维持性血液透析患者血浆游离氨基酸检测的临床意义

目的　对维持血液透析患者的血浆游离氨基酸进行测定和分析。方法　用氨基酸自动分析仪测定 15例血透患者在一次透析前后的血浆氨基酸谱。结果　血透患者在透析前的必需氨基酸除苯丙氨酸外均较正常对照组降低 ,其中以缬氨酸、亮氨酸和组氨酸下降为显著 ;非必需氨基酸中精氨酸、甘氨酸和鸟氨酸明显升高 ;酪氨酸/苯丙氨酸和丝氨酸 /甘氨酸的比值较对照组明显降低。患者在一次透析后的必需和非必需氨基酸均低于透析前水平。结论　血透患者氨基酸异常的原因可能与蛋白质摄入不足、尿毒症毒性物质和酸中毒等有关     

Changes in high-energy phosphate compounds of isolated rat hearts during Ca-free perfusion and reperfusion with Ca

Isolated rat hearts were perfused with a glucose-containing modified Tyrode solution at 37°C, according to Langendorff. After a 15 min stabilization period, the hearts were perfused for 4 min with a Ca²⁺-free medium and subsequently reperfused with Ca²⁺-containing medium. Reperfusion with Ca²⁺ caused irreversible loss of electrical and mechanical activity of the hearts (calcium paradox). After 30 s of reperfusion with Ca²⁺, myocardial creatine phosphate (CP) and ATP levels were decreased by 65% and 45% respectively. In the same period there was an increase in creatine (15%), ADP (85%) and AMP (2800%). Continued reperfusion with Ca²⁺ resulted in a gradual decrease in the tissue concentration of all compounds. The effluent fluid contained large amounts of creatine and AMP, and relatively minor amounts of CP, ATP and ADP. The results show that reperfusion with Ca²⁺-containing medium, after a short Ca²⁺-free period, produces a sudden and severe decline of myocardial high-energy stores, prior to the release of these compounds.     

Changes in high-energy phosphate compounds of isolated rat hearts during Ca2+-free perfusion and reperfusion with Ca2+.

Isolated rat hearts were perfused with a glucose-containing modified Tyrode solution at 37°C, according to Langendorff. After a 15 min stabilization period, the hearts were perfused for 4 min with a Ca²⁺-free medium and subsequently reperfused with Ca²⁺-containing medium. Reperfusion with Ca²⁺ caused irreversible loss of electrical and mechanical activity of the hearts (calcium paradox). After 30 s of reperfusion with Ca²⁺, myocardial creatine phosphate (CP) and ATP levels were decreased by 65% and 45% respectively. In the same period there was an increase in creatine (15%), ADP (85%) and AMP (2800%). Continued reperfusion with Ca²⁺ resulted in a gradual decrease in the tissue concentration of all compounds. The effluent fluid contained large amounts of creatine and AMP, and relatively minor amounts of CP, ATP and ADP. The results show that reperfusion with Ca²⁺-containing medium, after a short Ca²⁺-free period, produces a sudden and severe decline of myocardial high-energy stores, prior to the release of these compounds.     

兴奋性氨基酸测定对急性脑梗死恶化进展预测的意义

目的　研究急性脑梗死后谷氨酸 (Glu)、甘氨酸 (Gly)的变化规律及与梗死恶化进展的关系 ,寻找急性脑梗死恶化进展的预测指标。方法　采用高效液相色谱技术测定 1 1 2例发病 2 4 h内的急性脑梗死患者及 32例正常对照组血和脑脊液 (CSF)中 Glu、Gly浓度的变化。结果　脑梗死患者血和 CSF中 Glu、Gly浓度在发病 2 4 h内明显升高 ,与对照组比较有显著差异 (P<0 .0 0 1 )。其中急性脑梗死进展组血和 CSF中 Glu浓度(1 53.0 5± 35.80 ,78.80± 2 6.95)较稳定组血和 CSF中 Glu浓度 (1 0 7.44± 2 3.82 ,2 7.75± 9.89)有明显差异 (P<0 .0 0 1 )。血中 Glu浓度超过1 30 μmol/ L和 CSF浓度超过 50 μmol/ L与早期神经功能缺损症状进展有独立的显著联系 (2 5.7,41 .5) ,特别是 CSF中 Glu浓度超过 50 μmol/ L,其预测的灵敏性、特异性、准确性分别为 95.3%、99.7%、97.5%。结论　急性脑梗死早期神经功能缺损的进展与血和 CSF中 Glu浓度增高有关 ,血中 Glu浓度超过 1 30 μmol/ L和 CSF浓度超过 50 μmol/ L是发病 48h内病情恶化进展的重要预测指标。特别是 CSF中 Glu浓度超过 50 μmol/ L其预测价值更大。     

