雌二醇诱发大鼠高血压后相关组织中Ca，Cu及Zn含量的变化

①目的探讨雌二醇诱发大鼠血压升高与某些离子的关系。②方法用原子吸收分光光度法（火焰法），检测了雌二醇诱发血压升高组及对照组大鼠血清、延髓、肾上腺、心肌和肾脏组织中Ｃａ２＋，Ｃｕ２＋和Ｚｎ２＋的含量，经ｔ检验统计处理。③结果与对照组相比，实验组大鼠血清和延髓中Ｃａ２＋的含量增加（ｔ＝２．３０３，Ｐ＜０．０５；ｔ＝２．０８５，Ｐ＜０．０５），而肾上腺和心肌中Ｃａ２＋含量减少（ｔ＝３．５１０，Ｐ＜０．０１；ｔ＝２．１０４，Ｐ＜０．０５）。血清和肾脏中Ｃｕ２＋含量增加（ｔ＝２．４５４，Ｐ＜０．０５；ｔ＝２．５６４，Ｐ＜０．０１），而延髓中Ｃｕ２＋含量减少（ｔ＝２．２５４，Ｐ＜０．０５）。延髓和肾上腺Ｚｎ２＋含量增高（ｔ＝２．５０２，Ｐ＜０．０５；ｔ＝２．１４７，Ｐ＜０．０５），而心肌和肾脏Ｚｎ２＋含量减少（ｔ＝２．０７７，Ｐ＜０．０５；ｔ＝２．４９８，Ｐ＜０．０５）。④结论Ｃａ２＋，Ｃｕ２＋和Ｚｎ２＋可能参与雌二醇诱发大鼠高血压     

牛磺酸对缺血大鼠心肌细胞膜ATP酶活性的影响

研究缺血大鼠心肌细胞膜ＡＴＰ酶活性改变及牛磺酸的影响。给Ｗｉｓｔａｒ大鼠皮下注射异丙肾上腺素（ＩＳＰ５ｍｇ／ｋｇ）制造心肌缺血损伤模型，另一组在注射ＩＳＰ前３０ｍｉｎ腹腔注射牛黄酸２００ｍｇ／ｋｇ及对照组注射等量生理盐水。观测心肌细胞膜Ｋ＋·Ｎａ＋－ＡＴＰ酶，Ｃａ２＋－ＡＴＰ酶活性，丙二醛（ＭＤＡ）含量及心肌钙含量。结果显示，缺血组Ｃａ２＋－ＡＴＰ酶和Ｋ＋，Ｎａ＋－ＡＴＰ酶活性分别降低４８．２３％和４５．８５％（Ｐ＜０．０１），ＭＤＡ含量升高８０％（Ｐ＜０．０１），牛磺酸保护组未见显著性变化。并发现Ｋ＋、Ｎａ＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性与ＭＤＡ含量之间有显著负相关（Ｐ＜０．０５）。结果提示，牛磺酸可通过抑制心肌ＭＤＡ生成，实现它对心肌细胞膜Ｃａ２＋－ＡＴＰ酶和Ｋ＋·Ｎａ＋－ＡＴＰ酶活性的保护作用。     

