鼠急性肾功能衰竭时血浆心钠素动态变化及其与肾功能的关系

用顺铂（ＣＰ）复制大鼠急性肾功能衰竭动物模型，动态观察急性肾功能衰竭各阶段的血浆心钠素（ＰＡＮＰ）变化及其与肾功能的关系。在采用ＣＰ处理后２４ｈ和７２ｈ，血清肌酐分别升高为正常对照组的１．５和４倍，同时血浆心钠素水平升高到１．８和３．６倍。血浆ｃＧＭＰ水平也与血浆心钠素水平一道平行升高。这表明血浆心钠素水平的变化与肾功能损害程度密切相关。     

蜂王浆产量与密蜂幼虫日龄和取浆周期的关系研究

对蜜蜂幼虫移虫后７２ｈ，５５ｈ，４８ｈ３个取浆周期及１日龄、１．５日龄、２日龄、２．５日龄幼虫与王浆产量三者之间的关系进行了研究。结果表明，７２ｈ，５５ｈ，４８ｈ取浆周期，分别采用１日龄 、２日龄、２．５日龄幼虫的王浆产量比较高。     

蜂王浆产量与蜜蜂幼虫日龄和取浆周期的关系研究

对蜜蜂幼虫移虫后７２ｈ，５５ｈ，４８ｈ３个取浆周期及１日龄、１．５日龄、２日龄、２．５日龄幼虫与王浆产量三者之间的关系进行了研究。结果表明，７２ｈ，５５ｈ，４８ｈ取浆周期，分别采用１日龄、２日龄、２．５日龄幼虫的王浆产量比较高。其中以７２ｈ，１日龄的幼虫组合王浆产量最高，与其它２种组合差异显著。     

山羊十二指肠内灌注酸或碱对血浆胃动素水平的影响

选用２只装有永久性十二指肠瘘管的１周岁母山羊,禁食２４ｈ分别以５ｍＬ．ｍｉｎ＾－１的速度经瘘管灌注０．１ＭＨＣｌ,０．３Ｍｔｒｉｓ缓冲液和生理盐水各１００ｍＬ,重复进行２次,每隔７２ｈ灌注１次。分别于灌注后０,５,１０,２０,３０,６０,９０ｍｉｎ采集颈静脉血样,用放射免疫法测定血浆胃动素水平。结果如下：（１）山羊禁食２４ｈ无灌注时血浆胃动素水平为（１６８．４４－２３４．１７）ｎｇ．Ｌ＾－１,平均     

亚硝酸盐和氨对罗氏沼虾幼体的毒性

本文研究了ＮＯ２＾－Ｎ与ＮＨ３－Ｎ对罗氏沼虾幼体的毒性作用，分别给出了ＮＯ２％－－Ｎ与ＮＨ３－Ｎ对罗氏沼虾Ｚ５、Ｚ７与Ｚ９的２４ｈ、４８ｈ、７２ｈ、９６ｈ的ＬＣ５０值，提出ＮＯ２＾－－Ｎ对Ｚ５、Ｚ７和Ｚ９的安全浓主工分别为０．６４，１．３８和１．６８ｍｇ／ｌ，ＮＨ３－Ｎｔ（ＮＨ３－Ｎｍ（的安全浓度分别为２．０４（０．２８７），２．２６（０．３１８）和２．５５（０．３５８）ｍｇ／ｌ。Ｚ５与Ｚ７分别经     

亚硝酸盐和氨对罗氏沼虾幼体的毒性

本文研究了ＮＯ２＾－Ｎ与ＮＨ３－Ｎ对罗氏沼虾幼体的毒性作用，分别给出了ＮＯ２％－－Ｎ与ＮＨ３－Ｎ对罗氏沼虾Ｚ５、Ｚ７与Ｚ９的２４ｈ、４８ｈ、７２ｈ、９６ｈ的ＬＣ５０值，提出ＮＯ２＾－－Ｎ对Ｚ５、Ｚ７和Ｚ９的安全浓主工分别为０．６４，１．３８和１．６８ｍｇ／ｌ，ＮＨ３－Ｎｔ（ＮＨ３－Ｎｍ（的安全浓度分别为２．０４（０．２８７），２．２６（０．３１８）和２．５５（０．３５８）ｍｇ／ｌ。Ｚ５与Ｚ７分别经     