Myocardial injury with biomarker elevation in diabetic ketoacidosis

We report of two patients with severe ketoacidosis, minute elevations of myocardial biomarkers (troponin T and CK-MB) and initial ECG changes compatible with myocardial infarction (MI). All successive investigations, including coronary arteriography, were normal, and the patients recovered fully without further evidence of ischemic heart disease. We suggest that acidosis and very high levels of free fatty acids could cause membrane instability and biomarker leakage. Regardless of the pathogenesis, these two case stories suggest that nonspecific myocardial injury may occur in severe diabetic ketoacidosis and that the presence of minute biomarker elevation and ECG changes does not necessarily signify MI.     

辛伐他汀改善心肌梗死后心肌胶原含量变化及机制的实验研究

目的:探讨辛伐他汀对大鼠心肌梗死后心肌胶原含量的影响及其机制. 方法:建立大鼠心肌梗死模型,24 h后存活大鼠随机分成心肌梗死组(n=9)、辛伐他汀20 mg组[20 ms/(kg·d),n=10]和平伐他汀40 mg组[40 ms/(kg·d),n=9],另设假手术组(n=10).4周后观察血脂水平、左心室重指数和天狼猩红染色分析左心室非梗死区心肌胶原容积分数(表达心肌胶原含量),免疫组化检测基质金属蛋白酶-2(MMP-2),免疫印迹杂交方法(Western blot)和逆转录多聚酶链反应(RT-PCR)检测转化生长因子β1(TGF-β1)在非梗死区的表达. 结果:①各组血脂水平差异无统计学意义,心肌梗死组左心室重苗指数、非梗死区Ⅰ型、Ⅲ型胶原容积分数及Ⅰ型与Ⅲ型胶原容积分数比值较假手术组均明显升高(P均<0.05),差异均有统计学意义;辛伐他汀两组左心室重量指数、非梗死区Ⅰ型、Ⅲ型胶原容积分数及Ⅰ型与Ⅲ型胶原容积分数比值较心肌梗死组均卜降,但仍高于假手术组(P均<0.05),差异均有统计学意义.②心肌梗死组MMP-2和TGF-β1表达较假手术组均显著增加(P均<0.05),而辛伐他汀两组表达则明显降低,但仍高于假手术组(P均<0.05),差异均有统计学意义. 结论:辛伐他汀能有效改善大鼠心肌梗死后心肌胶原含量,机制与其渊脂作用无关,可能与下调MMP-2和TGF-β1的表达有关.     

Effect of free fatty acids and amino acids on glucagon and insulin secretions in normal and diabetic ducks

Summary The relationship between two metabolites, free fatty acids (FFA) and amino acids (AA), and the two main pancreatic hormones, insulin and glucagon, was studied by infusing small amounts of these metabolites into normal and diabetic Peking ducks, i. e. two days after subtotal pancreatectomy. Infusion of oleic acid (0.365 g/kg/30 min as an emulsion in plasma) indicated a suppressive effect of free fatty acids on glucagon secretion, but was without effect on insulin secretion, in normal as well as in diabetic ducks, indicating that insulin might not be directly involved in the FFA-glucagon feedback in the duck. Infusions of arginine for one hour (1 g/kg/h) into normal ducks, hyperglycaemic normal birds (as a result of glucose infusion: 1 g/kg/h) and diabetic ducks, suggested the persistence of an amino acid effect on glucagon secretion, and a slight reduction of the effect on insulin secretion in diabetes. This suggests that insulin may not be involved in amino acidinduced glucagon secretion in the duck.     