不同年龄自发性高血压大鼠血管平滑肌细胞Ca~（2＋）转运功能障碍及某些相关因素的变化

应用不同年龄自发性高血压大鼠（ＳＨＲ）血管平滑肌原代与传代细胞（ＶＳＭＣ），观察Ｃａ２＋转运功能障碍及某些相关因素的变化。结果表明：（１）在血压未升高的ＶＳＭＣＣａ２＋内流已较同龄对照组ＷＫＹ大鼠明显增加，而Ｃａ２＋外流量较ＷＫＹ大鼠显著降低。表明ＳＨＲＶＳＭＣ膜Ｃａ２＋转运功能障碍在血压升高前就已发生，并随年龄及血压增高有加重趋势；（２）ＶＳＭＣｃＡＭＰ及钙调素（ＣａＭ）含量变化与细胞膜Ｃａ２＋转运功能障碍基本同步，提示二者异常与细胞膜Ｃａ２＋转运功能障碍有密切关系；（３）血压升高前ＳＨＲＶＳＭＣ内ＡＮＧⅡ含量与ＷＫＹ大鼠相比无明显差异，但１６周龄５ＨＲＶＳＭＣ内ＡＮＧⅡ含量明显高于其幼鼠（Ｐ＜０．００１），与血压呈正相关。提示ＶＳＭＣ内ＡＮＧⅡ在血压升高过程中可能具有一定作用。以上结果表明高血压时ＶＳＭＣ膜Ｃａ２＋转运功能障碍有明显遗传倾向，ＶＳＭＣ内ＣＡＭＰ、ＣａＭ及ＡＮＧⅡ含量异常与上述障碍密切相关。     

1，6－二磷酸果糖对心肌细胞胞质游离Ca~（2＋）和pH的影响

考察外源性的１，６－二磷酸果糖（ＦＤＰ）对心肌细胞内游离Ｃａ２＋浓度和ｐＨ值的影响。用荧光探针（Ｆｕｒａ－２，ＢＣＥＣＦ）技术同时测定成年大鼠心肌细胞内游离Ｃａ２＋浓度和ｐＨ值，并观察其在缺氧／复氧条件下的变化。结果：在缺氧／复氧过程中，胞质游离Ｃａ２＋浓度缓慢升高，从基础值１３０±２９．５ｎｍｏｌ／Ｌ１升至７４２±１５４ｎｍｏｌ／Ｌ，胞质ｐＨ值则从７．１２±０．０８降至６．７１±０．１３。在含有５ｍｍｏｌ／ＬＦＤＰ的细胞悬液中，则胞质游离Ｃａ２＋上升幅度明显低于对照组（Ｐ＜０．０５），在复氧结束时的最高值为５３８±１９３ｎｍｏｌ／Ｌ，但胞质ｐＨ值的变化与对照组比较无显著差别。结论：ＦＤＰ可以减轻由缺氧／复氧所造成的心肌细胞内游离Ｃａ２＋浓度增高的程度，而对胞质ｐＨ值的变化无明显影响。     

三七总皂甙对大鼠脊髓损伤组织总钙和脂质过氧化的影响

打击法致大鼠脊髓损伤４ｈ后脊髓组织ＭＤＡ、ＦＦＡ含量均显著增加（Ｐ＜０．０１）；ＸＯＤ活性显著升高（Ｐ＜０．０５），ＳＯＤ活性显著降低（Ｐ＜０．０１）；［Ｃａ＾２＋］ｔ显著增加（Ｐ＜０．００１）。表明ＳＣＩ病理过程中伴随Ｃａ＾２＋介导的自由基生成和膜脂质过氧反应。不同剂量的（３０、９０、２７０ｍｇ／ｋｇ，ｉｖ）ＰＮＳ均可抑制ＭＤＡ生成（Ｐ＜０．０１）；大剂量（２７０ｍｇ／ｋｇ）ＰＮＳ还可抑制ＦＦＡ     

