血管紧张素转化酶抑制剂能提高冠心病患者血浆中人组织激肽释放酶的含量

目的探讨血管紧张素转化酶抑制剂(ACEI)对冠心病患者血浆中人组织激肽释放酶(TK)的含量的影响。方法采用生物素-亲和素双抗体夹心ELISA法检测730例冠心病患者血浆中TK的含量,其中有302例患者有ACEI服用史,428例患者无该类药物服用史。绘制TK含量的分布图并用独立样本T检验和logistic回归进行统计分析。结果冠心病患者血浆中TK含量服从正偏态分布(Skewness=0.617,SE=0.090,Kurtosis=0.774,SE=0.181)。ACEI能明显提高冠心病患者血浆TK水平(0.388±0.076mg/lvs.0.320±0.079mg/l,P0.001;OR=3.20,95%CI2.59～3.95,P0.001)。结论ACEI能通过提高冠心病患者血浆中TK的含量来发挥其部分心血管保护作用。     

HIV-1感染者血浆可溶性PD-1的含量及其临床意义北大核心

目的初步探索艾滋病病毒1型(HIV-1)感染者血浆中可溶性程序性细胞死亡受体1(sPD-1)表达水平及临床意义。方法建立检测血浆sPD-1含量的双抗体夹心酶联免疫吸附试验(ELISA);收集26份尚未接受抗病毒治疗的HIV-1感染者和37份健康人外周血;利用双抗体ELISA检测血浆sPD-1表达水平,并分析其与临床参数的相关性。结果 HIV-1感染人群血浆sPD-1含量为(1147.81±375.7)pg/mL,显著高于健康人群(361.75±187.7)pg/mL(P<0.0001);HIV-1感染人群血浆sPD-1含量与外周血CD4+T淋巴细胞数量呈负相关(P=0.0229,r=-0.4444),与血浆病毒载量呈正相关关系(P=0.0089,r=0.5027)。结论 sPD-1在HIV-1的致病过程中可能起重要调控作用。     

HIV-1感染者血浆可溶性PD-1的含量及其临床意义

目的初步探索艾滋病病毒1型(HIV-1)感染者血浆中可溶性程序性细胞死亡受体1(sPD-1)表达水平及临床意义。方法建立检测血浆sPD-1含量的双抗体夹心酶联免疫吸附试验(ELISA);收集26份尚未接受抗病毒治疗的HIV-1感染者和37份健康人外周血;利用双抗体ELISA检测血浆sPD-1表达水平,并分析其与临床参数的相关性。结果 HIV-1感染人群血浆sPD-1含量为(1147.81±375.7)pg/mL,显著高于健康人群(361.75±187.7)pg/mL(P0.0001);HIV-1感染人群血浆sPD-1含量与外周血CD4+T淋巴细胞数量呈负相关(P=0.0229,r=-0.4444),与血浆病毒载量呈正相关关系(P=0.0089,r=0.5027)。结论 sPD-1在HIV-1的致病过程中可能起重要调控作用。     

人血清载脂蛋白AⅤ的检测及与血脂的相关性

目的开发并利用了一种新的免疫学方法以检测人血清载脂蛋白AⅤ含量,进而观察健康中国人群中血清载脂蛋白AⅤ与血脂的相关性。方法血脂用酶法及匀相测定法测定;应用针对不同抗原位点的抗重组载脂蛋白AⅤ单克隆抗体配对,形成双夹心酶联免疫吸附方法以检测人血清载脂蛋白AⅤ。结果92例健康中国人群血清载脂蛋白AⅤ浓度为182.7±104.7μg/L(5.4～455.6μg/L)。所有研究对象中血清载脂蛋白AⅤ浓度与甘油三酯呈负相关(r=-0.225,P=0.031),在女性中更为显著(r=-0.496,P=0.001)。所有研究对象载脂蛋白AⅤ浓度与高密度脂蛋白胆固醇呈正相关(r=0.453,P<0.001),在女性中更为显著(r=0.617,P<0.001)。载脂蛋白AⅤ浓度与低密度脂蛋白胆固醇和总胆固醇均不相关。载脂蛋白AⅤ浓度与体质指数呈负相关(r=-0.345,P=0.001),在女性中更显著(r=-0.456,P=0.002)。结论人血清中载脂蛋白AⅤ含量极低,并与甘油三酯呈负相关,与高密度脂蛋白胆固醇呈正相关,与体质指数呈负相关。     

