依那普利联合吲达帕胺治疗中、重度高血压64例疗效观察

目的观察依那普利加吲达帕胺治疗中、重度高血压病的疗效。方法将128例中、重度高血压病人分为两组,观察组64例口服依那普利加吲达帕胺,疗程8周。对照组口服依那普利,疗程8周。结果观察组有效率为93.8%,对照组为79.7%,明显优于对照组,P<0.05。结论提示依那普利加吲达帕胺治疗中、重度高血压有较好疗效,优于单用依那普利,无严重不良反应,是治疗中、重度高血较理想治疗方案。     

吲达帕胺片的稳定性研究

目的：研究吲达帕胺片的稳定性以确定有效期。方法：采用紫外分光光度法测定吲达帕胺的含量，用薄层色谱法检查其降解产物^[1]，对制剂在强光、高温、高湿、空气中放置及加速实验、长期室温留样等条件下进行稳定性考察，结果：本品在光照、空气放置、室温留样2年条件下稳定，在高湿(92．5％)条件下，片面吸潮开裂，在高温(80℃)条件下片面出现暗黄色斑，但吲达帕胺含量及其他质量指标无明显变化，为防止储存、使用过程中吸潮霉变，仍需干燥密封条件下储存。有效期暂定为2年。     

反相高效液相色谱法测定吲达帕胺的含量

建立RP-HPLC法测定吲达帕胺含量的新方法.采用HPLC法,色谱柱为Kromasil C18柱;流动相中加入新的流动相-乙腈,V(水):V(乙腈):V(甲醇):V(冰醋酸)=65:17.5:17.5:0.1,流速1.0mL/min,检测波长240nm.该方法的线性范围为52.0～260.0μg/mL(r=0.9994),RSD=0.14%(n=6).本法简便、准确、灵敏、重现性好,适合吲达帕胺片的质量控制.     

硝苯地平治疗高血压疗效观察

目的探讨硝苯地平治疗高血压疗效。方法治疗分硝苯地平组及复方降压片对照组。所有病例均为门诊病例,治疗前常规体检,并且停用降压药物7天左右,用同一水银柱血压计在同一时间测定同日3次血压,以平均值作治疗前血压值。结果硝苯地平组40例治疗后,显效26例,有效10例,无效4例。复方降压片组38例治疗后,显效19例,有效13例,无效6例。结论硝苯地平是一种安全有效的抗高压制剂,可以作为农村治疗高血压的一线药物。     

硝苯地平缓释片联合倍他洛克治疗高血压的疗效观察

目的进一步了解高血压病联合用药的必要性。方法对120例高血压患者采取单独服用硝苯地平缓释片和联合倍他洛克两种不同治疗方法,观察治疗前后降压情况、副作用和实验室变化。结果硝苯地平联合倍他洛克治疗高血压疗效优于单独用药组,而且副作用少,耐受性好。结论联合应用硝苯地平和倍他洛克治疗高血压病既可减少药量,减少副作用,又可增加降压效应,值得进一步推广。     

银杏达莫联合阿司匹林治疗TIA疗效观察

目的探讨银杏达莫联合阿司匹林治疗短暂性脑缺血发作的疗效。方法将120例TIA病人分两组(A组与B组),B组单纯使用肠溶阿斯匹林治疗,A组在肠溶阿斯匹林治疗基础上,加用银杏达莫注射液治疗,观察病人3个月内、6个月内TIA复发情况。结果A组前3个月TIA复发1例,B组5例。后3个月A组TIA复发3例,B组10例,B组复发率高于A组,差异显著(P<0.05)。结论银杏达莫具有扩张脑血管改善脑缺血产生的症状和记忆功能,其与阿司匹林联合应用可以通过不同途经发挥抗血小板聚集作用。对TIA疗效明显优于单纯使用肠溶阿斯匹林。     

银杏达莫治疗老年不稳定性心绞痛的疗效观察

目的 观察银杏达莫注射液治疗老年不稳定性心绞痛的临床疗效。方法 将80例不稳定性心绞痛老年患者随机分为2组,每组40例,对照组给予扩冠、抗血小板等常规治疗,治疗组在常规治疗基础上给予银杏达莫静滴。观察2组患者治疗前及治疗后2周心绞痛发作次数、程度、心电图ST段总压低及药物的不良反应。结果 经2周治疗后,治疗组总有效率(90.0%)优于对照组(67.5%),2组比较,差异有统计学意义(P<0.05)。结论 应用银杏达莫注射液治疗不稳定型心绞痛疗效显著,值得临床推广应用。     

