Cells among Norwegian Blood Donors

Increased osmotic fragility of red blood cells was found in 9 out of 1008 Norwegian blood donors. In addition, increased osmotic fragility was found in 3 out of 23 first grade relatives and in 1 out of 4 spouses of individuals with the same condition. Finally, there was a positive correlation between increased osmotic fragility and morphological signs of spherocytosis (P < 0.05). No definite conclusions with respect to underlying mechanism(s) for this high prevalence of non-symptomatic increased osmotic fragility can be offered, but very mild hereditary spherocytosis, environmental factors and even a normal variant, never associated with haemolysis, may have contributed. Furthermore, until more specific and sensitive laboratory techniques have been introduced, a proper distinction between these 3 conditions cannot be made.     

Production of Spherocytosis and Increased Osmotic Fragility in Normal Erythrocytes by Sodium Stress

Red cells from normal human subjects were exposed to hypertonic sodium chloride solutions for varying periods of time. The cell changes commonly observed in hereditary spherocytosis were induced, including microspherocyte formation with corresponding increase in osmotic fragility. Solutions of magnesium sulphate of equal osmolarity did not produce these changes. These observations lend support to the theory that excessive sodium permeability is concerned in the pathogenesis of hereditary spherocytosis. Increased influx of sodium and water into erythrocytes leads to spherocytosis, but only increased efflux of sodium leads to irreversible microspherocytosis.     

Osmotic Erythrocyte Fragility and ABO Blood Groups

In a study of 1008 blood donors a reduced frequency of blood group A and an increased frequency of blood group O were observed in those with increased osmotic fragility of their red cells.     

The Normal Range of Osmotic Fragility of Red Blood Cells

With the technique of Parpart et al (1947), the normal range for osmotic fragility of red blood cells has been estimated to include 5%–45% haemolysis at a salt concentration corresponding to 4.5 g NaCl/1 (Dacie 1954). This estimate may be questioned, however. Thus, nearly 20% of the data obtained from 50 presumably healthy subjects fell outside these limits. Furthermore, the distribution pattern was very asymmetric with erroneously small standard deviation. On the other hand, if the technical conditions (salt concentration, buffer) were properly adjusted, nearly all the observations were located within the straight part of the s-shaped haemolysis curve and scattered symmetrically around the mean. Under these conditions, the normal range (mean ± 2 SD) included 22%–88% haemolysis. Moreover, this wider range included about 95% of the observations, even adapted to the original experimental situation. The present estimates should therefore replace earlier statements in the literature.     

Increased Sodium Influx into Erythrocytes in Diabetes Mellitus and Hypertension

A variety of abnormality has been reported in the cation transport systems in erythrocytes in essential hypertension. To determine the existence of similar abnormality in diabetics with hypertension, sodium (Na+) influx into erythrocytes in the presence of ouabain (measured by using 22Na+), and the Na+ and potassium (K+) content in intact erythrocytes were examined. Subjects, all of whom were Japanese, were divided into 4 groups; 23 nondiabetic, normotensive control subjects without family history of hypertension (control group), 20 patients with essential hypertension (group 1), 21 normotensive diabetics without family history of hypertension (group 2) and 15 hypertensive diabetics (group 3). Na+-K+ pump activity (measured by using 86Rb+) was studied in some of them, too. Na+ influx in group 1 was 0.451±0.111 m mol/Kg erythrocytes/h, significantly more elevated than that in the control group (0.345±0.080, p < 0.001). Na+ influx in group 2(0.435±0.094) was significantly greater than that in the control group(p < 0.005), but no significant difference was found between groups 1 and 2. Na+ influx in group 3 (0.551±0.128) was significantly higher than that in the control group (p < 0.001), in group 1(p < 0.02), or in group 2(p < 0.005). There were no significant differences in Na+-K+ pump activity, or Na+ and K+ content among the 4 groups. These findings suggested that: 1) Na+ influx into ouabain-treated erythrocytes was higher in patients with essential hypertension than in control subjects in Japanese, 2) diabetes mellitus per se might increase Na+ influx, and 3) the elevation of blood pressure in hypertensive diabetics as well as in essential hypertensives might be related to the increased Na+ influx.     