KLK6、KLK10在结直肠癌的表达及与临床病理的关系

目的探讨人组织激肽释放酶家族成员KLK6及KLK10蛋白在结直肠癌发生发展中的作用及与临床、病理的关系。方法采用SP免疫组织化学染色法检测57例结直肠腺癌、21例结直肠腺瘤及11例正常结直肠黏膜组织KLK6及KLK10的表达情况,并分析二者的表达与结直肠癌临床病理指标的关系。结果 KLK6及KLK10在结直肠腺癌的阳性率分别为52.6%(30/57)和66.7%(38/57),在结直肠腺瘤的阳性率分别为33.3%(7/21)和38.1%(8/21),在正常结直肠黏膜组织中的阳性率为9.1%(1/11)和27.3%(3/11)。KLK6及KLK10在结直肠腺癌、结直肠腺瘤及正常结直肠黏膜组织中的表达均具有显著差异(P均<0.05)。KLK6及KLK10的表达均与患者的TNM分期、淋巴结转移及肝转移情况相关(P均<0.05)。KLK6还与肿瘤的分化程度相关(P=0.015)。KLK6及KLK10在结直肠癌的表达呈正相关(r=0.745,P=0.000)。KLK10在KLK6阳性组中的表达明显高于在KLK6阴性组中的表达。结论 KLK6及KLK10参与结直肠癌的发生发展并与结直肠癌的转移相关,可作为较为理想的肿瘤标志物辅助判断患者预后并指导临床治疗。     

社区队列人群血浆氨基末端脑钠肽前体水平与左心室构型关系探讨

目的:探讨社区队列人群血浆氨基酸末端脑钠肽前体(NT-proBNP)水平与左心室构型的关系。方法:横断面调查北京首钢社区733例具有心血管疾病高危因素的队列人群,运用电化学发光免疫技术测定血浆NT-ProBNP水平。收集人群年龄、性别、身高及体质量等一般资料,以及心血管疾病病史情况如心肌梗死、心绞痛、高血压病及心房颤动并收集有无糖尿病、脑卒中/短暂性脑缺血发作(TIA)等病史;行超声心动图检查测量有关参数,并根据舒张末期室间隔厚度(IVSTd),左心室后壁厚度(LVP-WT)及左心室内径(LVDd)等参数对受试者左心室构型进行分型分组。分析血浆NT-ProBNP水平与左心室构型的关系。结果:在校正有差异因素后,有左心室肥厚组血浆NT-ProBNP水平高于无左心室肥厚组,中位数分别为96.79 ng/L和62.74 ng/L(P=0.0001),左心室构型的分型与血浆NT-ProBNP水平相关(r=0.159,P=0.0001),以向心性肥厚型血浆NT-ProBNP水平最高,为105.4 ng/L。多因素回归分析显示,左心室构型分型为血浆NT-ProBNP水平的独立影响因素。结论:血浆NT-ProBNP水平与左心室构型有关,左心室构型是血浆NT-ProBNP水平的独立影响因素之一。     

重症哮喘患者血脂组分与体重指数、肺功能及气道炎症的相关性研究

目的 探讨重症哮喘患者血脂组分与体重指数、肺功能和气道炎症的关系。方法 选择113例重症哮喘患者为研究对象,入院后抽取肘静脉血约5 mL,采用气相色谱-质谱法检测血浆中23种脂肪酸的表达水平。同时,检测患者肺功能及呼出气一氧化氮(FeNO)水平,统计分析重症哮喘患者血脂组分与肺功能的相关性。结果 (1)气相色谱-质谱鉴定结果显示,饱和脂肪酸约占血浆总脂肪酸的50.5%,主要是十六烷酸(72.1%)和硬脂酸(22.3%);其次是单不饱和脂肪酸(17.3%)。血浆ω-3脂肪酸和ω-6脂肪酸水平之间存在不平衡,ω-6脂肪酸占血浆总脂肪酸的30.4%,而ω-3仅占1.9%。(2)相关性分析结果显示,血浆总脂肪酸(r=-0.284,P=0.032)、总单不饱和脂肪酸(r=-0.263,P=0.035)、总多不饱和脂肪酸(r=-0.252,P=0.043)、总ω-6脂肪酸(r=-0.258,P=0.042)均与PEF_25%-75%呈负相关关系。血浆总脂肪酸(r=-0.296,P=0.034)、总单不饱和脂肪酸(r=-0.257,P=0.043)与FEV₁...     