增效磷对农药混剂的增效作用及增效比值研究

测定增效磷与氰戊菊酯、敌敌畏混用对褐稻虱和菜蚜的增效作用以及对其他几种害虫的增效比值结果表明,混剂对褐稻虱处理２４ｈ的触杀毒力ＬＣ５０值为１３．８５ｍｇ／ｋｇ,比单剂氰戊菊酯、敌敌畏和增效磷的触杀毒力分别高６．３５倍、２．５６倍和１．８６倍,共毒系数为２３９．７５,大于２００有明显增效作用。混剂对菜蚜处理２４ｈ的触杀毒力ＬＣ５０值为１．１０ｍｇ／ｋｇ,比单剂氰戊菊酯、敌敌畏和增效磷的触杀毒力分别高０．５倍、４．２倍和３２．５倍,共毒系数为２７１．３５,亦有明显增效作用。加有增效磷的混剂对棉蚜处理２４ｈ的触杀毒力ＬＣ５０值为３０．９９ｍｇ／ｋｇ,比不加增效磷混剂的增效比值高１．７倍;对棉红叶螨处理２４ｈ的触杀毒力ＬＣ５０值为４６．５７ｍｇ／ｋｇ,增效比值为１．７倍;对玉米螟处理２４ｈ的触杀毒力ＬＣ５０值为１１６．５０ｍｇ／ｋｇ,增效比值为２．０倍;对粘虫处理２４ｈ的触杀毒力ＬＣ５０值为２４．８１ｍｇ／ｋｇ,增效比值为１．３倍。     

盐胁迫下大豆小真叶愈伤组织过化和酶活性的变化

大豆小真叶愈伤组织在含ＮａＣｌ０％、０．４％、０．８％、１．２％、１．６％的培养基中进行２４、４８、７２ｈ短时间２和１６、２０、２４ｄ长时间培养，结果表明，愈伤组织对盐胁迫都有过氧化物酶活性同的适应性反应。短时间培养，高盐比低盐酸活升高快，且值高，长时间培养，低盐比高盐酶活升高幅度大。     

粒细胞系集落刺激因子对慢性肾功能衰竭患者影响的研究

为研究粒细胞系集落刺激因子对慢性肾功能衰竭的影响，方法；以酶标免疫测定法检测了３１例ＣＲＦ患者血清及尿－ＧＣＳＦ水平及４０例健康人血清及尿Ｇ－ＣＳＦ水平，并进行了相关分析。结果：ＣＲＦ患者血清及尿－ＧＣＳＦ水平分别是２４．１４±２．１ｐｇ／ｍｌ和３０．７２±１．８３ｐｇ／ｍｌ，高于健康对照组，Ｐ〈０．００１；ＣＲＦ血清Ｇ－ＣＳＦ与ＢＵＮ，Ｓｃｒ均无相关性，但血Ｇ－ＣＳＦ与尿Ｇ－ＣＳＦ水平呈正相关。     

