Adrenaline

肾上腺素
  • 文章类型: Journal Article
    背景:肾上腺素在治疗可逆性牙髓炎患者盖髓中的作用尚不清楚。
    目的:探讨肾上腺素在可逆性牙髓炎患者盖髓中的作用。
    方法:纳入2020年1月至2021年12月安徽省界首市人民医院收治的可逆性牙髓炎患者100例。将他们分为观察组(n=50;肾上腺素治疗)和对照组(n=50;氧化锌丁香酚糊剂治疗)。术后24小时疼痛,牙龈充血和发红的回归时间,临床疗效,比较两组不良反应发生率。根据临床疗效将患者进一步分为无效和有效治疗组。Logistic多元回归分析探讨了影响盖髓治疗疗效的因素。
    结果:术后24h疼痛组间差异有统计学意义(P<0.05),观察组Ⅰ级疼痛比例高于对照组(P<0.01)。观察组牙龈充血和肿胀消退时间较低(2.61±1.44d和2.73±1.36d,分别)比对照组(3.85±1.47d和4.28±1.61d,分别)(P<0.05)。对照组术后2周的总有效率(80.00%)低于观察组(94.00%)(P<0.05)。对照组(14.00%)和观察组(12.00%)不良反应发生率差异无统计学意义(P>0.05)。无效治疗组肾上腺素使用率低于有效治疗组(P<0.05),链球菌和核梭杆菌厌氧消化比例高于有效治疗组(P<0.05)。Logistic多元回归分析显示,肾上腺素是可逆性牙髓炎发生盖髓的保护因素(P<0.05),链球菌和核囊厌氧消化是可逆性牙髓炎发生盖髓的危险因素(P<0.05)。
    结论:肾上腺素在可逆性牙髓炎的盖髓治疗中具有治疗效果,安全地减轻疼痛和改善临床症状。它是纸浆封盖的保护因素,而链球菌和核仁F.是危险因素。可实施针对性措施,提高临床疗效。
    BACKGROUND: The role of epinephrine in the treatment of pulp capping in patients with reversible pulpitis is not clear.
    OBJECTIVE: To explore the role of epinephrine in the treatment of pulp capping in patients with reversible pulpitis.
    METHODS: A total of 100 patients with reversible pulpitis who were treated in Anhui Jieshou People\'s Hospital from January 2020 to December 2021 were included in the study. They were categorized into an observation group (n = 50; treatment with adrenaline) and a control group (n = 50; treatment with zinc oxide eugenol paste). The 24-h postoperative pain, regression time of gingival congestion and redness, clinical efficacy, and incidence of adverse reactions were compared between the groups. Patients were further categorized into the ineffective and effective treatment groups based on clinical efficacy. Logistic multiple regression analysis explored factors affecting the efficacy of pulp capping treatment.
    RESULTS: A significant difference in 24-h postoperative pain was observed between the groups (P < 0.05), with a higher proportion of grade I pain noted in the observation group than in the control group (P < 0.01). The regression time of gingival congestion and swelling was lower in the observation group (2.61 ± 1.44 d and 2.73 ± 1.36 d, respectively) than in the control group (3.85 ± 1.47 d and 4.28 ± 1.61 d, respectively) (P < 0.05). The 2-wk postoperative total effective rate was lower in the control group (80.00%) than in the observation group (94.00%) (P < 0.05). The incidence of adverse reactions was not significantly different between the control (14.00%) and observation (12.00%) groups (P > 0.05). The proportion of adrenaline usage was lower (P < 0.05) and that of anaerobic digestion by Streptococcus and Fusobacterium nucleatum was higher in the ineffective treatment group than in the effective treatment group (P < 0.05). Logistic multiple regression analysis revealed adrenaline as a protective factor (P < 0.05) and anaerobic digestion by Streptococcus and F. nucleatum as risk factors for pulp capping in reversible pulpitis (P < 0.05).
