心肌肥厚大鼠心肌组织中5-羟色胺及血管紧张素-Ⅱ含量的变化

目的：观察大鼠发生心肌肥厚时心肌组织中5-羟色胺（5-HT）及血管紧张素-Ⅱ（Ang-Ⅱ）含量的变化，探讨5-HT、Ang-Ⅱ与心肌肥厚发生的关系。方法：采用腹主动脉缩窄法建立压力超负荷心肌肥厚模型；腹腔注射甲状腺素法建立体液性心肌肥厚模型；荧光分光光度法和放射免疫分析法测定5-HT及Ang-Ⅱ含量。结果：大鼠腹主动脉缩窄后8周，心肌肥厚明显，分别于主动脉缩窄后4-8周内处死动物，发现心肌肥厚程度逐渐加重；心肌组中5-HT及Ang-Ⅱ含量也逐渐增加，并与肥厚程度呈正相关。腹腔注射甲状腺素2周后出现心肌肥厚，4周时症状加剧；于2、3、4周时处死动物，发现肥厚心肌组织中5-HT和Ang-Ⅱ含量均显著增加。结论：提示5-HT与心肌肥厚的形成有关，二者之间的相互关系尚待进一步研究。     

Cardiovascular risk factors in people with different genotypes in the insertion/deletion (I/D) polymorphism at the locus for angiotensin I-converting enzyme (ACE)

The deletion (D) allele of an insertion/deletion (I/D) polymorphism at the locus for angiotensin I-converting enzyme (ACE) has been reported to be an independent risk factor for myocardial infarction (MI), particularly in people lacking traditional risk factors. Furthermore, a borderline association between Lp(a) lipoprotein level and the I/D polymorphism at the ACE locus was reported in one study. We have searched for possible "level gene" or "variability gene" effects of ACE genes on Lp(a) lipoprotein, total cholesterol (TC), high density lipoprotein (HDL) cholesterol (HDLC), low density lipoprotein (LDL) cholesterol (LDLC), triglycerides (TG), apolipoprotein B (apoB), apolipoprotein A-I (apoA-I), and body mass index (BMI). None of these variables differed significantly between genotypes in the I/D polymorphism in any of three population samples. A single population sample created by combining the three series, exhibited an insignificant trend towards individuals carrying the D-allele having a higher level of Lp(a) lipoprotein than those lacking it, and DD homozygotes had a significantly higher Lp(a) lipoprotein level than the combined group of ID/II individuals (p = 0.03). These results may indicate that the D-allele of the I/D polymorphism at the ACE locus could influence the level of Lp(a) lipoprotein.     

Angiotensin II-induced depression of Purkinje cell firing and possible modulatory action on GABA responses

Effects of octapeptide angiotensin II (AII) were tested on cortical neurons of rat's cerebellum by means of microiontophoresis. It was observed that AII consistently depressed spontaneous firing of Purkinje cell, whereas other unidentified neurons were unaffected. When tested against responses of Purkinje cell to depressant putative neurotransmitters, namely, GABA, glycine, taurine, 5-hydroxytryptamine and noradrenaline, it was observed that AII specifically enhanced depressant action of GABA, while the responses to other substances were unaffected. Both AII-induced depression of cell firing and the AII-induced enhancement of GABA depression were antagonized by a specific GABA antagonist, bicuculline methochloride. We therefore suggest that AII exerts an inhibitory action on Purkinje cells through its modulatory action on bicuculline-sensitive GABA receptors.     

Neuronal histamine in the gut wall releasable by gastrin and cholecystokinin

Histamine accumulated in the ligated vagus nerve of the rat, both above and below the ligature; maximum accumulation was after 4 h. The finding is suggestive of axonal flow. Further evidence for histamine in peripheral nerves was obtained in experiments showing that the guinea-pig gut wall could be labelled with [3H]histamine. The experiments were carried out with isolated strips of stomach wall and taenia coli. Electrical stimulation released [3H]histamine from these specimens. The release could be blocked by Ca2+-free medium or by tetrodotoxin. The release was unaffected by vagal denervation or chemical sympathectomy (6-hydroxydopamine) but prevented by reserpinization. Gastrin-17 and cholecystokinin-39 released radioactivity by a tetrodotoxin-sensitive mechanism. The possible existence of a gastrin/cholecystokinin-sensitive neuronal pool of histamine in the gut wall offers a new perspective on the postulated role of histamine as a physiological stimulant of gastric acid secretion and might explain why H2-receptor antagonists block gastrin-stimulated acid secretion.     

Selectivity of angiotensin II antisera

A significant problem in the immunoassay of angiotensin II is the cross-reactivity of most available antisera with the peptide's metabolic products, (des-Asp1)-angiotensin II and (des-Asp1.Arg2)-angiotensin II. In order to attempt to generate antisera of greater selectivity, a variety of conjugates between angiotensin II or derivative peptides and carrier proteins were examined as immunogens with the aim of generating antisera that would selectively identify the amino terminal region of the peptide. Selectivity for the amino terminus was achieved by either (1) immunization with N-acetylated angiotensin II-amide which had been coupled to rabbit serum albumin by its carboxy terminus, or (2) immunization with angiotensin-(1-7)-heptapeptide which was randomly coupled to thyroglobulin. The antisera produced with the N-acetylated immunogen cross-reacted with the unacetylated ligand (Asn1-Val5)-angiotensin, but did not recognize the human hormone (Asp1,Ile5)-angiotensin. Carboxy-terminal coupling of angiotensin without N-acetylation did not induce selectivity for the amino terminus, nor did a conjugate which was linked to the carrier protein via a diazo bond to His6 of the peptide. These findings may be explained by the fact that N-acetylated angiotensin II resists degradation by amino peptidases and thus retains its structure in the immunogen and by the fact that the (1-7)-heptapeptide has lost the immunodominant carboxy-terminal epitope, thus emphasizing the desired amino terminal determinant.     