Myocardial infarction in diabetic and non-diabetic persons with and without prior myocardial infarction: the FINAMI Study

Aims/hypothesis We compared the risk of acute coronary events in diabetic and non-diabetic persons with and without prior myocardial infarction (MI), stratified by age and sex. Methods A Finnish MI-register study known as FINAMI recorded incident MIs and coronary deaths (n=6988) among people aged 45 to 74 years in four areas of Finland between 1993 and 2002. The population-based FINRISK surveys were used to estimate the numbers of persons with prior diabetes and prior MI in the population. Results Persons with diabetes but no prior MI and persons with prior MI but no diabetes had a markedly greater risk of a coronary event than persons without diabetes and without prior MI. The rate of recurrent MI among non-diabetic men with prior MI was higher than the incidence of first MI among diabetic men aged 45 to 54 years. The rate ratio was 2.14 (95% CI 1.40–3.27) among men aged 50. Among elderly men, diabetes conferred a higher risk than prior MI. Diabetic women had a similar risk of suffering a first MI as non-diabetic women with a prior MI had for suffering a recurrent MI. Conclusions/interpretation Both persons with diabetes but no prior MI, and persons with a prior MI but no diabetes are high-risk individuals. Among men, a prior MI conferred a higher risk of a coronary event than diabetes in the 45–54 year age group, but the situation was reversed in the elderly. Among diabetic women, the risk of suffering a first MI was similar to the risk that non-diabetic women with prior MI had of suffering a recurrent MI.     

冠状动脉造影正常的年轻人心肌梗死(附7例报告)

目的观察冠状动脉造影正常年轻人心肌梗死的临床和血管造影特点.方法 1996年1月～2000年3月315例心肌梗死患者中26例血管造影显示冠状动脉完全正常,其中7例年龄<45岁.回顾性分析患者的临床和冠状动脉造影特点.结果 7例患者均为男性,平均年龄41岁.既往均无高血压、糖尿病、高血脂及冠心病家族史,前壁梗死5例,下壁梗死2例.7例患者均有发病前大量吸烟、劳累和紧张等明确诱发因素,其中4例于发病后12小时内入院行静脉溶栓治疗,预后良好,另外3例入院时间超过12小时而行一般药物治疗,出院时留有不同程度心功能不全.结论年轻人心肌梗死可发生在冠状动脉完全正常患者中,一般都有明确诱因,及时入院行溶栓治疗预后良好.     

大鼠心肌梗塞超急性期压力反射敏感性变化

为研究急性心肌梗塞（ＡＭＩ）超急性期压力反射敏感性（ＢＲＳ）的动态变化规律，制备了ＳＤ大鼠ＡＭＩ模型，观察以ＡＭＩＯ～４ｈ的ＢＲＳ变化及其与血流动力学改变的关系，发现ＡＭＩ３０分钟时即有ＢＲＳ钝化现象，以１ｈ时最为明显。ＢＲＳ钝化与ＢＰ及心脏功能无关。     

Aromatic and branched-chain amino acids in autopsied brain tissue from cirrhotic patients with hepatic encephalopathy

Concentrations of the branched-chain amino acids (BCAAs) valine, leucine, and isoleucine and the aromatic amino acids (AAAs) phenylalanine and tyrosine were measured in three areas of dissected brain tissue obtained at autopsy from nine cirrhotic patients who died in hepatic encephalopathy. The controls were an equal number of subjects free from neurological, psychiatric or hepatic diseases, matched for age and time interval from death to freezing of autopsied brain samples. Amino acids were measured using high-performance liquid chromatography with fluorimetric detection. In brain tissue of cirrhotic patients, no changes in BCAA concentrations were observed compared with controls. On the other hand, phenylalanine levels were found to be increased 141% in prefrontal cortex, 86% in frontal cortex and 26% in caudate nucleus, and tyrosine content was increased by 71% in prefrontal cortex and 28% in frontal cortex with no significant increase in caudate nucleus. Alterations in the concentration of AAAs may lead to disturbances of monoamine neurotransmitters in brain. Such changes could play a role in the pathogenesis of hepatic encephalopathy resulting from chronic liver disease in man.     

Myocardial infarction and left ventricular free wall rupture in a patient with a prior pericardiectomy

A 59-year-old man with an inferolateral myocardial infarction and cardiogenic shock was found to have extensive intrathoracic hemorrhage in communication with the left ventricle. His remote pericardiectomy precluded hemopericardium and tamponade, and permitted the establishment of an unusual diagnosis and subsequent closure of the site of myocardial perforation.     