限食后追赶生长性肥胖与大鼠血浆葡萄糖依赖性胰岛素释放肽水平的关系

目的 探讨限食后追赶生长性肥胖与大鼠血浆葡萄糖依赖性胰岛素释放肽(GIP)水平的相关性.方法 6周龄健康雄性SD大鼠60只按随机数字表法随机分为普通饮食组(n=15,给予普通饮食)、普通饮食追赶生长组(n=15,给予同体重普通饮食组大鼠60%普通饲料限食喂养4周后饲以普通饲料)、高脂饮食组(n=15,给予高脂饮食)和高脂饮食追赶生长组(n=15,给予同体重普通饮食组大鼠60%普通饲料限食喂养4周后饲以高脂饲料),观察大鼠体重及进食量变化.分别于4、6、8周处死部分动物,检测体脂含量及血浆GIP浓度.采用配对t检验和单因素方差分析以及一元线性相关分析进行数据统计.结果 与普通饮食组相比,高脂饮食组、普通饮食追赶生长组和高脂饮食追赶生长组体脂含量[分别为(3.6±0.6)、(7.9±1.5)、(4.6±1.1)、(7.0±1.0)g;t值分别为-2.601、-2.305、-2.501,均P＜0.05]、血浆GIP水平升高[分别为(41±9)、(61±7)、(51±8)、(59±8)pmol/L;t值分别为-6.061、-3.452、-4.651,均P＜0.05].相关分析显示,体脂含量与血浆GIP水平显著相关(r2=0.9407).结论 限食后追赶生长性肥胖与大鼠血浆GIP水平高度相关,可能与追赶生长所引发的病理生理学变化有关.     

组织型激肽释放酶对脑缺血再灌注大鼠缺血脑组织缓激肽及其受体表达的影响

目的 探讨组织型激肽释放酶(tissue kallikrein,TK)对脑缺血再灌注大鼠缺血脑组织缓激肽、缓激肽B1受体(bradykinin B1 rgceptor,B1R)和缓激肽B2受体(bradykinin B2 receptor,B2R)表达的影响.方法 54只SD大鼠随机分为3组,每组18只.3组分别为假手术组;生理盐水(normal saline,NS)处理组(Ns组):NS 2 ml/(kg·d),连用3 d;TK(处理组(TK组):TK 17.5×10-3U/(kg·d),连用3 d.3 d后分别进行神经功能缺损评分、脑梗死体积测定.酶联免疫吸附法检测缺血区缓激肽含量;采用逆转录聚合酶链反应和Western印迹法分别检测缺血脑组织B1R、B2R mRNA和蛋白表达.结果 与NS组比较,TK组神经功能缺损显著减轻[(6.17±1.17)分对(8.17 4±1.33)分,t=2.000,P=0.004],脑梗死体积明显缩小[(29.67±3.78)%对(37.50±6.72)%,t=0.078,P=0.005];缺血脑组织缓激肽含量升高[(9.25 4±1.13)对(15.53±1.68),t=6.283,P:0.000];B2RmRNA表达显著上调[(1.21±0.17)对(2.15±0.20),t=0.943,P=0.000),而B1R mRNA表达上调不明显[(0.51±0.05)对(0.57±0.06),t=0.058,P=0.141)];B2R蛋白表达显著上调[(1.15±0.16)对(1.88 4±0.21),t=0.737,P=0.0001,B1R蛋白表达上调不明显[(0.50±0.04)对(0.53±0.05),t=1.326,P=0.214].结论 TK 对脑缺血再灌注大鼠具有保护作用,能使缺血脑组织缓激肽含量增高,B2R表达上调,而对B1R表达影响不大.由此推测,B2R在TK保护缺血脑组织中发挥着主要作用.     

