妊娠期高血压疾病患者影响因素分析及对妊娠结局和生命质量的影响

摘要 目的：分析妊娠期高血压疾病(HDCP)患者影响因素,并探讨HDCP对妊娠结局和生命质量的影响。方法：选取2018年1月～2021年1月我院收治的100例HDCP患者为HDCP组,另选取同期于我院产检的健康孕产妇100例为对照组。收集两组临床资料和妊娠结局,采用36项健康调查简表(SF-36)评价两组孕产妇的生命质量。单因素及多因素Logistic回归分析HDCP的影响因素。结果：单因素及多因素Logistics回归分析显示,年龄＞35岁、孕前体质量指数≥28 kg/m²、焦虑/抑郁、高血压家族史为HDCP的独立危险因素,文化程度大专及以上、孕期规律补充钙剂为HDCP的独立保护因素(P＜0.05)。与对照组比较,HDCP组剖宫产、新生儿窒息、产后出血、低体重儿、胎儿窘迫比例增加(P＜0.05)。与对照组比较,HDCP组躯体功能、生理职能、一般健康状况、生命活力、社会功能、情感功能、精神健康评分降低,躯体疼痛评分增加(P＜0.05)。结论：HDCP受多种因素影响,其发病会对患者妊娠结局和生命质量产生不良影响,临床应做好相关预防措施。     

早期康复护理对肠内营养治疗的高血压颅内出血 患者预后的影响

目的：研究早期康复护理对肠内营养治疗的高血压颅内出血患者预后的影响。方法：选取2010 年1 月~2012 年10 月间入 院诊治的高血压颅内出血并应用肠内营养支持治疗的患者120 例,随机分为实验组（60 例）和对照组（60 例）。对照组应用常规护 理办法,实验组在其基础上应用早期康复护理,随访1 年后观察两组患者预后的生活质量情况、GCS（格拉斯哥昏迷指数）评分以 及并发症的发生情况。结果：随访1 年后,实验组的生活质量显著高于对照组（P<0.05）;护理干预前两组患者的GCS 评分无差异, 护理干预后实验组的GCS 评分显著高于对照组（P<0.05）;实验组在肺部感染、下肢静脉血栓、肩手综合征等并发症的发生例数均 显著低于对照组（P<0.05）。结论：针对肠内营养支持治疗的高血压颅内出血患者应用早期康复护理可有效改善患者的昏迷程度、 预防并发症,有助于提高患者的生活质量。     

心理干预对高血压合并脑梗塞患者负性情绪及生活质量的影响

目的:探讨心理干预措施对高血压合并脑梗塞患者负性情绪及生活质量的影响。方法:本次选择的研究对象共92例,均为住院的高血压合并脑梗塞患者,采用简单随机分组方法,分为干预组和对照组,每组46例。对照组给予常规治疗及护理,干预组在对照组的基础上给予心理干预。在入组时、入组后1个月采用抑郁自评量表(SDS)、焦虑自评量表(SAS)、症状自评量表(SCL一90)作为测评工具,测评两组患者干预前后负性情绪和生活质量情况。结果:入组时两组患者的SDS评分、SAS评分及SCL-90各项分值比较差异无统计学意义(P0.05);干预治疗1个月后干预组较对照组患者的SDS评分、SAS评分及SCL-90各项分值均降低,差异有统计学意义(P0.05)。结论:心理干预不仅能缓解患者抑郁焦虑等负性情绪,而且有利于患者生活质量的提高。     

入院时血清钙水平与高血压性脑出血血肿体积、神经功能及预后的关系研究

摘要 目的：探讨入院时血清钙水平与高血压性脑出血血肿体积、神经功能及预后的关系。方法：选择2018年9月-2020年4月我院收治的高血压性脑出血患者102例,根据患者入院时血清钙水平将其分为低血钙组（血清钙<2.1 mmol/L, n=34）、正常血钙组（2.1 mol/L≤血清钙≤2.7 mmol/L, n=39）和高血钙组（血清钙>2.7 mmol/L, n=29）,比较各组性别、血肿体积、入院美国国立卫生研究院卒中量表（NIHSS）评分等临床资料。所有患者随访1年,观察患者格拉斯哥预后量表（GOS）评分,根据患者预后情况将患者分为预后良好组（n=84）和预后不良组（n=18）,比较两组血清钙、血肿体积、入院NIHSS评分、GOS评分。应用受试者工作特征（ROC）曲线分析血清钙水平对患者预后的预测价值。结果：三组血肿体积、入院NIHSS评分、GOS评分、1年病死率、1年再出血率、总预后不良率比较有统计学差异（P<0.05）。预后不良组血清钙水平、GOS评分显著低于预后良好组,血肿体积、入院NIHSS评分显著高于预后良好组（P<0.05）。Pearson相关性分析显示：高血压性脑出血患者入院时血清钙水平与脑出血血肿体积、入院NIHSS评分呈负相关,与GOS评分呈正相关（P＜0.05）。ROC曲线分析显示入院时血清钙预测高血压脑出血不良预后的曲线下面积为0.129（95%CI：0.073~0.179）。结论：高血压性脑出血患者入院时血清钙水平与血肿体积、神经功能及预后存在一定关联,且入院时血清钙对高血压性脑出血不良预后具有一定预测价值。     