    CONCLUSIONS: Adrenaline demonstrated therapeutic efficacy in pulp capping treatment for reversible pulpitis, reducing pain and improving clinical symptoms safely. It is a protective factor for pulp capping, whereas Streptococcus and F. nucleatum are risk factors. Targeted measures can be implemented to improve clinical efficacy.
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  • 文章类型: Case Reports
    肾上腺素,应激性心肌病,过敏反应,和Kounis综合征(肾上腺素,Takotsubo,过敏反应,Kounis情结,ATAK)构成一种复杂的临床综合征,通常与内源性或外源性肾上腺素有关。由于它的快速发作,严重程度,和治疗挑战,它值得临床医生的极大关注。本文报道了1例II型Kounis综合征合并由latamoxef引起的过敏引发的应激性心肌病(ATAK)。
    一名67岁男性慢性阻塞性肺疾病急性加重患者入院呼吸内科治疗。出院前一天,在接受latamoxef输注27分钟后,病人出现喘息,呼吸困难,发冷,大量出汗,体温升高,需要转移到ICU进行监测和治疗。心电图提示疑似心肌梗塞,床旁超声心动图显示左心室射血分数为40%,左心室节段功能障碍,和顶端四舍五入。急诊冠状动脉造影显示左前降支和右冠状动脉中段有50%的节段性偏心狭窄。最终诊断为II型Kounis综合征合并因latamoxef引起的过敏引起的应激性心肌病,即,ATAK.尽管积极治疗,患者在ICU第3天死于严重心源性休克.
    ATAK是一个进展迅速的临界条件。对于出现严重过敏反应的患者,监测生物标志物如肌钙蛋白和心电图的变化对于及时识别至关重要。如果一个病人被诊断为库尼斯综合征,应谨慎使用肾上腺素以预防ATAK。
    UNASSIGNED: Adrenaline, stress cardiomyopathy, allergic reactions, and Kounis syndrome (Adrenaline, Takotsubo, Anaphylaxis, Kounis Complex, ATAK) constitute a complex clinical syndrome often associated with endogenous or exogenous adrenaline. Due to its rapid onset, severity, and treatment challenges, it warrants significant attention from clinicians. This article reports a case of Type II Kounis syndrome combined with stress cardiomyopathy (ATAK) triggered by a latamoxef-induced allergy.
    UNASSIGNED: A 67-year-old male patient with an acute exacerbation of chronic obstructive pulmonary disease was admitted to the respiratory department for treatment. The day before discharge, after receiving a latamoxef infusion for 27 min, the patient developed wheezing, dyspnea, chills, profuse sweating, and an elevated body temperature, necessitating transfer to the ICU for monitoring and treatment. The ECG suggested a suspected myocardial infarction, while bedside echocardiography showed a left ventricular ejection fraction of 40%, segmental dysfunction of the left ventricle, and apical rounding. Emergency coronary angiography revealed 50% segmental eccentric stenosis in the mid-segment of the left anterior descending branch and right coronary artery. The final diagnosis was Type II Kounis Syndrome combined with stress cardiomyopathy due to a latamoxef-induced allergy, i.e., ATAK. Despite aggressive treatment, the patient succumbed to severe cardiogenic shock on the third day in the ICU.
    UNASSIGNED: ATAK is a critical condition that progresses rapidly. For patients experiencing severe allergic reactions, monitoring biomarkers such as Troponin and ECG changes is crucial for timely recognition. If a patient is diagnosed with Kounis syndrome, caution should be exercised in using adrenaline to prevent ATAK.