Failure of Ouabain to Influence the Osmotic Fragility in Hereditary Spherocytosis

No effect of 3 μmol ouabain on the osmotic fragility of red blood cells in subjects suspected of being carriers of hereditary spherocytosis, as well as in patients with overt disease could be demonstrated. These results are in disagreement with a recent report. Some possible explanations for these discrepant results are discussed. It is concluded that ouabain probably adds little to the diagnostic capability of the osmotic fragility test.     

原发性高血压患者血浆非对称性二甲基精氨酸浓度升高

背景 非对称性二甲基精氨酸是一种内源性一氧化氮(NO)合成酶抑制剂,可以抑制NO的生成,影响血管内皮功能.目的 探讨原发性高血压患者血浆非对称性二甲基精氮酸(ADMA)浓度的变化及可能意义.方法 选取经冠状动脉造影检查排除冠状动脉粥样硬化性心脏病且无糖尿病的住院病人56例,其中原发性高血压(EH)患者30例,对照组(26例)为血压正常并无高血压史患者.通过高效液相色谱联合质谱法(HPLC)测定各患者的血浆ADMA、L精氨酸(L-Arg)含量,比色法测定血糖、肌酐、尿素氮、高密度脂蛋白胆固醇(HDL-C)、总胆固醇(TC)、三酰甘油(TG)和尿酸(UA).结果 EH组血浆ADMA浓度[(0.029±0.010)mmol/L]显著高于对照组[(0.023±0.010)mmol/L,P＜0.05].两组间血浆L-Arg、HDL-C、TC、TG、UA浓度比较,差异无统计学意义(P＞0.05).血浆ADMA、L-Arg浓度与患者年龄、HDL-C、TC、TG、UA浓度无相关性(P＞0.05).结论 EH患者血浆ADMA浓度升高.     

原发性高血压患者血浆非对称性二甲基精氨酸浓度升高

背景非对称性二甲基精氨酸是一种内源性一氧化氮(NO)合成酶抑制剂,可以抑制NO的生成,影响血管内皮功能。目的探讨原发性高血压患者血浆非对称性二甲基精氨酸(ADMA)浓度的变化及可能意义。方法选取经冠状动脉造影检查排除冠状动脉粥样硬化性心脏病且无糖尿病的住院病人56例,其中原发性高血压(EH)患者30例,对照组(26例)为血压正常并无高血压史患者。通过高效液相色谱联合质谱法(HPLC)测定各患者的血浆ADMA、L精氨酸(L-Arg)含量,比色法测定血糖、肌酐、尿素氮、高密度脂蛋白胆固醇(HDL-C)、总胆固醇(TC)、三酰甘油(TG)和尿酸(UA)。结果EH组血浆ADMA浓度[(0.029±0.010)mmol/L]显著高于对照组[(0.023±0.010)mmol/L,P<0.05]。两组间血浆L-Arg、HDL-C、TC、TG、UA浓度比较,差异无统计学意义(P>0.05)。血浆ADMA、L-Arg浓度与患者年龄、HDL-C、TC、TG、UA浓度无相关性(P>0.05)。结论EH患者血浆ADMA浓度升高。     

The Osmotic Fragility of Red Blood Cells: A Re-Evaluation of Technical Conditions

The osmotic fragility of red blood cells is influenced by even modest environmental changes. Consequently, the technical procedure must be strictly standardized. This implies that temperature equilibrium of the buffered salt solutions should be reached prior to the addition of blood. Furthermore, since erroneous statements concerning the composition of phosphate buffers regularly used to secure correct pH of the salt solutions have repeatedly appeared in the literature, pH control of such solutions prior to use becomes essential.     