肾康注射液对伴高同型半胱氨酸血症高血压肾病患者肾功能和心功能的影响

目的:探讨肾康注射液对伴高同型半胱氨酸血症的高血压肾病患者心、肾功能的影响。方法:采用随机数字表法将76例高血压肾病伴高同型半胱氨酸血症患者随机分成研究组和对照组,每组各38例。两组均予以常规治疗措施,研究组则在上述基础上联合肾康注射液方案,持续治疗4周。观察比较两组治疗前后肾功能指标[血肌酐(SCr)、血尿素氮(BUN)、内生肌酐清除率(Ccr)]、肾损伤标志物[血清β2-微球蛋白(β2-MG)、血清胱抑素C(Cys-C)]、心功能指标[左室射血分数(LVEF)、心室舒张期末内径(LVIDd)、左心室收缩末期内径(LVIDs)]、炎性因子[C反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)]及动脉粥样硬化危险因子[同型半胱氨酸(Hcy)、内皮素]水平及不良反应的发生情况。结果:治疗4周后,两组患者部分肾功能指标(SCr、BUN)、肾损伤标志物(血清β2-MG、血清Cys-C)、部分心功能指标(LVIDd、LVIDs)、炎性因子(CRP、TNF-α、IL-6)及动脉粥样硬化危险因子(Hcy、内皮素)水平均较治疗前明显降低,且研究组以上指标均显著低于对照组(P均0.05);LVEF及Ccr水平则较治疗前明显提升,且研究组以上指标均显著高于对照组,差异均有统计学意义(P均0.05)。两组患者均无不良反应发生(P0.05)。结论:肾康注射液用于高血压肾病伴高同型半胱氨酸血症患者的临床治疗对延缓其肾损伤进程、改善患者心、肾功能及降低动脉粥样硬化形成风险等具有积极意义。     

微创颅内血肿清除术治疗高血压脑出血的效果分析

目的:探讨微创颅内血肿清除术在高血压脑出血治疗中的应用效果。方法:选择我院收治的80例高血压脑出血患者(2014年12月至2015年12月),通过随机数字表将其分为实验组和对照组。在患者知情同意基础上,实验组患者(42例)采用微创颅内血肿清除术进行治疗,而对照组患者(38例)使用开颅血肿清除术进行治疗。观察并比较两组患者治疗前后颅内压、GCS评分(格拉斯哥昏迷评分)、神经功能,同时对两组患者治疗有效性以及安全性进行评价。结果:治疗前,两组患者颅内压、神经功能以及GCS评分无明显差异性(P0.05),而治疗后,实验组患者上述指标值明显优于对照组,且差异性明显(P0.05)。实验组患者总有效率明显高于对照组(P0.05),而不良反应发生率却低于对照组(P0.05)。结论:颅内血肿清除术治疗高血压脑出血不仅能有效降低颅内压,改善患者神经功能及其昏迷症状,并且安全性较高。     

颅内压参数联合血清caveolin-1、AQP-4对高血压脑出血患者术后预后不良的预测价值

摘要 目的：探讨颅内压参数联合血清小窝蛋白-1（caveolin-1）、水通道蛋白4（AQP-4）对高血压脑出血（HICH）患者术后预后不良的预测价值。方法：选择2020年1月至2022年1月河北省胸科医院收治的106例HICH患者,术后随访3个月,根据格拉斯哥预后（GOS）评分将患者分为预后良好组（55例）,预后不良组（51例）。术后监测颅内压参数[压力反应指数（PRx）、平均颅内压波幅（MWA）、20 mmHg阈值下颅内压剂量（Dicp20）],检测血清caveolin-1、AQP-4水平。多因素Logistic回归分析HICH患者术后预后不良的因素。受试者工作特征曲线（ROC）分析颅内压参数联合血清caveolin-1、AQP-4预测HICH患者术后预后不良的价值。结果：预后不良组PRx、MWA、Dicp20以及血清caveolin-1、AQP-4水平高于预后良好组（P＜0.05）。低术前格拉斯哥昏迷评分（GCS）评分、高PRx、高Dicp20、高caveolin-1、高AQP-4是HICH患者术后预后不良的危险因素（P＜0.05）。联合PRx、Dicp20、caveolin-1和AQP-4预测HICH患者术后3个月预后不良的的曲线下面积为0.823,大于PRx、Dicp20、caveolin-1和AQP-4单独预测。结论：高PRx、Dicp20、caveolin-1、AQP4是HICH患者术后预后不良的危险因素,联合颅内压参数PRx、Dicp20及血清caveolin-1、AQP4预测HICH患者术后预后不良具有较高的价值。     