NIDDM患者血小板Ca_(2+)转运及其与聚集功能的关系

３２例ＮＩＤＤＭ患者，分血小板聚集功能亢进组（ｎ＝１７）和无亢进组（ｎ＝１５），探讨Ｃａ２＋转运影响血小板胞浆游离Ｃａ２＋（［Ｃａ２＋］ｉ）变化与最大聚集（ＭＡＲ）的关系。结果：亢进组血小板静息［Ｃａ２＋］ｉ高于对照组（１３４．４±２６．４对１０１．５±１３．３ｎｍｏｌ／Ｌ，Ｐ＜０．０１）。［Ｃａ２＋］ｉ与ＭＡＲ呈正相关（ｒ＝０．３２１９，Ｐ＜０．０５）以凝血酶刺激，有胞外Ｃａ２＋内流及胞内Ｃａ２＋释放时，亢进组［Ｃａ２＋］ｉ高于对照组（９１８．９±２０７．６对７９１．２±１１９．６ｎｍｏｌ／Ｌ，Ｐ＜０．０１），并与ＭＡＲ呈正相关（ｒ＝０．３３７１，Ｐ＜０．０１）；以ＴＭＢ８阻滞胞内Ｃａ２＋释放，组间差异仍然显著（Ｐ＜０．０５）；当缺乏胞外Ｃａ２＋内流时，则组间不呈显著差异（Ｐ＞０．０５）。以钙载体Ａ２３１８７刺激，在有或无胞外Ｃａ２＋时，亢进组［Ｃａ２＋］ｉ均高于对照组（Ｐ均＜０．０５）然而，无亢进组上述各指标与对照组间均未呈显著差异。提示ＮＩＤＤＭ患者血小板聚集功能亢进与［Ｃａ２＋］ｉ变化有关，可能涉及胞浆内Ｃａ２＋稳态异常，凝血酶刺激胞外Ｃａ２＋内流及Ａ２３１８７作用胞内Ｃａ２＋释放增强等环节     

败血症大鼠肝细胞内核膜三磷酸肌醇受体的改变

目的：观察早期、晚期败血症大鼠肝细胞内核膜上１,４,５三磷酸肌醇受体（ｉｎｏｓｉｔｏｌ１,４,５ｔｒｉｐｈｏｓｐｈａｔｅｒｅｃｅｐｔｏｒｓ,ＩＰ３Ｒ）的变化。方法：通过结扎并穿刺盲肠制作大鼠败血症模型,差速离心分离内核膜,［３Ｈ］ＩＰ３放射配体分析肝内核膜ＩＰ３Ｒ与其配体的最大结合容量（Ｂｍａｘ）及亲和力（Ｋｄ）。４５Ｃａ２＋转运测定内核膜ＩＰ３Ｒ释放Ｃａ２＋功能。结果：早期和晚期败血症Ｂｍａｘ分别增加１４％（Ｐ＜０．０５）和９１％（Ｐ＜０．０１）。但Ｋｄ值无明显变化（Ｐ＞０．０５）。ＩＰ３引起４５Ｃａ２＋转运在败血症时也相应增加。结论：在败血症时肝细胞核被膜ＩＰ３Ｒ发生上调,其释放Ｃａ２＋的能力增强,但结构可能未发生变化。     

内皮素-1对成纤维细胞内游离钙的影响

目的研究内皮素（ＥｎｄｏｔｈｅｌｉｎＥＴ）对成纤维细胞（ＨＬＦ）内钙离子浓度（［Ｃａ＋２］ｉ）的影响及维拉帕米（Ｖｅｒ）对ＥＴ促［Ｃａ＋２］ｉ效应的阻断作用。方法采用Ｆｕｒａ－２／ＡＭ钙荧光指示剂测定ＨＬＦ细胞内Ｃａ＋２浓度。结果ＥＴ在很短时间内即可明显提高ＨＬＦ细胞内Ｃａ＋２浓度（Ｐ＜０．０１～０．００１）。并且在细胞外液无Ｃａ＋２存在情况下，亦可提高［Ｃａ＋２］ｉ，且有明显的量效关系（Ｐ＜０．０５～０．０１）。同时，Ｖｅｒ对ＥＴ的上述作用具有显著的作用（Ｐ＜０．０５）。结论ＥＴ对Ｖｅｒ的调控作用是通过［Ｃａ＋２］ｉ转运而产生的。     