大鼠心肌梗死后血浆PⅢNP和PⅠCP的变化及其与心肌胶原含量的相关性研究

目的 :了解血浆中 P NP和 P CP含量能否反映心肌梗死 (心梗 )后梗死区 (IZ)和非梗死区 (NIZ)胶原沉积。方法 :通过结扎左冠主干建立大鼠心梗模型 ,分别在术后第 1、3、7、14、42天 ,采血后处死动物 ,获取左心室 IZ和 NIZ组织。应用放免法测定血浆 P NP和 P CP,用羟脯氨酸法测定心肌胶原含量。结果 :血浆 P N P和 P CP含量于术后第 3天开始明显升高 ,至第 14天达高峰 ,第 42天时下降 ,但 P N P含量仍高于非梗死组。IZ和 NIZ胶原含量也是术后第 3天开始升高 ,以后逐渐增高 ,以 IZ增高为明显。血浆 P NP和 P CP与心肌组织胶原的相关分析发现 ,在非梗死组 ,血浆 P NP和 P CP与左室胶原含量无明显相关性。而心梗组 ,血浆P NP与 IZ胶原含量明显相关 (r =0 .6 8,P <0 .0 1) ,与 NIZ胶原含量无明显相关 (r =0 .16 ,P >0 .0 5 )。血浆P CP与 IZ胶原含量亦明显相关 (r =0 .5 2 ,P <0 .0 1) ,且与 NIZ胶原含量亦弱相关 (r =0 .43;P <0 .0 5 )。结论 :心梗后血浆 P NP和 P CP含量变化主要反映 IZ胶原合成 ,而与 NIZ胶原之间的相关性较差     

Immunolocalization and expression of kallistatin and tissue kallikrein in human inflammatory bowel disease

The distribution of tissue kallikrein (TK) and its plasma inhibitor, kallistatin in plasma and intestinal tissue, was studied in patients with active ulcerative colitis (UC) and Crohn's disease (CD). TK was localized to goblet cells and kallistatin to epithelial cells of normal human intestine. Both proteins are visualized in macrophages inside granulomas in CD as well as in plasmocytes in both CD and UC. Intestinal tissue kallikrein (ITK) and kallistatin are significantly decreased in inflamed intestine compared to noninflammatory controls. TK mRNA is significantly decreased in intestinal biopsy samples from active UC patients compared with inactive patients or controls. Immunoreactive TK is present in plasma in very low concentrations in patients and did not differ in normal subjects. Plasma kallistatin was significantly decreased in patients with active disease compared to normal controls. Our data suggest that release of TK during inflammation plays a role in inflammatory bowel disease.     

Plasma beta-endorphin levels in primary aldosteronism

Excessive production of an as yet unidentified aldosterone-stimulating factor may cause idiopathic hyperaldosteronism (IHA). This putative factor may be related to proopiomelanocortin-derived peptides, some of which have aldosterone-stimulating properties. The present study evaluated plasma beta-endorphin, ACTH, cortisol, and aldosterone levels in patients with IHA (n = 10), aldosterone-producing adenomas (n = 4), essential hypertension (n = 11), and normal subjects (n = 10). Plasma and urinary hormone measurements were obtained at timed intervals during an isocaloric, fixed electrolyte intake (Na+, 128 meq/day; K+, 80 meq/day) in a metabolic unit. Plasma for beta-endorphin assay was preincubated with sepharose-bound anti-beta-lipotropin to remove beta-lipotropin that cross-reacted with the beta-endorphin RIA. Mean +/- SE plasma beta-endorphin levels at 0800 h were elevated in IHA patients (47 +/- 13 fmol/ml) compared to those in aldosterone-producing adenoma (25 +/- 9), essential hypertension (16 +/- 1), and normal control (20 +/- 2; P less than 0.05) subjects. Plasma ACTH, plasma cortisol, and urinary cortisol levels were not different in these four groups. These data support the hypothesis that excess production of either beta-endorphin or related proopiomelanocortin-derived peptides may function as aldosterone secretogogue(s) in IHA.     

A very sensitive direct radioimmunoassay system for plasma angiotensin II and its clinical application in various hypertensive diseases

A very sensitive and simplified direct radioimmunoassay system for plasma angiotensin II was developed using the antiserum against synthetic angiotensin II (final dilution = 1: 1,500,000) in combination with 125I-labeled angiotensin II (specific activity = 1,600 microCi/micrograms). In this assay system, it was possible to carry out a direct assay using 100 microliter of plasma without any extraction procedure. This conclusion was supported by 100% recovery, parallelism of plasma samples against the standard curve, and no difference in hormone levels, there was also a high positive correlation between the plasma angiotensin II levels measured by this direct assay and the dowex column extraction method. The sensitivity of this assay system was 0.1 pg/tube, which is the highest sensitivity in studies reported to date. The cross-reactivities of angiotensin III and I against this antiserum were 100% and less than 0.1%, respectively, suggesting that the antiserum was very specific for the C-terminal of angiotensin II. Plasma angiotensin II levels in normal subjects after overnight fasting ranged from 3.0 to 21.3 pg/ml (12.0 +/- 2.1 pg/ml, mean +/- SE). By comparison, plasma angiotensin II levels of patients with essential hypertension were similar to those in the normal renin group, lower than those in low renin group and higher than those in high renin group. In patients with secondary hypertension, levels were lower in those with primary aldosteronism and higher in those with renovascular hypertension when compared to normal subjects.     