苯磺酸左旋氨氯地平治疗老年高血压56例疗效观察

目的探讨新型长效钙拮抗剂苯磺酸左旋氨氯地平对老年高血压病的疗效。方法口服苯磺酸左旋氨氯地平片(吉林天风制药集团生产,商品名施慧达),每次2.5～5mg,1次/d,疗程6周。结果 56例患者经施慧达治疗6周以后,显效30例(53.6%),有效25例(44.7%),无效1例(1.7%),总有效率为98.3(55/56)。结论施慧达对老年人原发性高血压降压疗效好,且对其他心血管疾病防治有利,不良反应少。     

沙利度胺与地塞米松联合治疗复发、难治性多发性骨髓瘤的疗效观察

目的观察沙利度胺(Thal)联合地塞米松(Dex)治疗复发、难治性多发性骨髓瘤的疗效。方法Tha l200mg/d,分早晚2次口服,持续2周;300mg/d,第3周,分早晚2次服用;400mg/d,第4～12周,分早晚2次口服。结果20例复发、难治性多发性骨髓瘤患者中,2例骨髓(BM)完全缓解(CR),CR率为10%,部分缓解(PR)4例,PR率为20%,骨髓未达PR及CR标准,但病情稳定,一般症状有所改善,此类患者所占比例为40%,无效6例,总有效率为70%。结论Thal联合Dex的方案是治疗复发、难治性多发性骨髓瘤的有效方案。     

甲钴胺与前列地尔联合治疗糖尿病周围神经病变的疗效观察

目的 观察及探讨甲钴胺与前列地尔联合治疗糖尿病周围神经病变的临床疗效,并对2种药物联合作用的机制进行分析。方法 入选的82例糖尿病周围神经病变患者按照随机数字表法随机分成观察组和对照组2组,每组各42例,2组均给予糖尿病饮食,采用胰岛素控制血糖等基础治疗,观察组在此基础上给予前列地尔l0g静注加用甲钴胺1000ug加入250mL生理盐水中避光静滴治疗,每天1次。在治疗前和治疗3周后观察临床症状改善情况,测定下肢肌电图。治疗后比较2组的疗效。结果 观察组42例患者,总有效率90.5%;对照组42例患者,总有效率76.2%。采用χ2检验,对2组的总有效率进行比较,差异有统计学意义(P<0.05)。观察组和对照组MNCV、SNCV均较治疗前明显降低,且观察组较对照组降低更明显,P<0.05,差异有统计学意义。结论 甲钴胺与前列地尔联合治疗糖尿病周围神经病变疗效明确、副作用少、并发症少,值得临床推广和应用。     

非洛地平治疗老年高血压病疗效观察

目的 观察非洛地平缓释片对老年高血压病的治疗效果、不良反应及时患者代谢的影响.方法 选择92例老年高血压病患者,每日早晨顿服非洛地平缓释片2.5mg,采用逐渐增量的方法,最大剂量为10mg/d,疗程4周.比较治疗前后患者血压情况,观察用药前后血生化指标.结果 服药4周后,血压明显下降,与治疗前相比差异有统计学意义(P＜0.05).92例患者中显效64例(69.56%),有效20例(21.73%),总有效率达91.3%(84例).治疗前后空腹血糖、血脂、肾功能及电解质无显著变化(P＞0.05),不良反应发生率为8.7%.结论 非洛地平缓释片对于老年高血压病患者是一种较理想的降血压药物.     

Hypertension in Patients with Insulin Resistance: Etiopathogenesis and Management in Children

Insulin resistance (IR) is a key component in the etiopathogenesis of hypertension (HS) in patients with diabetes mellitus (DM). Several pathways have been found to be involved in this mechanism in recent literature. For the above-mentioned reasons, treatment of HS should be specifically addressed in patients affected by DM. Two relevant recently published guidelines have stressed this concept, giving specific advice in the treatment of HS in children belonging to this group: the European Society of HS guidelines for the management of high blood pressure in children and adolescents and the American Academy of Pediatrics Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents. Our aim is to summarize the main pathophysiological mechanisms through which IR causes HS and to highlight the specific principles of treatment of HS for children with DM.     