高血压病人红细胞变形能力与红细胞ATP酶活性及细胞内离子水平关系的研究

通过观察６６例高血压病（ＥＨ）病人红细胞变形能力（ＥＤ）和红细胞ＡＴＰ酶活性，细胞内离子浓度变化及其相互关系。结果显示，ＥＨ病人红细胞滤过指数（ＩＦ）较对照组明显增高（Ｐ＜０．００１），红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰ酶和Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性、细胞内Ｋ＋，Ｍｇ２＋－浓度明显降低（Ｐ＜０．００１），而细胞内Ｎａ＋，Ｃａ２＋浓度明显增高（Ｐ＜０．００１），且随着ＥＨ病程进展而逐渐明显（Ｐ＜０．００１）。ＥＨ病人红细胞ＩＦ与红细胞Ｎａ＋－Ｋ＋－ＡＴＰ酶、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性及Ｋ＋，Ｍｇ２＋浓度呈明显负相关（Ｐ＜０．００１），与Ｃａ２＋，Ｎａ＋浓度呈正相关（Ｐ＜０．００１）。结果提示ＥＨ病ＨＥＤ降低与红细胞膜ＡＴＰ酶活性降低及离子浓度异常有关。     

氯化钐、氯化镨对大鼠肝脏形态及LPO、SOD活性的影响

本实验采用不同途径给予断乳Ｗｉｓｔａｒ大鼠小剂量（０．０５ｍｇ／ｋｇ、０．０２５ｍｇ／ｋｇ）氯化角钐（ＳｍＣｌ３）、氯化镨（ＰｒＣｌ３）后，测定了肝脏中过氧化脂质（ＬＰＯ）和超氧化物歧化酶（ＳＯＤ）的含量，观察了肝脏的超微结构。结果表明：ＳｍＣｌ３和ＰｒＣｌ３均使肝脏中ＬＰＯ活性降低、ＳＯＤ活性升高，二者比较ＰｒＣｌ３的作用更为明显，肝脏未见明显形态学改变。     

Erythrocyte and plasma Ca2+, Mg2+ and cell membrane adenosine triphosphatase activity in patients with essential hypertension

OBJECTIVE: To assess the relationships between plasma and intracellular Ca2+, Mg2+ and blood cell membrane adenosine triphosphatase (ATPase) activity in normotensive and hypertensive subjects. METHODS: Plasma and intracellular Ca2+, Mg2+ were measured with atomic absorption spectrophotometry, and red blood cell membrane Na(+)-K+ ATPase and Ca(2+)-ATPase activities were determined with colorimetric method in 55 patients with essential hypertension and 32 normotensive controls. RESULTS: The results showed that the hypertensive group consistently demonstrated a significant decreased activity of ATPase studied, with significantly lower plasma Ca2+ and higher cytosolic Ca2+ levels when compared with those in normotensive group (P < 0.01 or P < 0.05, respectively). No significant differences were found in either plasma Mg2+ or intracellular Mg2+ level between the two groups. CONCLUSIONS: This study suggests that patients with essential hypertension have widespread depression of cell membrane Na(+)-K(+)-ATPase and Ca(2+)-ATPase activities with plasma Ca2+ depletion and cytosolic Ca2+ overload, which may reflect an underlying membrane abnormality in essential hypertension. The cellular abnormalities may be related to the defective transport mechanisms that in turn may be aggravated by plasma Ca2+ depletion.     

Lack of deficiency in extracellular and intralymphocyte free Mg2+ in genetically hypertensive rats

Recently it has been suggested that Mg deficiency may play a key role in hypertension and several cardiovascular diseases. In order to investigate the status of Mg in genetic hypertension, the cytosolic free Mg2+ concentration ([Mg2+]i) in the lymphocytes and serum concentrations of free Mg2+ and total Mg were measured in spontaneously hypertensive rats/Izumo (SHR/Izm), stroke-prone spontaneously hypertensive rats/Izumo (SHRSP/Izm), and Wistar-Kyoto rats/Izumo (WKY/Izm). In addition, the basal cytosolic free Ca2+ concentration ([Ca2+]i) was assessed in the three strains. Systolic blood pressure was highest in SHRSP/Izm and lowest in WKY/Izm. No significant differences were found in either the serum free Mg2+ concentrations or the serum total Mg concentrations among WKY/Izm, SHR/Izm, and SHRSP/Izm. [Mg2+]i in the lymphocytes was significantly higher in SHR/Izm than in WKY/Izm (254 +/- 51 versus 201 +/- 36 mumol/liter, p < 0.05), but the [Mg2+]i in SHRSP/Izm (211 +/- 34 mumol/liter) was at the same level as in WKY/Izm. No significant correlation was found between [Mg2+]i in the lymphocytes and systolic blood pressure. Basal [Ca2+]i did not differ among the three strains. Thus, an increase in [Ca2+]i is not obligatory in all cells of genetically hypertensive rats. Mg deficiency may not exist in the intracellular or extracellular space in genetically hypertensive rats.     