鹿复合麻醉剂对鹿无创血压、血浆ANP、CGRP及RAAS影响

为明确鹿复合麻醉剂作用下鹿血压变化与血浆肾素-血管紧张素-醛固酮系统、心钠素、降钙素基因相关肽相关性。试验选取6只健康成年梅花鹿,肌注鹿复合麻醉剂0.04 m L·kg-1,注药前及注药后0、15、30、45、60、75、90及120 min血压监测,并同步采集颈静脉血样测定肾素(PRA)、血管紧张素(AⅡ)、醛固酮(ALD)、心钠素(ANP)和降钙素基因相关肽(CGRP)含量。结果表明,梅花鹿麻醉期血浆中ANP、PRA、AⅡ和ALD含量下降,与对照组相比显著降低(P0.01或P0.05);CGRP含量升高,与对照组相比极显著升高(P0.01);SBP、DBP和MAP显著低于对照组(P0.01)。说明鹿复合麻醉剂引起肾素-血管紧张素-醛固酮系统、心钠素、降钙素基因相关肽变化,参与鹿血压变化调节。     

Atrial natriuretic peptide elevation in congestive heart failure in the human

A sensitive radioimmunoassay for atrial natriuretic peptide was used to examine the relation between circulating atrial natriuretic peptide and cardiac filling pressure in normal human subjects, in patients with cardiovascular disease and normal cardiac filling pressure, and in patients with cardiovascular disease and elevated cardiac filling pressure with and without congestive heart failure. The present studies establish a normal range for atrial natriuretic peptide in normal human subjects. These studies also establish that elevated cardiac filling pressure is associated with increased circulating concentrations of atrial natriuretic peptide and that congestive heart failure is not characterized by a deficiency in atrial natriuretic peptide, but with its elevation.     

脑钠肽生物学特性及其在心血管病中的应用

脑钠肽（BNP）主要是由心脏分泌和存储的一种神经内分泌激素,为32个氨基酸组成的多肽片段,具有抑制肾素-血管紧张素-醛固酮系统（RAAS）和交感神经系统（SNS）等功能,BNP水平的检测已逐渐被应用于临床,在诊断心力衰竭、心源性哮喘与支气管哮喘的鉴别、评估急性心肌梗死范围等方面具有较大的应用价值,现已成为广大学者关注的焦点.     

新生儿缺氧缺血性脑病心房利钠多肽血浆水平的检测及其与低钠血症的关系

目的 :观察血浆心房利钠多肽 (ANP)在新生儿缺氧缺血性脑病 (HIE)中的变化及与低钠血症的关系。方法 :采用放射免疫法分别检测 49例 HIE足月儿在治疗前后及 2 0例正常足月儿血浆 ANP水平 ,同时测定血清钠浓度 ,并将 ANP与血钠作相关性分析。结果 :HIE组血浆 ANP水平明显高于对照组 (P<0 .0 1 ) ,HIE程度愈重 ,ANP水平愈高 ,HIE组治疗后血浆 ANP水平明显低于治疗前水平 (P<0 .0 0 1 ) ;血浆 ANP与血清钠浓度呈显著负相关 (r=- 0 .6632 ,P<0 .0 0 1 )。结论 :血浆 ANP可反映 HIE患儿脑损伤的程度和预后 ,并可影响新生儿 HIE水盐代谢 ,引起失钠性低钠血症。     

Cardiac atria of BIO 14.6 hamsters are deficient in natriuretic factor

The hearts of 220-day-old hamsters of the BIO 14.6 strain are deficient in atrial natriuretic factor; saline extracts of atria produce one-third the natriuretic and diuretic effects of extracts of atria from age-matched normal hamsters. BIO 14.6 hamsters are known to develop congestive heart failure with edema when they are about 200 days old, and the venous congestion and edema are preventable by parabiosis with normal hamsters. The humoral mediator, the deficiency of which causes venous congestion and edema in BIO 14.6 hamsters, may be atrial natriuretic factor.     

