Decreased Cell Membrane Magnesium in Some Essential Hypertension Patients

The concentrations of total ([T-Mg]), ultrafilterable ([UF-Mg]), and protein-bound or nonfilterable ([NF-Mg]) magnesium were measured in the plasma and in the intracellular compartment of blood from 8 essential hypertensive patients and 9 normotensive subjects. In the former, [T-Mg] was unchanged in the plasma but decreased in whole blood due to decreases of both [UF-Mg] and [NF-MG]; [UF-Mg] was increased in plasma but decreased intracellularly while [NF-Mg] was decreased in plasma and unchanged intracellularly. These concentrations correlated significantly with the average blood pressures. Decreased Mg binding to the erythrocyte membrane was also observed in 13 additional essential hypertensive patients. This decreased binding may well be responsible for the decreased intracellular [UF-Mg] in the blood of such patients. The cause of the decreased Mg binding to the erythrocyte membrane is unknown, but the binding is returned to normal by incubating erythrocytes from essential hypertensive patients with blood plasma from normotensive subjects. Decreased Mg binding to cell membranes must also occur in frankly Mg-deficient patients, some of whom, as a consequence of the primary deficiency of this mineral, are hypertensive. Normal Mg binding to erythrocyte membranes was observed in two patients with hypertension indicating that hypertension per se does not cause decreased Mg binding to cell membranes.

These observations suggest that decreased Mg binding to cell membranes may be an important contributing factor in some cases of essential hypertension.     

Comparison of normal saline versus Lactated Ringer's solution for fluid resuscitation in patients with mild acute pancreatitis,A randomized controlled trial

Background/Objectives

Aggressive fluid resuscitation is recommended for initial management of acute pancreatitis. However, there are few studies which focus on types of fluid therapy.

中性粒细胞/淋巴细胞比值等4项指标对溃疡性结肠炎内镜活动度的判断价值

目的探讨中性粒细胞/淋巴细胞比值(neutrophils-lymphocytes ratio,NLR)、单核细胞/淋巴细胞比值(monocyte-lymphocytes ratio,MLR)、C反应蛋白(C-reactive protein,CRP)、红细胞沉降率(erythrocyte sedimentation rate,ESR)判断溃疡性结肠炎(ulcerative colitis,UC)内镜活动度的价值。方法收集广西医科大学第一附属医院2012年8月至2018年8月住院的112例UC患者,87例肠易激综合征(irritable bowel syndrome,IBS)患者数据,依据改良Mayo评分及蒙特利尔分型分组,并采用改良Mayo评分评估UC患者内镜活动度,探究NLR、MLR、CRP、ESR对UC内镜活动度的判断价值。结果(1)UC组NLR、MLR、CRP、ESR均高于IBS组;(2)UC活动期组NLR、MLR、CRP、ESR均高于愈合期组,NLR、MLR、CRP、ESR水平与内镜下改良Mayo评分呈正相关,除ESR外,NLR、MLR、CRP水平在不同病变范围组中无差异;(3)根据ROC曲线分析,四者中NLR判断UC内镜活动度的效能最佳,其曲线下面积(AUC)为0.795,当截断值为1.56时,敏感度为0.844,特异度为0.687;NLR、MLR、CRP、ESR联合较各指标独立判断效能更佳,其AUC为0.850,当截断值为0.88时,敏感度为0.667,特异度为0.937。结论NLR、MLR、CRP、ESR均可判断UC内镜活动度,可用于UC内镜活动度的监测,其中NLR判断效能最佳,四者联合效能更佳。     

Erythrocyte deformability has no influence on the rate of erythrophagocytosis in vitro by autologous human monocytes/macrophages

Summary. Erythrocytes with decreased deformability are known to be rapidly removed from the circulation by splenic macrophages. The exact mechanism is, however, not well understood. We have analysed the phagocytosis of less-deformable erythrocytes by macrophages in vitro. Human monocytes/macrophages were isolated from peripheral blood and cultured for a total time of 6 h at 37°C with 5% CO₂. Autologous erythrocytes of the rhesus positive donor were rigidified by heat treatment (47°C for 1 h). The change in erythrocyte deformability was assessed with a filter aspiration technique; the membrane elastic modulus was found to be increased about 2·5-fold. For controls, untreated erythrocytes and erythrocytes incubated with anti-RhD-antibodies were prepared. The rate of phagocytosis during 2 h at 37°C and 5% CO₂ was 0·74·0±59 (erythrocytes per monocyte/macrophage) for controls, 3·58·2±72 for anti-RhD-loaded erythrocytes and 0·82·0±74 for heat-treated erythrocytes, respectively. We conclude that decreased erythrocytes deformability does not cause an increased rate of phagocytosis by monocytes/macrophages compared to normally deformable erythrocytes in our in vitro model. This suggests that the preferential removal of rigid cells in vivo is probably not a specific process, but is due to the increased splenic transit time of rigid erythrocytes and hence longer interaction time between erythrocytes and phagocytes.     

Modified osmotic fragility test for the laboratory diagnosis of hereditary spherocytosis

A modified osmotic fragility test, based on measurement of hemolysis in four hypotonic NaCl solutions and logarithmic linearization of osmotic fragility curve is, like the "Pink test," a specific and sensitive test for the laboratory diagnosis of hereditary spherocytosis.     