肉桂酸对小鼠运动疲劳的实验研究

目的：探讨肉桂酸对提升小鼠运动耐力的影响。方法通过建立力竭性游泳来建立小鼠力竭性运动模型,比较安静对照组、运动训练组和运动给药组小鼠力竭游泳持续时间,血浆中乳酸（LAC）含量来探讨肉桂酸对小鼠的耐力提升;检测肝脏组织匀浆中超氧化物歧化酶（SOD）、丙二醛（MDA）和过氧化酶（CAT ）的含量来探讨肉桂酸的抗氧化能力,通过Western blot方法检测肉桂酸对小鼠股四头肌中Na＋／K＋‐ATP酶、Ca2＋／Mg2＋‐ATP酶表达水平来进一步研究其对小鼠运动能力提升的影响。结果肉桂酸显著延长小鼠的游泳时间;运动给药组与安静对照组比较：血浆 LAC含量虽然有所升高,但差异无统计学意义（P＞0．05）,肝脏组织匀浆中SOD和CAT 显著下降（P＜0．05）,MDA显著上升（P＜0．01）,CAT 虽下降但差异无统计学意义（P＞0．05）,Na＋／K＋‐ATP酶和Ca2＋／Mg2＋‐ATP酶的表达水平显著下降（P＜0．01）;运动训练组与安静对照组比较,血浆LAC含量显著升高（P＜0．01）,肝脏组织匀浆中SOD和CAT 显著下降（P＜0．01）,MDA显著上升（P＜0．01）,Na＋／K＋‐ATP酶和Ca2＋／Mg2＋‐ATP酶的表达水平显著降低（P＜0．01）;运动给药组与运动训练组比较,血浆LAC含量显著降低（P＜0．01）,肝脏组织匀浆中SOD和CAT显著上升（P＜0．01）,MDA显著下降（P＜0．01）,CAT 显著下降（P＜0．01）,Na＋／K＋‐ATP酶和Ca2＋／Mg2＋‐ATP酶的表达水平显著降低（P＜0．05）。结论肉桂酸具有良好的抗氧化能力和抗疲劳能力。     

风心瓣膜病变患者红细胞膜钠、钙泵活性和脂质过氧化的变化

用酶解法和Ｈ２Ｏ２分解法分别测定２８例风心瓣膜病变患者红细胞膜钠泵（Ｎａ＋、Ｋ＋－ＡＴＰ酶）、钙泵（Ｃａ２＋、Ｍｇ２＋－ＡＴＰ酶）活性和膜过氧化氢酶（ＣＡＴ）活性，并用硫代巴比妥酸比色法测定患者红细胞膜脂质过氧化物（ＬＰＯ）含量。患者红细胞膜Ｎａ＋、Ｋ＋－ＡＴＰ酶活性和Ｃａ２＋、Ｍｇ２＋－ＡＴＰ酶活性分别显著低于正常人３４．７５％（Ｐ＜０．０１）和２６．７７％（Ｐ＜０．０１）；ＣＡＴ活性显著低于正常人２０．０７％（Ｐ＜０．０１）；而患者ＬＰＯ含量却显著高于正常人９７．５０％（Ｐ＜０．０１）。结果提示风心病患者瓣膜病变与质膜钠、钙泵活性变化以及膜脂质过氧化作用有关。     

Cross-sectional survey of intralymphocytic and serum elements in hypertensive patients