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  • 文章类型: Journal Article
    下丘脑视交叉上核(SCN)容纳哺乳动物的中央昼夜节律振荡器。SCN中产生的主要神经递质是γ-氨基丁酸,精氨酸加压素(AVP),血管活性肠肽(VIP),垂体衍生的腺苷酸环化酶激活肽(PACAP),前动力蛋白2,神经介肽S,和胃泌素释放肽(GRP)。除了这些,在SCN中也检测到儿茶酚胺及其受体。在这项研究中,我们通过免疫组织化学证实了SCN和小鼠SCN衍生的永生化细胞系中β-肾上腺素受体的存在,免疫细胞化学,和药理学技术。然后,我们表征了β-肾上腺素能激动剂和拮抗剂对cAMP调节元件(CRE)信号传导的影响。此外,我们研究了β-肾上腺素能信号与影响平行信号通路的物质的相互作用。我们的发现对压力(肾上腺素升高)对生物钟的作用具有潜在的影响,并且可以解释用作抗高血压药物的β受体阻滞剂的某些副作用。
    The suprachiasmatic nucleus of the hypothalamus (SCN) houses the central circadian oscillator of mammals. The main neurotransmitters produced in the SCN are γ-amino-butyric acid, arginine-vasopressin (AVP), vasoactive intestinal peptide (VIP), pituitary-derived adenylate cyclase-activating peptide (PACAP), prokineticin 2, neuromedin S, and gastrin-releasing peptide (GRP). Apart from these, catecholamines and their receptors were detected in the SCN as well. In this study, we confirmed the presence of β-adrenergic receptors in SCN and a mouse SCN-derived immortalized cell line by immunohistochemical, immuno-cytochemical, and pharmacological techniques. We then characterized the effects of β-adrenergic agonists and antagonists on cAMP-regulated element (CRE) signaling. Moreover, we investigated the interaction of β-adrenergic signaling with substances influencing parallel signaling pathways. Our findings have potential implications on the role of stress (elevated adrenaline) on the biological clock and may explain some of the side effects of β-blockers applied as anti-hypertensive drugs.
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  • 文章类型: Journal Article
    肥胖和糖尿病是心血管疾病的主要危险因素。Zucker脂肪型糖尿病(ZFDM)大鼠是肥胖和2型糖尿病的新型动物模型。我们最近报道ZFDM-Leprfa/fa(人)大鼠血压正常,而血液肾上腺素水平和心率低于对照ZFDM-Leprfa/(Heterio)大鼠。这里,我们比较了Hetero和Homo大鼠离体肠系膜动脉的反应性。去氧肾上腺素引起的收缩增加,与异株大鼠相比,21-23周龄的人鼠中异丙肾上腺素诱导的松弛减少。人大鼠中α1A而不是β2肾上腺素受体的mRNA表达增加。一氧化氮(NO)介导的乙酰胆碱诱导的松弛减少,而内皮NO合成酶(eNOS)的mRNA表达在人鼠肠系膜动脉中相当增加。这些发现首次揭示了在血浆肾上腺素减少的人鼠中,通过增加的α1肾上腺素受体表达和减弱的β2肾上腺素受体信号增强肾上腺素诱导的血管收缩力,可以维持血压。此外,NO介导的内皮依赖性舒张功能受损,可能是由于eNOS功能障碍,这也可能有助于维持人鼠的血压。
    Obesity and diabetes are major risk factors for cardiovascular diseases. Zucker fatty diabetes mellitus (ZFDM) rats are novel animal model of obesity and type 2 diabetes. We have recently reported that blood pressure in ZFDM-Leprfa/fa (Homo) rats was normal, while blood adrenaline level and heart rate were lower than those in control ZFDM-Leprfa/+ (Hetero) rats. Here, we compared the reactivity in isolated mesenteric artery between Hetero and Homo rats. Contraction induced by phenylephrine was increased, while relaxation induced by isoprenaline was decreased in Homo rats at 21-23 weeks old compared with those in Hetero rats. The mRNA expression for α1A but not β2 adrenoreceptor in Homo rats was increased. Nitric oxide (NO)-mediated relaxation induced by acetylcholine was decreased, while the mRNA expression for endothelial NO synthase (eNOS) was rather increased in mesenteric artery from Homo rats. These findings for the first time revealed that in Homo rats with reduced plasma adrenaline, blood pressure could be maintained by enhancing vascular contractility induced by adrenaline through the increased α1 adrenoceptor expression and the attenuated β2 adrenoceptor signaling. Additionally, NO-mediated endothelium-dependent relaxation is impaired perhaps due to eNOS dysfunction, which might also contribute to maintain the blood pressure in Homo rats.