急性心肌梗死发作期间组织因子途径变化的观察

目的：观察急性心肌梗死（AMI）发作期间组织因子途径的变化。方法：69列临床确诊的AMI患和30例健康中老年人（作对照）被纳入研究对象。血浆中的组织因子（TF）和组织因子途径抑制物（TFPI）的活性测定采用发色底物法,TF和TFPI抗原采用ELISA法。激活的凝血因子Ⅶa采用重组可溶性TF法。凝血因子Ⅶ促凝活性采用活性测定法。结果：与对照组相比,AMI患血浆中TF、TFPI的活性均显增加[分别为5．67（1．77－54．95）mU/ml vs2.36(1.13-6.42)mU/ml,P＜0．01;224．85（86．65－512．12）％vs 138．75（51．72－297．2）％,P＜0．01]。同时TF、TFPI的抗原、凝血因子Ⅶa的活性亦有明显升高,但凝血因子Ⅶ促凝活性无显变化。结论：AMI发作期间体内组织因子途径被启动,血液呈现高凝状态。     

不稳定性心绞痛和急性心肌梗塞肌钙蛋白T变化的比较

目的 :比较不同急性冠状动脉综合征患者肌钙蛋白 T(Tn T)变化。　　方法 :不稳定性心绞痛 (UAP)、Q波型和非 Q波型急性心肌梗塞 (AMI)患者于急诊就诊时、住院后第 2、第 3和第 6日取血测定 Tn T水平。　　结果 :35 %的 UAP患者 Tn T表现为升高 ,其升高的幅度 (均 <3.0 ng/ ml)明显 <非 Q波型 AMI(2 4% >3.0 ng/ml)和 Q波型 AMI(90 % >3.0 ng/ ml) ,且一般 3天后即转为阴性 ,而 AMI患者 6天后多数仍为阳性。非 Q波型 AMI和Q波型 AMI急诊就诊时 Tn T的阳性率分别为 79.1%和 90 .7% ,住院后第 2日均达 10 0 % ,均明显高于同时间谷草转氨酶和肌酸激酶同工酶的阳性率 ,两组 Tn T阳性在持续时间上相似 ,但在升高幅度上有明显的区别。再灌注治疗可能会影响 Q波型 AMI患者 Tn T的自然变化规律。　　结论 :UAP患者 Tn T的变化与非 Q波型 AMI和 Q波型 AMI有显著的不同。     

Effects of amino acids on pancreatic polypeptide before and after vagotomy in the dog

Summary We have previously indicated a marked influence of the vagus nerve on postprandial pancreatic polypeptide secretion. The present study was designed to determine whether the vagus nerve also plays a role in the regulation of pancreatic polypeptide secretion by absorbed nutrients. The pancreatic polypeptide responses to 17 intravenously administered amino acids, as well as arginine and glucose, were measured and compared with those 1 year after truncal vagotomy in conscious dogs. In response to the infusion of a mixture of amino acids (20 g during 60 min), plasma pancreatic polypeptide concentrations decreased in normal dogs. The effect was, however, completely reversed by vagotomy, with a significant pancreatic polypeptide release being observed (p < 0.05). Arginine (5 g during 60 min) also showed a similar, although not statistically significant, effect. After intravenous bolus-injection of glucose (0.5 g/kg body weight), a transient decrease of pancreatic polypeptide secretion was found; vagotomy abolished this response. These results suggest that the vagus nerve may have a suppressive role in the process of pancreatic polypeptide secretion induced by intravenous amino acid(s) and glucose.     

Effects of free fatty acids on insulin secretion in obesity

The prevalence of obesity in Western society has reached epidemic proportions and its aetiological role in the development of type 2 diabetes has made finding an effective treatment for the condition of crucial importance. Of the many consequences of obesity, derangements in glucose metabolism present one of the greatest problems to health. While the role of obesity in causing insulin resistance has received much attention, the effect of obesity on β‐cell failure and the consequent development of type 2 diabetes requires re‐emphasis. In this review, the current understanding of the effects of elevated free‐fatty acids on β‐cell function will be examined, including a discussion of potential mechanisms. In particular, dysregulation of biochemical pathways and alterations in key enzymes, proteins and hormones will be considered as grounds for the progression to a diabetic phenotype.     