Oxygen availability from the blood and the effect of phosphate replacement on erythrocyte 2,3-diphosphoglycerate and haemoglobin-oxygen affinity in diabetic ketoacidosis

Summary Eleven patients with diabetic ketoacidosis were given intravenous phosphate in doses (mean 118 mmol; range 83–320 mmol) adequate to maintain normal plasma phosphate, in addition to a standard treatment regime. Prevention of hypophosphataemia stimulated recovery of the initially low red-cell 2,3-diphosphoglycerate concentrations (10.6 ±5.8 (SD) mol/g Hb) after twenty-four hours. In ten control patients (initial concentration 8.1±4.4 mol/g Hb) treated without phosphate replacement, significantly lower red-cell 2,3-diphosphoglycerate concentrations were found between 2 and 6 days after admission (forty-eight hour value for control patients 14.6±1.6 and for phosphate-treated patients 18.9±4.1 mol/g Hb; p<0.01). However, no effect onin vivo p 50 or on the availability of oxygen from the blood resulted from the higher 2,3-diphosphoglycerate levels. Maintenance of normal plasma phosphate levels by intravenous phosphate is, therefore, not indicated to improve tissue oxygenation in diabetic ketoacidosis.     

Prognostic value of erythrocyte sedimentation rate in ST segment elevation myocardial infarction: interaction with hyperglycaemia

OBJECTIVES: Many inflammatory markers are associated with an adverse prognosis after ST segment elevation myocardial infarction (STEMI). Hyperglycaemia may exacerbate this inflammatory response. We investigated whether the erythrocyte sedimentation rate (ESR) was associated with an adverse prognosis and whether this was mediated by glucose levels. RESEARCH DESIGN AND METHODS: It concerns a post hoc analysis of a prospective randomised trial. In 346 patients with STEMI treated with reperfusion therapy, we investigated long-term outcome. Patients with ESR in the upper quartile (>14 mm h(-1)) were compared to patients with a normal ESR. Hyperglycaemia was defined as admission glucose >or=7.8 mmol L(-1). Median follow up was 7.4 years (range: 5.7-8.3). MAIN OUTCOME MEASURES: All cause mortality, cardiovascular mortality, sudden death, death as a result of heart failure. RESULTS: Both elevated ESR and hyperglycaemia were associated with a worse prognosis and increased mortality. Elevated ESR was particularly associated with an increased risk of sudden death (OR: 3.3, 17% vs. 6%, P < 0.01) whereas hyperglycaemia was especially associated with an increased risk of death because of heart failure (OR: 6.5, 8% vs. 1%, P < 0.01). There was no association between increased ESR and elevated glucose levels. Multivariate analysis did reveal that both elevated ESR and admission glucose were independent predictors of long-term mortality. CONCLUSIONS: Elevated ESR and admission glucose are independent predictors of mortality in STEMI patients treated with reperfusion therapy. There is no association or interaction between glucose levels and the inflammatory response as reflected by ESR.     

Effect of replacement of extracellular sodium ions and of D-600 on the activation by adrenalin of adenylate cyclase in intact pigeon erythrocytes

The effect of replacement of extracellular Na⁺ by Li⁺, choline, K⁺ or sucrose on cyclic AMP formation in pigeon erythrocytes has been investigated. Replacement of extracellular Na⁺ by Li⁺, choline or sucrose but not by K⁺ inhibited the stimulation by adrenalin of cyclic AMP formation, but had no detectable effect on cyclic AMP content in the absence of adrenalin. This inhibition was observed in the presence or absence of extracellular Ca²⁺. The relative inhibition caused by Na⁺ removal decreased with increasing adrenalin concentration. It was concluded that extracellular Na⁺ or K⁺ ions were required for maximal activation of adenylate cyclase by low concentrations of adrenalin, and that this effect of monovalent cations may have been due to an effect on the affinity of the receptor for adrenalin.The verapamil derivative D-600 also inhibited the stimulation by adrenalin of cyclic AMP formation. This effect occurred in the absence of extracellular Ca²⁺ and hence seemed to be unrelated to the inhibition by D-600 of the slow Ca²⁺ channel in electrically excitable tissues.     

Oxidative stress and erythrocyte damage in Kenyan children with severe Plasmodium falciparum malaria

Anaemia causes significant morbidity in children with Plasmodium falciparum malaria, but the mechanism(s) are unclear. During malarial infection, increased reactive oxygen species (ROS) are generated that may contribute to erythrocyte damage and anaemia. This study measured the concentrations of alpha-tocopherol in plasma and erythrocyte membranes, and the percentage polyunsaturated fatty acid composition (%PUFA) (an indirect marker of ROS damage) in erythrocyte membranes in children with severe P. falciparum malaria from Kilifi, Kenya, and asymptomatic children from the same district. Malarial subjects were stratified into complicated malaria and malaria anaemia. Results demonstrated significant reductions in erythrocyte membrane alpha-tocopherol concentration (1.63 +/- 0.16 versus 3.38 +/- 0.18 micromol/mg protein; P < 0.001) and total %PUFA (30.7 +/- 0.49 versus 32.8 +/- 0.44% P < 0.005) for the malarial subjects (non-stratified) compared with controls. Malarial subjects showed a significant positive correlation between membrane alpha-tocopherol and haemoglobin concentrations (P < 0.005 r = 0.63 complicated malaria group; P < 0.05 r = 0.36 non-stratified data). There were no significant differences in plasma alpha-tocopherol concentration between malaria patients and controls. In conclusion, malarial infection may be associated with oxidative damage and reduced alpha-tocopherol reserve in the erythrocyte membrane, suggesting that local antioxidant depletion may contribute to erythrocyte loss in severe malaria. Erythrocyte membrane alpha-tocopherol appeared a better indicator of ROS exposure than plasma.