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  • 文章类型: Case Reports
    慢性疲劳综合征(CFS)是一种异质性疾病,具有儿茶酚胺代谢的遗传相关脆弱性(例如,儿茶酚O-甲基转移酶多态性),其中环境因素具有重要影响。α-甲基-对-酪氨酸(AMPT;也称为甲酪氨酸)是用于治疗嗜铬细胞瘤的批准的药物。作为酪氨酸羟化酶抑制剂,AMPT可能是治疗涉及儿茶酚胺改变的疾病的潜在候选者。然而,只有小规模的临床试验测试了AMPT在其他一些疾病中的再利用。目前的病例报告汇编了对一名连续诊断为持续过度压力的男性患者进行一年多随访的遗传和纵向生化数据。神经衰弱,CFS(根据疾病控制中心(CDC/Fukuda)于2012年诊断),和体位性心动过速综合征(POTS)在10年期间,并报告患者的症状改善响应低-中剂量的AMPT。该病例被认为是与压力相关的CFS病例。从患者提供的医疗记录中报告数据,以允许对针对患者呈现的高肾上腺素能状态的治疗的详细反应。我们强调对治疗CFS的经典方法缺乏积极的回应,反映了CFS诊断的局限性和缓解患者症状的可用治疗方法。当前的病理机制假设强调DA/肾上腺素能系统中的单胺改变(高肾上腺素能状态)和由交感神经过度活动引起的功能失调的自主神经系统。患者对AMPT治疗的反应突出了起搏与紧张情况和活动增加的相关性。重要的是,结果不表明AMPT与其对单胺系统的作用之间存在因果关系,未来的研究应该评估其他目标的影响。
    Chronic fatigue syndrome (CFS) is a heterogeneous disorder with a genetically associated vulnerability of the catecholamine metabolism (e.g., catechol O-methyltransferase polymorphisms), in which environmental factors have an important impact. Alpha-methyl-p-tyrosine (AMPT; also referred to as metyrosine) is an approved medication for the treatment of pheochromocytoma. As a tyrosine hydroxylase inhibitor, AMPT may be a potential candidate for the treatment of diseases involving catecholamine alterations. However, only small-scale clinical trials have tested AMPT repurposing in a few other illnesses. The current case report compiles genetic and longitudinal biochemical data for over a year of follow-up of a male patient sequentially diagnosed with sustained overstress, neurasthenia, CFS (diagnosed in 2012 as per the Center for Disease Control (CDC/Fukuda)), and postural orthostatic tachycardia syndrome (POTS) over a 10-year period and reports the patient\'s symptom improvement in response to low-medium doses of AMPT. This case was recognized as a stress-related CFS case. Data are reported from medical records provided by the patient to allow a detailed response to treatment targeting the hyperadrenergic state presented by the patient. We highlight the lack of a positive response to classical approaches to treating CFS, reflecting the limitations of CFS diagnosis and available treatments to alleviate patients\' symptoms. The current pathomechanism hypothesis emphasizes monoamine alterations (hyperadrenergic state) in the DA/adrenergic system and a dysfunctional autonomic nervous system resulting from sympathetic overactivity. The response of the patient to AMPT treatment highlights the relevance of pacing with regard to stressful situations and increased activity. Importantly, the results do not indicate causality between AMPT and its action on the monoamine system, and future studies should evaluate the implications of other targets.