40例老年患者手术麻醉处理研究

目的对老年患者手术麻醉处理进行研究。方法 2008年10月至2010年10月之间在我院进行手术的老年患者40例,其中麻醉处理中硬膜外阻滞27例,静吸复合麻醉7例,腰麻2例,颈丛臂丛阻滞3例,其他1例。结果所有患者术后并发症观察,术后随访48h内无死亡病例,1例为中毒性休克,局麻药毒性反应1例,轻度肺功能不全2例。结论高龄并不是手术和麻醉的禁忌证,麻醉中要全面考虑患者身体条件,合理选择麻醉方法和麻醉药,尽量缩短手术时间,预防并发症。     

认知心理干预对高血压病患者遵医行为和临床疗效的影响

目的观察认知心理干预对高血压病患者遵医行为和临床疗效的影响。方法100例高血压患者随机分为干预组和对照组,各50例2组均接受内科常规治疗,干预组患者进行贝克认知疗法(Beck’s cognitive therapy)。采用自行设计的高血压患者遵医行为调查问卷,焦虑自评量表(SAS)、抑郁自评量表(SDS),对患者进行评估。结果治疗后2组患者遵医行为,SAS、SDS评分,疗效间差别有统计学意义(P<0.05)。结论认知心理干预可以改善患者的焦虑和抑郁等负性情绪,提高近期医从性及治疗效果。     

Anti-Inflammatory Effect of Allicin Associated with Fibrosis in Pulmonary Arterial Hypertension

Pulmonary arterial hypertension (PAH) is characterized by pulmonary vascular remodeling. Recent evidence supports that inflammation plays a key role in triggering and maintaining pulmonary vascular remodeling. Recent studies have shown that garlic extract has protective effects in PAH, but the precise role of allicin, a compound derived from garlic, is unknown. Thus, we used allicin to evaluate its effects on inflammation and fibrosis in PAH. Male Wistar rats were divided into three groups: control (CON), monocrotaline (60 mg/kg) (MCT), and MCT plus allicin (16 mg/kg/oral gavage) (MCT + A). Right ventricle (RV) hypertrophy and pulmonary arterial medial wall thickness were determined. IL-1β, IL-6, TNF-α, NFκB p65, Iκβ, TGF-β, and α-SMA were determined by Western blot analysis. In addition, TNF-α and TGF-β were determined by immunohistochemistry, and miR-21-5p and mRNA expressions of Cd68, Bmpr2, and Smad5 were determined by RT-qPCR. Results: Allicin prevented increases in vessel wall thickness due to TNF-α, IL-6, IL-1β, and Cd68 in the lung. In addition, TGF-β, α-SMA, and fibrosis were lower in the MCT + A group compared with the MCT group. In the RV, allicin prevented increases in TNF-α, IL-6, and TGF-β. These observations suggest that, through the modulation of proinflammatory and profibrotic markers in the lung and heart, allicin delays the progression of PAH.     

Thermoase-Derived Flaxseed Protein Hydrolysates and Membrane Ultrafiltration Peptide Fractions Have Systolic Blood Pressure-Lowering Effects in Spontaneously Hypertensive Rats

Thermoase-digested flaxseed protein hydrolysate (FPH) samples and ultrafiltration membrane-separated peptide fractions were initially evaluated for in vitro inhibition of angiotensin I-converting enzyme (ACE) and renin activities. The two most active FPH samples and their corresponding peptide fractions were subsequently tested for in vivo antihypertensive activity in spontaneously hypertensive rats (SHR). The FPH produced with 3% thermoase digestion showed the highest ACE- and renin-inhibitory activities. Whereas membrane ultrafiltration resulted in significant (p < 0.05) increases in ACE inhibition by the <1 and 1–3 kDa peptides, only a marginal improvement in renin-inhibitory activity was observed for virtually all the samples after membrane ultrafiltration. The FPH samples and membrane fractions were also effective in lowering systolic blood pressure (SBP) in SHR with the largest effect occurring after oral administration (200 mg/kg body weight) of the 1–3 kDa peptide fraction of the 2.5% FPH and the 3–5 kDa fraction of the 3% FPH. Such potent SBP-lowering capacity indicates the potential of flaxseed protein-derived bioactive peptides as ingredients for the formulation of antihypertensive functional foods and nutraceuticals.     