原发性高血压患者中血浆肾上腺紧张素的浓度变化

目的 :探讨肾上腺紧张素在高血压发病机制中的主要作用。方法 :用特异性放射免疫顺序饱和分析法测定血浆肾上腺紧张素浓度。结果 :正常人和Ⅰ期、Ⅱ期、Ⅲ期原发性高血压患者的血浆肾上腺浓度有极显著差异 (F =399.6 4,P =0 0 0 0 1) ,且随病情加重而减少 (P值均小于 0 0 1)。结论 :在高血压发病机制中 ,肾上腺紧张素的信号调节作用远强于其血管活性作用。     

Prolactin Secretion in Essential Hypertension

This study was designed to evaluate prolactin (PRL) secretion in patients with essential hypertension. PRL secretory pattern was assessed by hourly blood sampling between 2200 and 0800 hours. Additional samples were collected at 0810 and 1000 hours (10 and 120 minutes after assumption of upright posture), as well as at 1200, 1400, and 1800 hours under normal simulated activities. No difference could be detected between the two study groups at any of the sampling times, and the number of secretory episodes were similar. Basal plasma renin activity levels were inversely related to simultaneous PRL levels in the hypertensive patients (r= -0.60, p<0.05). In the normal subjects mean overnight PRL levels were inversely related (r= -0.78, p<0.05) to the overnight urinary Na/K excretion. There was no PRL response to posture in either group. Hypertensive patients had a greater early response to the dopamine antagonist, metoclopramide than did normal subjects. Our data do not support the previously introduced concept of enhanced PRL responses to normal physiologic stimuli in essential hypertensives. However, it appears that dopaminergic control of PRL secretion may be altered in this disease state.     

伴胰岛素抵抗高血压患者中的红细胞胰岛素受体

目的研究伴胰岛素抵抗(IR)的原发高血压患者(EH)及治疗前后红细胞胰岛素受体(EIR)变化的意义.方法 (1)伴IR的EH患者37例(男25例,女12例.平均年龄(60±6.7)岁,健康对照30例(男19例,女11例.平均年龄(62±7.5)岁的红细胞胰岛素低亲合受体结合位数EIR(RT-2)及相关指标,并计算胰岛素敏感性指数(ISI).(2)伴IR的EH患者分别给予三种不同治疗方案(组111例,福辛普利5～20 mg,QD;吲达帕胺2.5 mg, QD.组212例,阿替洛尔12.5～50 mg,QD;尼群地平10～20 mg,Bid.组314例,阿替洛尔12.5～50 mg,QD;尼群地平10～20 mg,Bid;二甲双胍250 mg,Tid),疗程1年,治疗前后观察EIR(RT-2),ISI,及相关指标的变化.结果 (1)EH组EIR(RT-2),ISI较对照组明显降低(P<0.01).相关分析显示,EIR与ISI、餐后 2 h血糖正相关;与收缩期血压、血浆餐后两小时胰岛素水平(IN)及甘油三酯(TG)呈负相关.(2)3组治疗,血压控制均良好.3组间无统计学差异.治疗前组3 RT-2低于组1、2,有统计学差异(P<0.01);组1、2间无差异.治疗后组3 RT-2、ISI明显高于治疗前.结论胰岛素受体水平下调是伴胰岛素抵抗高血压患者关键环节.红细胞胰岛素受体一定程度的反映机体胰岛素敏感性.治疗组3方案可能对上调胰岛素受体水平有一定价值.     

原发性高血压患者血浆肾上腺髓质素水平变化意义的研究

目的探讨肾上腺髓质素(ADM)在原发性高血压(EH)的病理生理作用.方法在大鼠离体主动脉血管条上观察ADM与血管紧张素Ⅱ(ATⅡ)释放的相互影响.同时观察EH患者治疗前、后ADM的变化.结果大鼠离体主动脉血管组织中ADM、ATⅡ释放存在着相互影响;ATⅡ增加大鼠离体主动脉血管条ADM的分泌,ADM则抑制ATⅡ的释放.EH患者血浆ADM水平较正常对照组升高,有显著性差异(P<0.05);且与血浆ATⅡ水平、平均动脉压、动脉舒张压呈显著正相关.药物治疗后,伴随平均动脉压和血浆ATⅡ降低,ADM水平亦有不同程度的下降,尤以服用巯甲丙脯酸治疗后ADM改变更为明显,有显著性差异(P<0.05).结论血压和ATⅡ可能与ADM的分泌及(或)合成有关,EH患者血浆ADM水平升高可能是机体的代偿反应.药物治疗后的不同反应与药物的特性有关.     