Glial-vascular reactions to angiotensin II in the rat brain

Reactions of the glia and blood vessels in the sensomotor cortex of adult rats to intraperitoneal injection of angiotensin II were studied electron-microscopically. Repeated injections of the hormone led to edema of increasing severity of the astrocytes, constriction of the lumen of the capillaries, and changes in the structure of their endothelium. It is suggested that these disturbances may be the cause of the cerebrovascular insufficiency and of functional changes in the CNS.Laboratory of Morphology of the Central Nervous System and Laboratory of Experimental Pathology and Therapy of Higher Nervous Activity, Institute of Higher Nervous Activity and Neurophysiology, Academy of Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR V. S. Rusinov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 88, No. 11, pp. 615–617, November, 1979.     

肺癌患者化疗前后血清Hcy、IGF-Ⅱ和TSGF检测的临床意义

目的：探讨肺癌患者化疗前后血清Hcy、IGF-Ⅱ和TSGF水平的变化及临床意义。方法：应用免疫法和放射免疫分析对35例肺癌患者进行了血清Hcy、IGF-Ⅱ和TSGF含量检测,并与30名正常健康人作比较。结果：肺癌患者在化疗前血清Hcy、IGF-Ⅱ和TSGF水平均非常显著地高于正常人组（P〈0.01）,化疗后6个月在未复发的27例中明显下降接近于正常人组,而复发的8例,其数值又回升至化疗前水平（P〈0.05）。结论：检测肺癌患者血清Hcy、IGF-Ⅱ和TSGF水平的变化可作为诊断和疗效观察的参考。     

Frequent expression of the multi-drug resistance-associated protein BCRP/MXR/ABCP/ABCG2 in human tumours detected by the BXP-21 monoclonal antibody in paraffin-embedded material

The expression and cellular localization of angiotensin II (Ang II) and AT(1) receptor proteins were examined in the normal human prostate and benign prostatic hyperplasia (BPH) by immunohistochemistry. In the normal prostate, Ang II immunoreactivity was localized to the basal layer of the epithelium and AT(1) receptor immunostaining was found predominantly on stromal smooth muscle and also on vascular smooth muscle of prostatic blood vessels. Ang II immunoreactivity was markedly increased in hyperplastic acini in BPH compared with acini in the normal prostate (normal: 7.4+/-0.2%, n=5 vs. BPH: 22.7+/-1.9%, n=5, p<0.001). However, AT(1) receptor immunoreactivity was significantly decreased in BPH compared with the normal prostate [normal: 16.4+/-2.2%, n=4 vs. BPH: 9.4+/-1.3%, n=5, p<0.05 (p=0.025)]. The present study demonstrates the presence of Ang II peptide in the basal layer of the epithelium and AT(1) receptors on stromal smooth muscle, suggesting that Ang II may mediate paracrine functions on cellular growth and smooth muscle tone in the human prostate. Furthermore, AT(1) receptor down-regulation in BPH may be due to receptor hyperstimulation by increased local levels of Ang II in BPH. These data extend previous findings in support of the novel concept that overactivity of the renin-angiotensin system (RAS) may be involved in the pathophysiology of BPH.     

ADA、ACE、LDH、CEA的联合检测在结核性和恶性胸腔积液中的鉴别诊断价值

目的测定血清和胸水中腺苷脱氨酶（ADA）、血管紧张素转化酶（ACE）、乳酸脱氢酶（LDH）与癌胚抗原（CEA）的水平,探讨其指标联合检测对结核性和恶性胸水的鉴别诊断意义。方法对临床已确诊的72例胸腔积液患者（结核性40例,恶性32例）的胸水和血清分别采用酶免疫法和化学发光法进行ADA、ACE、LDH和CEA含量测定。结果结核性胸水中ADA的含量为（60.2±20.10）U/L,ACE的含量为（35±9.6）U/L,LDH的含量为（338±41）U/L,CEA的含量为（12.8±5.82）μg/L;在恶性胸水中,ADA为（11.02±5.23）U/L,ACE为（16±11.0）U/L,LDH为（379±69.0）U/L,CEA为（39.9±19.7）μg/L。结核性胸水ADA和ACE含量较恶性胸水组明显增高（P〈0.01）,CEA在恶性胸水中含量较结核性胸水组明显增高（P〈0.01）。胸水中ADA和ACE的检测对结性性胸膜积液诊断的敏感性分别为84.3%、87.5%,特异性分别为87.5%、80.0%;而胸水中LDH和CEA的检测对恶性胸膜积液诊断的敏感分别为84.3%、75.0%,特异性分别为80.0%、93.0%。四项指标联合检测敏感性性为78.1%,特异性为97.5%,较单一指标的特异性高。结论胸水中ADA、ACE、LDH和CEA的联合检测对结核性和恶性胸水的鉴别诊断具有一定价值,有助于临床胸水性质的诊断。