ＯｂｊｅｃｔｉｖｅＴｏｉｎｖｅｓｔｉｇａｔｅｔｈｅｄｉｓｔｒｉｂｕｔｉｏｎｃｈａｒａｃｔｅｒｉｓｔｉｃｓｏｆｓｏｍｅｃｏｍｍｏｎａｎｄｔｒａｃｅｅｌｅｍｅｎｔｓｉｎｂｏｔｈｓｅｒｕｍａｎｄｌｙｍｐｈｏｃｙｔｅｉｎｐａｔｉｅｎｔｓｗｉｔｈｅｓｓｅｎｔｉ...     

植酸钠对饮食所致高脂血症大鼠心血管的保护作用

目的研究植酸钠对饮食所致高脂血症大鼠心血管保护作用机制。方法5周龄的Wistar大鼠按体重随机分成4组：正常饮食组（对照组）、高脂饮食组（高脂模型对照组）、高脂饮食＋100mg／kg植酸钠（高剂量植酸钠组）、高脂饮食＋50mg／kg植酸钠（低剂量植酸钠组）。4周后测定各组大鼠血脂、氧化应激、心肌瘦素、心肌Na^＋，K^＋-ATPase和Ca^2＋，Mg^2＋-ATPase酶水平。结果与对照组相比，高脂血症显著提高血清总胆固醇、甘油三脂、高密度脂蛋白、低密度脂蛋白的含量，提高血清丙二醛（MDA）水平，显著降低血清超氧化物岐化酶（SOD）、谷胱甘肽过氧化物酶（GSH—Px）、过氧化氢酶（CAT）3种抗氧化酶水平，降低心肌Na^＋，K^＋-ATPase、Ca^2，Mg^2＋-ATPase和瘦素水平；高剂量或低剂量植酸钠组均可显著升高血清SOD、GSH—Px、CAT抗氧化酶水平，增高心肌Na^＋，K^＋-ATPase、Ca^2＋，Mg^2＋-ATPase水平，降低MDA含量，但对血脂水平无显著影响。高剂量植酸钠组还可显著增加心肌瘦素水平。结论植酸钠具有心血管保护作用，其作用机制至少包括抗氧化作用和增加心肌细胞的瘦素表达两个方面。     

电子探针X线微区分析1－烯丙基氯－3引起神经组织内Na、K、Ca等元素的改变

用ＥＰＭＡ技术测定了１－烯丙基氯－３染毒后鸡胚脑神经细胞、大鼠坐骨神经轴浆和脑干内Ｎａ、Ｋ、Ｃａ、Ｍｇ、Ｃｌ、Ｐ元素的百分含量变化。结果显示，在鸡胚脑神经细胞、大鼠坐骨神经轴浆和脑干内Ｎａ、Ｃａ明显增加，Ｋ则明显减少（Ｐ＜０．０１）。在鸡胚脑神经细胞内Ｃｌ明显增加（Ｐ＜０．０１），而在大鼠坐骨神经轴浆和脑干内无明显变化。在大鼠坐骨神经轴浆和脑干内Ｍｇ明显增加，而在鸡胚脑神经细胞内明显减少（Ｐ＜０．０５，Ｐ＜０．０１）。在鸡胚脑神经细胞内和大鼠坐骨神经轴浆内Ｐ明显减少（Ｐ＜０．０５），而在大鼠脑干内减少不明显。１－烯丙基氯－３引起神经组织内Ｎａ、Ｋ、Ｃａ、Ｍｇ、Ｃｌ、Ｐ元素稳态失调，这可能与其引起的中毒性周围神经病有关     