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  • 文章类型: Journal Article
    高电压门控Ca2通道(HVCCs)可塑造大多数内分泌细胞的电活动并控制激素释放。HVCC是由成孔α1和辅助β形成的多亚基蛋白质复合物,α2δ和γ亚基。四个基因编码α2δ同种型。在mRNA水平,小鼠嗜铬细胞(MCC)主要表达编码α2δ-1同种型的CACNA2D1基因。在这里,我们显示α2δ-1缺失导致~60%的HVCCCa2+流入减少,失活动力学较慢。药理学解剖显示,与野生型(WT)相比,HVCC组成在α2δ-1-/-MCC中保持相似,证明α2δ-1对所有HVCC同工型发挥相似的功能作用。与减少的HVCCCa2+流入量一致,α2δ-1-/-MCC显示出减少的自发电活动,动作电位(AP)具有较短的半最大持续时间,这是由较快的上升和衰减斜率引起的。然而,与WT相比,诱导的电活动显示出相反的作用,α2δ-1-/-MCC在强直激发模式下显示出显着更高的AP频率,并且激发AP爆发的细胞数量增加。这种功能获得表型是由Ca2依赖性K电流的功能激活降低引起的。此外,尽管HVCCCa2+流入减少,在持续刺激期间,与WT相比,α2δ-1-/-MCC中的细胞内Ca2+瞬变和囊泡胞吐作用或内吞作用未改变。总之,我们的研究表明,α2δ-1基因缺失减少了培养的MCC中的Ca2流入,但由于兴奋性增加,导致儿茶酚胺分泌矛盾地增加。关键点:α2δ-1高电压门控Ca2+通道(HVCC)亚基的缺失使小鼠嗜铬细胞(MCC)Ca2+内流降低~60%,但引起诱导兴奋性的矛盾增加。MCC细胞内Ca2+瞬变不受HVCCCa2+流入减少的影响。α2δ-1的缺失减少了可立即释放的池囊泡胞吐作用,但对持续刺激的儿茶酚胺(CA)释放没有影响。来自MCC的增加的电活动和CA释放可能有助于先前报道的携带α2δ-1功能丧失突变的患者的心血管表型。
    High voltage-gated Ca2+ channels (HVCCs) shape the electrical activity and control hormone release in most endocrine cells. HVCCs are multi-subunit protein complexes formed by the pore-forming α1 and the auxiliary β, α2δ and γ subunits. Four genes code for the α2δ isoforms. At the mRNA level, mouse chromaffin cells (MCCs) express predominantly the CACNA2D1 gene coding for the α2δ-1 isoform. Here we show that α2δ-1 deletion led to ∼60% reduced HVCC Ca2+ influx with slower inactivation kinetics. Pharmacological dissection showed that HVCC composition remained similar in α2δ-1-/- MCCs compared to wild-type (WT), demonstrating that α2δ-1 exerts similar functional effects on all HVCC isoforms. Consistent with reduced HVCC Ca2+ influx, α2δ-1-/- MCCs showed reduced spontaneous electrical activity with action potentials (APs) having a shorter half-maximal duration caused by faster rising and decay slopes. However, the induced electrical activity showed opposite effects with α2δ-1-/- MCCs displaying significantly higher AP frequency in the tonic firing mode as well as an increase in the number of cells firing AP bursts compared to WT. This gain-of-function phenotype was caused by reduced functional activation of Ca2+-dependent K+ currents. Additionally, despite the reduced HVCC Ca2+ influx, the intracellular Ca2+ transients and vesicle exocytosis or endocytosis were unaltered in α2δ-1-/- MCCs compared to WT during sustained stimulation. In conclusion, our study shows that α2δ-1 genetic deletion reduces Ca2+ influx in cultured MCCs but leads to a paradoxical increase in catecholamine secretion due to increased excitability. KEY POINTS: Deletion of the α2δ-1 high voltage-gated Ca2+ channel (HVCC) subunit reduces mouse chromaffin cell (MCC) Ca2+ influx by ∼60% but causes a paradoxical increase in induced excitability. MCC intracellular Ca2+ transients are unaffected by the reduced HVCC Ca2+ influx. Deletion of α2δ-1 reduces the immediately releasable pool vesicle exocytosis but has no effect on catecholamine (CA) release in response to sustained stimuli. The increased electrical activity and CA release from MCCs might contribute to the previously reported cardiovascular phenotype of patients carrying α2δ-1 loss-of-function mutations.