Atrial natriuretic factor ameliorates chronic metabolic alkalosis by increasing glomerular filtration

The kidney maintains the elevated plasma concentration of bicarbonate that occurs in chronic metabolic alkalosis. A reduction in the glomerular filtration rate (GFR) can maintain the filtered bicarbonate load at a normal level so that a normal rate of bicarbonate reabsorption suffices to prevent urinary excretion of this anion. It is also possible that bicarbonate reabsorption might increase so as to maintain the alkalosis if GFR were not reduced. To examine this latter possibility, atrial natriuretic factor was used in alkalotic rats to restore a more normal GFR and to increase the amount of bicarbonate filtered by the glomerulus. Proximal bicarbonate reabsorption remained relatively static. Higher than normal amounts of bicarbonate were then delivered out of the proximal tubule, bicarbonate appeared in the urine, and the plasma concentration of bicarbonate fell. A reduction in GFR is thus necessary for the maintenance of chronic metabolic alkalosis. Normalizing GFR induces bicarbonaturia and initiates repair of the alkalosis.     

Physiological role of silent receptors of atrial natriuretic factor

A ring-deleted analog of atrial natriuretic factor--des[Gln18, Ser19, Gly20, Leu21, Gly22] ANF4-23-NH2 (C-ANF4-23)--binds with high affinity to approximately 99% of ANF receptors in the isolated perfused rat kidney. In this preparation, C-ANF4-23 is devoid of detectable renal effects and does not antagonize any of the known renal hemodynamic and natriuretic actions of biologically active ANF1-28. In contrast, both C-ANF4-23 and ANF1-28 increase sodium excretion and decrease blood pressure in intact anesthetized rats. This apparent contradiction is resolved by the finding that the ring-deleted analog markedly increases plasma levels of endogenous immunoreactive ANF in the rat. The results show that the majority of the renal receptors of ANF are biologically silent. This new class of receptors may serve as specific peripheral storage-clearance binding sites, acting as a hormonal buffer system to modulate plasma levels of ANF.     

Inhibition of vasopressin action by atrial natriuretic factor

Atrial natriuretic factor results in diuresis in animals and humans, perhaps because atrial natriuretic factor increases renal blood flow. The possibility that this diuresis is due to direct inhibition of renal tubular epithelial water transport was examined in rabbit collecting tubules perfused in vitro. Atriopeptin III inhibition of the hydraulic conductivity response to the hormone arginine vasopressin but not to either 3'5'-cyclic adenosine monophosphate or forskolin was found. These results suggest that atriopeptin III acts proximal to cyclic adenosine monophosphate formation to directly affect vasopressin-stimulated water transport in the mammalian nephron. They also suggest a potential role for inhibition by atrial natriuretic factor of the renal response to arginine vasopressin as a contributor to a diuretic state.     

Atrial natriuretic factor: a hormone produced by the heart

Systematic studies on the significance of the secretory-like morphological characteristic of cardiac atrial muscle cells of mammals led to the finding that these cells produce a polypeptide hormone. This hormone, described in 1981 as atrial natriuretic factor (ANF), is diuretic (natriuretic), hypotensive, and has an inhibitory effect on renin and aldosterone secretion. Thus, ANF probably intervenes in the short- and long-term control of water and electrolyte balance and of blood pressure. Phylogenetically, ANF appears early, suggesting different functions for this peptide in accordance with each species' environment. Knowledge of the properties of the hormone should provide insights into the pathophysiology of important clinical entities and lead to the development of new pharmaceutical products.     

Coronary vasoconstrictor effects of atriopeptin II

Atrial natriuretic peptides lower arterial pressure, cardiac filling pressure, and cardiac output. In isolated, Langendorff-perfused guinea pig hearts, atriopeptin II, the 23-amino acid atrial natriuretic peptide, is also a potent coronary vasoconstrictor. The median effective dose for atriopeptin II in guinea pig hearts is 26 nanomoles, the threshold constrictor dose is 5 nanomoles, and flow nearly ceases at a dose of 100 nanomoles in perfused hearts at constant pressure. Similar concentrations of atriopeptin II also cause coronary vasoconstriction in rat and dog heart preparations. The disulfide bridge is necessary for vasoconstrictor activity; reduction of this bridge abolishes the activity, as it does the other biological activities of atrial natriuretic peptides.