铁污染软化水用树脂的改进复苏剂

铁污染软化水用树脂常用复苏剂是ＨＣｌ。为使树脂充分复苏，需用浓度高达１０％ＨＣｌ溶液浸泡树脂。本法用ＨＣｌ－ＮａＣｌ－Ｎａ２ＳＯ３混合溶液作复苏剂，各组份浓度依次为４％、４％、０．０８％，能快速使树脂充分复苏。酸浓度低、腐蚀性弱，所以对国内现有的小型软化水系统更为适用。

铁污染软化水用树脂的改进复苏剂

铁污染软化水用树脂常用复苏剂是盐酸。为使树脂充分复苏，需用浓度高达１０％ＨＣＩ溶液浸泡树脂。作者用氯化氢—氯化钠—亚硫酸钠混合溶液作复苏剂，各组份浓度依次为４％、４％、０．０８％，能快速使树脂充分复苏。酸浓度低、腐蚀性弱，对国内现有的小型软化水系统更为适用。

铁污染离子交换树脂复苏剂的改进

在软化水系统运行中 ,铁污染是离子交换最常见的现象。软化水树脂复苏通常采用 10 %的盐酸浸泡。为降低树脂处理成本和防止高浓度盐酸损坏软化水系统的防腐层 ,用 4 %HCl 4 %NaCl 0 .0 8%Na2 SO3混合溶液作复苏剂对树脂进行复苏试验。不仅能够快速使树脂充分复苏 ,而且对进一步降低软化水系统的运行成本 ,提高生产效率具有现实意义。

阴离子交换树脂有机物污染的次氯酸钠复苏机理与方法

在电厂高参数机组凝结水处理中,阴树脂常受到有机物污染[1]。将NaClO应用到阴树脂的复苏中,通过试验确定了NaClO的最佳浓度为0.4%。测定浸出液有机物含量、渗磨圆球率、树脂含水率、树脂工作交换容量,试验表明0.4%NaClO+10%NaNO3的复苏效果优于电厂广泛采用的0.1%NaOH+10%NaNO3复苏液和3%Na2SO3+10%NaNO3复苏液的复苏效果。将该复苏液应用于中试试验,结果表明复苏后树脂能够达到一等品的要求。

离子交换树脂污染原因分析及复苏方法

对某热电厂由于离子交换树脂污染造成除盐系统运行状况恶化进行分析、论证 ,并提出解决方案。指出污染物主要为铁和悬浮物杂质 ,复苏方法是用压缩空气擦洗除去悬浮物杂质 ,分离破碎树脂 ,并应用自行研制的树脂复苏剂除铁。另外 ,更换已达到报废标准的 0 0 1× 7强酸阳树脂 ,调整混床树脂的配比。经复苏和调试 ,树脂基本恢复了工交 ,酸碱耗降到正常值 ,出水水质完全合格 ,每年可为厂里节约酸碱费用 12 0万元。

离子交换树脂的复苏

对由于离子交换树脂污染造成除盐系统运行状况恶化进行了分析、论证,并提出离子交换树脂污染机理、污染程度的判断、复苏后达到标准、树脂复苏剂的选择及实际应用效果,进而阐明树脂污染复苏处理是解决树脂污染问题的有效途径,经复苏和调试,树脂基本恢复了工交,酸、碱耗降到正常值,出水水质完全合格。

离子交换树脂污染及复苏处理

介绍了离子交换树脂机理、污染程度的判断、复苏后达到标准、树脂复苏剂的选择及实际应用效果,进而阐明树脂污染复苏处理是解决树脂污染问题的有效途径,具有很好的经济效益、社会效益和应用价值。

铁污染阳离子交换树脂的复苏比较及测定

铁污染阳离子交换树脂常用HCI进行复苏。为使树脂充分复苏,需用浓度高达10％HCI溶液浸泡树脂。采用HCI-NaCl-Na_（2）SO_（3）复合复苏剂,其各组分浓度依次为5％、4％、0.06％,能快速使树脂充分复苏,因酸浓度低,腐蚀性弱。并对HCI复苏剂和复合复苏剂浸泡后的树脂进行工作交换容量测定。复合复苏剂对树脂复苏效果好,而且树脂的工作交换容量高。

Effect of hypertensive reperfusion on the changes between cerebral oxygen delivery and uptake after cardiac arrest and resuscitation in dogs

Objective: To study the changes between cerebral oxygen (O 2) delivery and uptake in dogs resuscitated under normotension or hypertension for 4 h. Methods: The model of ventricular fibrillation of 8 min in 12 dogs was made, followed by open cardiopulmonary resuscitation, reperfusion with normal or high mean arterial pressure (MAP), and controlled ventilation to 4 h. Animals were randomly assigned into Group NT (normotensive reperfusion, n=6) and Group HT (hypertensive reperfusion, n=6). Cerebral arteriovenous (sagittal sinus) O 2 content difference (Ca-ssO 2) and venous (sagittal sinus) PO 2 (PssO 2) were determined before cardiac arrest (CA) and 30, 60, 120, and 240 min after CA. Results: In Group NT, Ca-ssO 2 was lower at 30 min (P<0.05) but higher at 240 min (P<0.01) after CA than that before CA. In Group HT, Ca-ssO 2 was not significantly different from that in Group NT before CA but was lower than that in Group NT at 30 min after CA (P<0.01). Ca-ssO 2 was not significantly different in Group NT and HT thereafter. In both groups, PssO 2 was both higher at 30 min after reperfusion (P<0.01) and at 240 min after reperfusion lower (P<0.05) than those before CA .At 30 min after reperfusion, PssO 2 was higher (P<0.01) in Group HT than that in Group NT, with insignificant difference between two groups. Conclusion: Cerebral O 2 delivery and uptake are mismatched after CA and resuscitation. Hypertensive reperfusion improves oxygen delivery to the brain early after CA.