高血压病红细胞ATP酶活性和离子浓度的改变及其药物干预的影响

观察59例高血压病（EH）患者红细胞ATP酶活性和细胞内离于浓度以及尼群地平和卡托普利降压治疗后的变化，结果：EH患者Na －K －ATP酶、Ca2 －Mg2 －ATP酶活性显著低于正常人，细胞Na 和Ca2 浓度显著升高，Mg2 －ATP酶活性无显著差异，且平均动脉压与Ca2 －Mg2 －ATP酶活性和细胞Ca2 浓度呈显著相关性。降压治疗后，尼群地平组Na －K －ATP酶和Ca2 －Mg2 －ATP酶显著升高，细胞Na 和Ca2 浓度显著降低；卡托普利组Ca2 －Mg2 -ATP酶和细胞Ca2 浓度亦分别显著升高与降低。结果表明EH患者存在细胞钠和钙离子转运障碍，ATP酶活性受抑制可能是发病的重要环节，两种降压药至少在一定程度上对离子转运系统有影响。     

冠心病患者红细胞膜ATP酶活性及血脂水平的变化

观察２１例冠心病患者及正常对照组的空腹血浆甘油三酯（ＴＧ）、总胆固醇（ＴＣ）、低密度脂蛋白胆固醇（ＬＤＬＣ）、高密度脂蛋白胆固醇（ＨＤＬＣ）,红细胞膜Ｎａ＋Ｋ＋ＡＴＰ酶、Ｃａ２＋ＡＴＰ酶,Ｍｇ２＋ＡＴＰ酶及红细胞内Ｃａ２＋浓度（［Ｃａ２＋］）的变化。发现冠心病组ＴＧ,ＴＣ,ＬＤＬＣ及红细胞内［Ｃａ２＋］高于对照组;而血浆ＨＤＬＣ,红细胞膜Ｎａ＋Ｋ＋ＡＴＰ酶与Ｃａ２＋ＡＴＰ酶活性低于后者;Ｍｇ２＋ＡＴＰ酶无变化;Ｎａ２＋Ｋ＋ＡＴＰ酶,Ｃａ２＋ＡＴＰ酶分别与血浆ＴＧ,ＴＣ和ＬＤＬＣ呈负相关,与血浆ＨＤＬＣ呈正相关。根据测定结果,对其发病机制进行了讨论     

Studies on Hypokalemia Induced by Trimethyltin Chloride

To determine the possible relationship between plasma potassium concentration and severity of acute trimethyltin chloride (TMT) poisoning and to assess the mechanism of TMT induced hypokalemia. Methods SD rats were treated with various dosages of TMT (ip). All the indices were measured and analysed for determing their possible relations with plasma K+. Results With increase of dosage, the plasma K+ level dropped rapidly, and deaths appeared more quickly. The LDs0 of TMT (ip) was 14.7 mg/kgbw. In the low dosage group (10 mg/kgbw), the plasma K+ level dropped slowly with the lowest dosage on day 6 (4.85 mmol/L). It rose again on day 11 (5.06 mmol/L), and recoverd on day 28. The poisoning signs corresponded with decline of the span of K+ level. The plasma Na+ level dropped half an hour after TMT treatment, but recovered 24 h later. In the high dosage group (46.4 mg/kgbw), the levels of plasma K+ and Na+ fell rapidly within half an hour (P＜0.05), the intracellular potassium concentration of RBC did not decrerase obviously (P＞0.05), the activities of Na+-K+-ATPase and Mg2+-ATPase in RBC membrane were depressed remarkably (P＜0.01, P＜0.05, respectively), the plasma aldosterone concentrations rose as high as tenfold (P＜0.01), the arterial blood pH fell from 7.434 to 7.258 (P＜0.01),pCO2 was raised from 29.62 to 45.33 mmHg (P＜0.01). In the 24 h urine test, when rats were treated with TMT (21.5 mg/kgbw, ip), urine volume, urinary potassium, sodium and chloride increased significantly in comparison with those in the controls (P＜0.01). Conclusion TMT could induce hypokalemia in SD rats. The available evidence suggests that TMT can induce acute renal leakage of potassium. At the same time, a significant rise of plasma aldosterone may play an important role in promoting potassium leakage from kidney to result in severe hypokalemia with inhaling acid-base abnormalities produced, which aggravate the poisoning symptoms. In the end the rats would die of respiratory failure.