19F NMR measurements of NO production in hypertensive ISIAH and OXYS rats

Recently we demonstrated the principal possibility of application of 19F NMR spin-trapping technique for in vivo *NO detection [Free Radic. Biol. Med. 36 (2004) 248]. In the present study, we employed this method to elucidate the significance of *NO availability in animal models of hypertension. In vivo *NO-induced conversion of the hydroxylamine of the fluorinated nitronyl nitroxide (HNN) to the hydroxylamine of the iminonitroxide (HIN) in hypertensive ISIAH and OXYS rat strains and normotensive Wistar rat strain was measured. Significantly lower HIN/HNN ratios were measured in the blood of the hypertensive rats. The NMR data were found to positively correlate with the levels of nitrite/nitrate evaluated by Griess method and negatively correlate with the blood pressure. In comparison with other traditionally used methods 19F NMR spectroscopy allows in vivo evaluation of *NO production and provides the basis for in vivo *NO imaging.     

Exposure to stress differential vascular adaptive response in spontaneously hypertensive and Wistar rats: Role of nitric oxide, and prehypertensive and hypertensive states

Stress-induced vascular adaptive response in SHR was investigated, focusing on the endothelium. Noradrenaline responses were studied in intact and denuded aortas from 6-week-old (prehypertensive) and 14-week-old (hypertensive) SHR and age-matched Wistar rats submitted or not to acute stress (20-min swimming and 1-h immobilization 25 min apart), preceded or not by chronic stress (2 sessions 2 days apart of 1-h day immobilization for 5-consecutive days). Stress did not alter the reactivity of denuded aorta. Moreover, no alteration in the EC50 values was observed after stress exposure. In intact aortas, acute stress-induced hyporeactivity to noradrenaline similar between strains at both age. Chronic stress potentiated this adaptive response in 6- and 14-week-old Wistar but not in 6-week-old SHR, and did not alter the reactivity of 14-week-old SHR. Maximum response (g) in intact aortas [6-week-old: Wistar 3.25+/-0.12, Wistar/acute 1.95+/-0.12*, Wistar/chronic 1.36+/-0.21*(+), SHR 1.75+/-0.11, SHR/acute 0.88+/-0.08*, SHR/chronic 0.85+/-0.05*; 14-week-old: Wistar 3.83+/-0.13, Wistar/acute 2.72+/-0.13*, Wistar/chronic 1.91+/-0.19*(+), SHR 4.03+/-0.17, SHR/acute 2.26+/-0.12*, SHR/chronic 4.10+/-0.23; inside the same strain: *P < 0.05 relate to non-stressed rat, +P < 0.05 related to acute stressed rat; n = 6-18]. Independent of age and strain, L-NAME and endothelium removal abolished the stress-induced aorta hyporeactivity. CONCLUSION: The vascular adaptive response to stress is impaired in SHR, independently of the hypertensive state. Moreover, this vascular adaptive response is characterized by endothelial nitric oxide-system hyperactivity in both strains.     

Proteome changes in the myocardium of experimental chronic diabetes and hypertension: role of PPARα in the associated hypertrophy

Diabetes with or without the presence of hypertension damages the heart. However, there is currently a lack of information about these associated pathologies and the alteration of linked proteins. For these reasons, we were interested in the potential synergistic interaction of diabetes and hypertension in the heart, focusing on the proteome characterization of the pathological phenotypes and the associated hypertrophic response. We treated normotensive and spontaneously hypertensive (SHR) rats with either streptozotocin or vehicle. After 22 weeks, type-I diabetic (DM1), SHR, SHR/DM1 and control left-ventricles were studied using proteomic approaches. Proteomics revealed that long-term DM1, SHR and SHR/DM1 rats exhibited 24, 53 and 53 altered proteins in the myocardia, respectively. DM1 myocardium showed over-expression of apoptotic and cytoskeleton proteins, and down-regulation of anti-apoptotic and mitochondrial metabolic enzymes. In both SHR and SHR/DM1 these changes were exacerbated and free fatty-acid (FFA) ß-oxidation enzymes were additionally decreased. Furthermore, SHR/DM1 hearts exhibited a misbalance of specific pro-hypertrophic, anti-apoptotic and mitochondrial ATP-carrier factors, which could cause additional damage. Differential proteins were validated and then clustered into different biological pathways using bioinformatics. These studies suggested the implication of FFA-nuclear receptors and hypertrophic factors in these pathologies. Although key ß-oxidation enzymes were not stimulated in DM1 and hypertensive hearts, peroxisome proliferator-activated receptors-α (PPARα) were potentially activated for other responses. In this regard, PPARα stimulation reduced hypertrophy and pro-hypertrophic factors such as annexin-V in high-glucose and angiotensin-II induced cardiomyocytes. Thus, activation of PPARα could reflect a compensatory response to the metabolic-shifted, apoptotic and hypertrophic status of the hypertensive-diabetic cardiomyopathy.