Elevated levels of plasma prorenin (inactive renin) in diabetic and nondiabetic patients with autonomic dysfunction

We measured plasma inactive renin (prorenin) levels in 46 diabetic patients, 4 nondiabetic patients with idiopathic autonomic dysfunction, and 115 normal subjects. Plasma inactive renin levels were normal in the diabetic patients who had no complications (n = 6) and in those with microvascular disease (n = 8) who did not have coexistent autonomic dysfunction. Plasma inactive renin was either grossly elevated or in the upper limit of the normal range in diabetic patients with autonomic dysfunction (n = 18). No correlation was found between plasma inactive renin and glycemic control, as measured by hemoglobin A1c. High plasma inactive renin levels were also found in the 4 nondiabetic patients with idiopathic autonomic dysfunction. These data suggest that increased plasma inactive renin levels in diabetic patients are a consequence of coexistent autonomic dysfunction. This finding is consistent with other evidence that suggests autonomic regulation of the processing of prorenin to renin within the kidney.     

Rat peripheral mononuclear cell thymidine kinase activity increases during liver regenerative processes after partial hepatectomy

Deoxythymidine kinase (TK; EC 2.7.1.21) activity in the liver has been used as a marker of liver regeneration after partial hepatectomy. In this study we examined TK activity of various organs, plasma and peripheral blood mononuclear cells (PMNC) in 70% partially hepatectomized rats. TK activity of lymph nodes, small intestine, heart, lung, kidney and thymus did not increase significantly during the course of the study, except for spleen at 72 h. On the other hand, PMNC-TK and liver cystolic TK activity increased in a parallel fashion at all times after partial hepatectomy; they began to increase 12 h after surgery and peaked 48 h post-surgery. Fractionation of PMNC into T cells and B cells revealed that both populations increased and peaked 48 h post-surgery. Plasma TK peaked 12–24 h after surgery, then declined at 36, 48 and 72 h after partial hepatectomy. This change paralleled plasma levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT). PMNC-TK activity correlated significantly with liver cystolic TK activity 24 h (r = 0.743; P < 0.05) and 48 h (r = 0.708; P < 0.05) after partial hepatectomy. However, it did not correlate with plasma levels of TK, AST and ALT. The results indicate that in the early stage of liver regeneration PMNC-TK may provide a marker of liver regenerative processes.     

Total and individual free fatty acid concentrations in liver cirrhosis

The finding of high plasma free fatty acid (FFA) levels in cirrhotic patients has been attributed either to decreased hepatic clearance or to enhanced fat mobilization. To better clarify these hypotheses, total and individual FFA and glycerol levels were determined in 21 cirrhotic patients with different degrees of hepatocellular damage (evaluated by liver function tests), portal hypertension (evaluated by endoscopy and clinical signs), and nutritional status (evaluated by anthropometric and biohumoral parameters) and in 10 age- and sex-matched healthy subjects. Glucose tolerance and insulin and glucagon levels were determined in all individuals. Well-nourished and malnourished patients were identified within the cirrhotic group. Plasma FFA and glycerol concentrations were well correlated (r = 0.47, P less than 0.05), levels being significantly higher in cirrhotic individuals than in controls (746.6 +/- 46.29 SE v 359.22 +/- 40.82 mumol/L, P less than 0.001 for plasma FFA; 150.1 +/- 3.12 v 82.5 +/- 9.2 mumol/L, P less than 0.01 for glycerol). Plasma FFA and glycerol showed no correlation with the liver function test results or portal hypertension parameters. Interestingly, plasma levels of FFA and glycerol were influenced by the nutritional status, significantly higher FFA levels being observed in the well-nourished than in the malnourished patients (842.5 +/- 47.5 v 563.4 +/- 78 mumol/L, P less than 0.005). Furthermore, a positive correlation was found between plasma glycerol level and percentage of triceps skinfold (r = 0.45, P less than 0.05). No correlation was found between plasma levels of FFA or glycerol and glucose tolerance, insulin and glucagon.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pentagastrin promotes prolactin release in patients with medullary carcinoma of the thyroid