盐与高血压研究进展

大量流行病学调查及实验研究表明,盐作为重要的环境因素与高血压的发生发展密切相关,其不仅影响了血压调节,而且还可能独立于血压对心、脑、肾等器官的损害产生作用。此外通过研究肾脏排钠与高血压的关系也已筛选出许多与高血压有关的易感基因。本文就以上几方面对盐与高血压的研究进展作一综述。     

Clearance of Erythrocytes and the Immune Response An Experimental Study

Abstract. The effect of accelerating the clearance rate of isologous erythrocytes on the immune response to antigens present on the erythrocytes was studied in rabbits. Hg^A negative rabbits injected with 80 μg anti-Hg^A antibody 5 h before challenge with Hg^A positive erythrocytes cleared these erythrocytes significantly faster than controls and their anti-Hg^A antibody response was suppressed as compared with controls. Rabbits injected with heated erythrocytes (49°C for 10 min) or given 350 μg anti-Hg^A antibody 3 months before challenge cleared the donor erythrocytes even faster. Despite this their anti-Hg^A antibody response was not significantly suppressed as compared with controls. It is considered that in the Hg^A system the prime factor causing immunosuppression by IgG iso-antibody is competition for antigenic determinants by passive antibody with antibody-like receptors on antigen sensitive cells and that a similar mechanism is responsible for the prevention of Rh isoimmunisation by anti-D antibody.     

原发性高血压遗传模式研究

目的为分析原发性高血压的遗传模式及其环境协变量的作用。方法我们对３９个原发性高血压家系共２９６人用Ｐｅｎｒｏｓｅ＇ｓ法估计一般遗传模式，用Ｆａｌｃｏｎｅｒ法估算遗传度，并用ＳＡＧＥ软件拟合Ａ型回归Ｌｏｇｉｓｔｉｃ模型，进行复合分离分析。结果原发性高血压为多基因遗传，遗传度为７０．００％±１１．８６％；接受隐性模型，主基因模型处于临界状态，虽在０．０５界值上拒绝，但不能否认可能是主基因模型中存在隐性孟德尔遗传效应，拒绝单纯环境模型、非传递模型、显性模型、共显性模型，；协变量体重指数、血浆总胆固醇、尿酸均增加患病危险。结论认为原发性高血压为多因子遗传疾病，环境协变量与遗传因素交互作用     

Association Between Increased Plasma Levels of Aldosterone and Decreased Systemic Arterial Compliance in Subjects With Essential Hypertension

We previously observed that, in subjects with essential hypertension, acute ouabain constricts the brachial artery diameter in the presence of spironolactone treatment, a finding that is not observed in the absence of aldosterone antagonist and therefore suggests a specific effect of aldosterone on the arterial wall. To evaluate whether aldosterone excess may contribute to modulate arterial function, we investigated 56 patients with sustained essential hypertension in comparison with 36 normotensive controls. Systemic arterial compliance was measured from intraarterial blood pressure and cardiac output measurements using a classical Windkessel model to determine the elasticity of the proximal arterial tree. Radial artery compliance was determined using a previously described echo tracking technique. In hypertensive, but not in normotensive, subjects, systemic arterial compliance was strongly and negatively correlated with plasma aldosterone. The correlation was observed even after adjustment for age and blood pressure. Plasma potassium and renin activity did not interfere in the correlation. Acute administration of diltiazem did not change systemic compliance but significantly decreased plasma aldosterone, suggesting that, in the presence of calcium blockade, the same compliance was achieved for a lower plasma aldosterone level. Taken together, these findings strongly suggest that significant interactions exist between aldosterone and central conduit arteries and that aldosterone might modulate arterial function in subjects with essential hypertension.     

Renal Surrogates in Essential Hypertension

The kidney can be considered both as culprit and victim in the hypertensive process. Renal functional derangement contributes to the development of arterial hypertension and the development of secondary vascular damage both at the glomerular and arteriolar level accounts for the development of progressive nephrosclerosis. The most common alteration of renal function observed in humans since the early stages of essential hypertension is the presence of renal vasoconstriction. This can be accompanied by the appearance of hyperuricemia, increased urinary excretion of enzymes such as N-acetyl-beta-glucosaminidase and of proteins like albumin and beta2-microglobulin. Later on, a progressive fall in glomerular filtration rate accompanied or not by proteinuria can be observed if high blood pressure persists.