Myocardial infarction during factor IX infusion in hemophilia B: case report and review of the literature

There are very few reports in the literature of acute myocardial infarction (MI) occurring during infusion of factor concentrates, particularly cryosupernatant in patients with hemophilia B. We describe a case of a 61-year-old man with hemophilia B who suffered an acute MI while receiving cryosupernatant infusion as factor replacement therapy. Cryosupernatant is rich in coagulation factor IX and contains low levels of fibrinogen and von Willebrands factor. Factor IX and other factors present in cryosupernatant can possibly become activated during the manufacturing process causing thrombus formation in patients who are prone to it.     

Plasma fatty acids and kidney function decline in post-myocardial infarction patients of the Alpha Omega Cohort

Background and aimsAge-related kidney function decline is accelerated in patients with coronary heart disease (CHD). CHD and chronic kidney disease may share common etiologies. We examined plasma fatty acids (FAs) as novel biomarkers of kidney function decline after myocardial infarction (MI).Methods and resultsThe analysis included 2329 Dutch post–MI patients aged 60-80y (Alpha Omega Cohort) most receiving state-of-the-art medications. Plasma FAs (% total FAs) in cholesteryl esters were assessed at baseline (2002–2006), and ～40 months change in creatinine-cystatin C based glomerular filtration rate was estimated (eGFR, in ml/min per 1.73 m²). Beta coefficients for annual eGFR change in relation to plasma linoleic acid (LA; 50.1% of total FAs in CE), omega-3 FAs (EPA + DHA; 1.7%), odd-chain FAs (C15:0 and C17:0; 0.2%), and C14:0 (0.7%) were obtained from linear regression analyses adjusted for age, sex, smoking, and alcohol intake. Mean baseline eGFR ±SD was 78.5 ± 18.7, which declined by 4.7 ± 13.1 during follow-up, or 1.4 ± 3.9 per year. The annual decline in eGFR was less in patients with higher plasma LA (adjusted beta: 0.40 for LA >47 vs ≤ 47%, 95% CI: 0.01; 0.78; p = 0.046). Associations of plasma LA with annual eGFR decline were stronger in 437 patients with diabetes (1.21, 0.24; 2.19) and in 402 patients with CKD (eGFR<60; 0.90, ?0.09; 1.89). Weaker, non-significant associations with kidney function decline were observed for the other plasma FAs.ConclusionHigher plasma LA may be a good predictor of less kidney function decline after MI, particularly in patients with diabetes.The Alpha Omega Cohort is registered with clinicaltrials.gov, NCT03192410.     

Development of brain damage after neonatal hypoxia-ischemia: Excitatory amino acids and cysteine

The aim of this study was to investigate the possible role of excitatory amino acids (EAAs) and cysteine in the development of brain damage after hypoxia-ischemia (HI) in neonates. In a rat model of neonatal HI, changes in extracellular (ec) amino acids in cerebral cortex were measured with microdialysis and correlated with the extent of brain damage at the site of probe placement. Extracellular concentrations of glutamate, aspartate and cysteine increased during HI and remained elevated during reperfusion. During HI the pattern of EAA changes was the same in the infarcted, undamaged and border zone regions. During reperfusion, however, the ec concentrations of glutamate, aspartate and cysteine were higher in infarcted and border zone areas compared to undamaged tissue. HI also produced a slight increase of tissue concentration of cysteine and decrease of tissue concentration of glutamate in parietal cortex of the HI hemisphere. The effect of cysteine on brain damage induced by HI and glutamate was also investigated. A subtoxic dose of cysteine potentiated glutamate toxicity in the arcuate nucleus and enhanced brain infarction after HI in neonatal rats. The results show that in neonatal HI the extracellular levels of EAAs during HI are not directly related to brain injury but the EAA levels during reflow predict the extent of infarction. Cysteine increases HI-induced brain injury and potentiates glutamate toxicity in neonatal rats. Speculatively, elevated level of cysteine during reperfusion may participate in the excitotoxic cascade leading to brain injury.