Both calcitonin and gastrin have been found in the mammalian central nervous system, including the pituitary. Following a pentagastrin infusion in several patients with medullary carcinoma of the thyroid, we noted a coincident increase in plasma calcitonin and prolactin (PRL) levels. In order to evaluate further the influence of pentagastrin on human PRL release, a pentagastrin infusion was administered to 13 patients with active medullary carcinoma of the thyroid (MTC), eight subjects with inactive MTC, eight family members without MTC, and ten normal subjects. Plasma mean +/- SE PRL levels were significantly (P less than 0.01) increased in the active MTC patients from 7.6 +/- 0.5 to 12 +/- 1.4 ng/mL by 15 minutes post pentagastrin. Plasma mean +/- SE calcitonin levels increased in parallel with the plasma PRL levels from 0.28 +/- 0.1 to a peak of 1.9 +/- 0.9 ng/mL at 5 minutes post pentagastrin. A significant (P less than 0.05) correlation was found between the percentage increase in plasma calcitonin concentrations and plasma PRL levels at five and ten minutes post pentagastrin stimulation in this group of active MTC patients. Significant increases in serum calcitonin levels in the other groups post pentagastrin were of lesser magnitude and were not associated with a significant increase in PRL release. This latter observation suggested that neither the stress of the infusion nor the multiple endocrine neoplasia type 2 nor the pentagastrin was responsible for the observed increase in plasma PRL levels in the active MTC patients. These findings suggest, but do not prove, that calcitonin is a PRL-releasing factor in humans.     

Circulating thyroglobulin measurements by homologous radioimmunoassay in dogs with thyroid carcinoma

Circulating thyroglobulin was measured in 20 dogs with thyroid cancer, using a homologous polyclonal radioimmunoassay. Plasma Tg levels exceeded the normal range in 14 (70%) dogs, and ranged from 6 to 2902 micrograms/l (median 608). Plasma Tg levels tended to decrease from follicular carcinomas to solid-follicular carcinomas, to solid carcinomas (p less than 0.05). Plasma Tg levels were also higher in scintigraphically hot tumours than in cold ones. Other relationships between circulating Tg and clinical, pathological, and functional parameters were not found, except a poor (R = 0.49) but significant (p = 0.04) correlation between Tg and T4 levels. Plasma Tg was measured before surgery and at least once during follow-up, in 9 dogs. After hemithyroidectomy, a decrease was observed in 8 dogs. In 7 of these 8 dogs, plasma Tg levels declined within the reference range at the first postoperative sample. In the ninth dog, where metastases were detected 14 months after surgical treatment, plasma Tg slightly increased, yet within normal range. It is concluded that measurement of plasma Tg levels might be useful for monitoring the postoperative course of the disease in individual dogs with thyroid cancer.     

Changes of plasma levels of TRH and its target hormones by two hour constant intravenous infusion of TRH tartrate in man (author's transl)]

Constant iv infusion of TRH tartrate for 2 hours was administered to normal men in a dosage of 0.5 (n=4), 1.0 (n=2) and 2 (n=4) mg/120 minutes. Measurements at every 15 minutes were performed for plasma levels of TRH, TSH, Thyroxine (T4) and Triiodothyronine (T3) by radioimmunoassay. Plasma levels of TRH increased promptly and stayed at the same levels until the end of the infusion. The Mean Clearance Rate (MRC), Half-life and Volume of Distribution of TRH were respectively, 4.62 +/- 0.53 L/min. (M +/- SE), 17.8 +/- 3.8 minutes and 112 +/- 15 L in the 0.5 mg administered group and 6.38 +/- 2.50 L/min., 9.0 +/- 1.4 minutes and 82 +/- 30 L in the 2 mg administered group. Plasma levels of TRH increased in two phases, and increments of plasma TSH were dose dependable to the dosage of TRH. Plasma levels of T4 increased gradually in the course of TRH infusion and stayed at high levels even in the withdrawal phase of TRH. Plasma levels of T3 increased markedly during and after the TRH infusion in the 0.5 mg administered group, while increments of plasma T3 were minute in the 2 mg administered group. From the above data, it is suggested that the amount of TRH production in man, which is much more than has previously been reported, may indicate the existence of an extrahypothalamic synthesis of TRH in man.