KCNK3 Mutation Causes Altered Immune Function in Pulmonary Arterial Hypertension Patients and Mouse Models

Loss of function KCNK3 mutation is one of the gene variants driving hereditary pulmonary arterial hypertension (PAH). KCNK3 is expressed in several cell and tissue types on both membrane and endoplasmic reticulum and potentially plays a role in multiple pathological process associated with PAH. However, the role of various stressors driving the susceptibility of KCNK3 mutation to PAH is unknown. Hence, we exposed kcnk3^fl/fl animals to hypoxia, metabolic diet and low dose lipopolysaccharide (LPS) and performed molecular characterization of their tissue. We also used tissue samples from KCNK3 patients (skin fibroblast derived inducible pluripotent stem cells, blood, lungs, peripheral blood mononuclear cells) and performed microarray, immunohistochemistry (IHC) and mass cytometry time of flight (CyTOF) experiments. Although a hypoxic insult did not alter vascular tone in kcnk3^fl/fl mice, RNASeq study of these lungs implied that inflammatory and metabolic factors were altered, and the follow-up diet study demonstrated a dysregulation of bone marrow cells in kcnk3^fl/fl mice. Finally, a low dose LPS study clearly showed that inflammation could be a possible second hit driving PAH in kcnk3^fl/fl mice. Multiplex, IHC and CyTOF immunophenotyping studies on human samples confirmed the mouse data and strongly indicated that cell mediated, and innate immune responses may drive PAH susceptibility in these patients. In conclusion, loss of function KCNK3 mutation alters various physiological processes from vascular tone to metabolic diet through inflammation. Our data suggests that altered circulating immune cells may drive PAH susceptibility in patients with KCNK3 mutation.     

Toll-Like Receptors in the Pathogenesis of Essential Hypertension. A Forthcoming Immune-Driven Theory in Full Effect

Essential hypertension (EH) is a highly heterogenous disease with a complex etiology. Recent evidence highlights the significant contribution of subclinical inflammation, triggered and sustained by excessive innate immune system activation in the pathogenesis of the disease. Toll-like receptors (TLRs) have been implied as novel effectors in this inflammatory environment since they can significantly stimulate the production of pro-inflammatory cytokines, the migration and proliferation of smooth muscle cells and the generation of reactive oxygen species (ROS), facilitating a low-intensity inflammatory background that is evident from the very early stages of hypertension. Furthermore, the net result of their activation is oxidative stress, endothelial dysfunction, vascular remodeling, and finally, vascular target organ damage, which forms the pathogenetic basis of EH. Importantly, evidence of augmented TLR expression and activation in hypertension has been documented not only in immune but also in several non-immune cells located in the central nervous system, the kidneys, and the vasculature which form the pathogenetic core systems operating in hypertensive disease. In this review, we will try to highlight the contribution of innate immunity in the pathogenesis of hypertension by clarifying the deleterious role of TLR signaling in promoting inflammation and facilitating hypertensive vascular damage.     

Neuroprotective Effect of Statins in a Rat Model of Chronic Ocular Hypertension

Glaucoma is an optic neuropathy in which the degeneration of retinal ganglion cells (RGCs) results in irreversible vison loss. Therefore, neuroprotection of RGCs from glaucomatous afflictions is crucial for glaucoma treatment. In this study, we aimed to investigate the beneficial effects of statins in the protection of RGCs using a rat model. Glaucomatous injury was induced in rats by chronic ocular hypertension (OHT) achieved after performing a circumlimbal suture. The rats were given either statins such as simvastatin and atorvastatin or a solvent weekly for 6 weeks. Retina sections underwent hematoxylin and eosin, Brn3a, or cleaved casepase-3 staining to evaluate RGC survival. In addition, modulation of glial activation was assessed. While the retinas without statin treatment exhibited increased RGC death due to chronic OHT, statins promoted the survival of RGCs and reduced apoptosis. Statins also suppressed chronic OHT-mediated glial activation in the retina. Our results demonstrate that statins exert neuroprotective effects in rat retinas exposed to chronic OHT, which may support the prospect of statins being a glaucoma treatment.