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  • 文章类型: Journal Article
    (1)花生过敏与过敏反应的高风险相关,口服免疫疗法可以预防。符合免疫治疗条件的患者是根据食物挑战选择的。尽管目前评估针对主要花生分子(Arah1、2、3和6)的抗体被认为是另一种选择。(2)本研究评估了上述抗体之间的关系,挑战结果,花生致敏儿童的皮肤测试和其他一些参数。涉及74名儿童,分成两组,基于他们对食物挑战的反应。(3)两组皮肤试验结果不同,成分特异性抗体水平和花生接触史。然后使用抗体水平来计算预测攻击结果或症状严重程度的阈值。虽然基于抗体的攻击预测显示出统计学意义,在出现严重症状的情况下,它失败了。此外,抗体水平之间没有观察到显著的相关性,症状引发剂量和严重过敏反应的风险。尽管在某些患者中,它可能是由IgG4的干扰引起的,但后者并不是对这种现象的普遍解释。(4)尽管有一些限制,基于抗体的筛查可能是食物挑战的替代方案,尽管其临床相关性仍需进一步研究。
    (1) Peanut allergy is associated with high risk of anaphylaxis which could be prevented by oral immunotherapy. Patients eligible for immunotherapy are selected on the basis of a food challenge, although currently the assessment of antibodies against main peanut molecules (Ara h 1, 2, 3 and 6) is thought to be another option. (2) The current study assessed the relationship between the mentioned antibodies, challenge outcomes, skin tests and some other parameters in peanut-sensitized children. It involved 74 children, divided into two groups, based on their response to a food challenge. (3) Both groups differed in results of skin tests, levels of component-specific antibodies and peanut exposure history. The antibody levels were then used to calculate thresholds for prediction of challenge results or symptom severity. While the antibody-based challenge prediction revealed statistical significance, it failed in cases of severe symptoms. Furthermore, no significant correlation was observed between antibody levels, symptom-eliciting doses and the risk of severe anaphylaxis. Although in some patients it could result from interference with IgG4, the latter would not be a universal explanation of this phenomenon. (4) Despite some limitations, antibody-based screening may be an alternative to the food challenge, although its clinical relevance still requires further studies.
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  • 文章类型: Case Reports
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  • 文章类型: Journal Article
    在这项研究中,我们创新性地合成了源自燕麦片的氮掺杂碳微球(NCS)。通过利用多金属氧酸盐(POM)作为还原剂和连接剂,我们实现了铂纳米颗粒(PtNP)均匀负载到NCS的表面。由Pt/多金属氧酸盐/氮掺杂碳微球(Pt/POM/NCS)构建的复合纳米颗粒充分利用了协同催化作用,在肾上腺素检测中表现优异。该方法的线性范围为2.59至1109.59μM,检测限低至0.25μM(S/N=3),灵敏度为0.74μAμM-1cm-2。此外,它具有高稳定性和强抗干扰能力。在人血清中的回收率为98.51%至101.25%。
    In this study, we innovatively synthesized nitrogen-doped carbon microspheres (NCS) derived from oatmeal. By utilizing polyoxometalates (POM) as both reducing and linking agents, we achieved uniform loading of platinum nanoparticles (Pt NPs) onto the surface of the NCS. The composite nanoparticles constructed from Pt/polyoxometalate/nitrogen-doped carbon microspheres (Pt/POM/NCS) fully exploit the synergistic catalytic effect, demonstrating superior performance in adrenaline detection. The method has a linear range of 2.59 to 1109.59 μM, a detection limit as low as 0.25 μM (S/N = 3), and a sensitivity of 0.74 μA μM-1 cm-2. Additionally, it exhibits high stability and strong anti-interference ability. The recoveries in human serum were 98.51 % to 101.25 %.
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