心脏彩超对感染性心内膜炎的诊断意义

目的探讨感染性心内膜炎心脏彩超声像图特点及诊断价值。方法对2003年1月至2010年3月在南宁市第八人民医院住院的25例感染性心内膜炎患者的心脏彩超声像图特征进行分析。结果 25例均探及瓣膜上赘生物,其中二尖瓣上赘生物9例,主动脉瓣上赘生物8例,室间隔缺损右室面赘生物5例,三尖瓣上赘生物2例,肺动脉瓣上赘生物1例,两个瓣膜同时有赘生物的有8例;赘生物最大20mm×13mm,最小3mm×3mm,其中15例有基础心脏病变。结论心脏彩超对感染性心内膜炎赘生物的诊断及定位,以及心脏基础病的诊断,对治疗的决策及预后判断均有重要意义。     

感染性心内膜炎与脑栓塞

感染性心内膜炎由多种病原微生物引起, 20%～40%的患者可同时合并神经系统并发症,其中又以脑栓塞发生率居多,严重影响患者预后。其诊断和治疗均需多科合作,多数病例需要接受心脏外科手术。本文就感染性心内膜炎合并脑栓塞的发病机理、诊断、治疗及近年来的研究进展作一回顾。     

感染性心内膜炎的超声诊断价值

目的:探讨超声心动图(UCG)对感染性心内膜炎(IE)的诊断价值。方法:对2005年—2007年住院的8例感染性心内膜炎患者彩色多普勒超声心动图特征进行分析。结果:8例中6例有基础心脏病变,包括先天性心脏病、瓣膜钙化、瓣叶脱垂。结论:超声心动图可发现基础心脏病、赘生物,对感染性心内膜炎的诊断具有重要价值。     

超声心动图在感染性心内膜炎诊断中的应用

近年来，感染性心内膜炎由于其易感人群、致病微生物的变化、临床表现的多样性及临床医生对该病的认识不足等因素，使得该病的临床诊断阳性率低。而超声心动图在临床上的广泛应用，为临床诊断感染性心内膜炎提供了重要依据。本文回顾性总结了15例感染性心内膜炎患者的临床和超声资料，现报告如下。     

超声心动图在感染性心内膜炎诊断中的应用

目的探讨超声心动图在感染性心内膜炎中的诊断及临床价值。方法总结36例经手术证实的感染性心内膜炎术前超声心动图资料与术中资料进行比较,结果超声心动图对赘生物的大小、位置及数量的判断与术中基本一致;且超声心动图还可发现心脏有无基础病变及由感染性心内膜炎导致的新的心脏血流动力学改变。结论超声心动图对感染性心内膜炎赘生物能进行准确定位,并确定其数目、大小及伴随的心脏病情况,为临床诊断及治疗提供可靠的依据。     

超声心动图诊断感染性心内膜炎赘生物的价值

目的探讨感染性心内膜炎赘生物的超声心动图特点及临床价值。方法对本院16例感染性心内膜炎（IE）患者做超声心动图检查,结合临床资料进行分析。结果超声心动图对赘生物附着的部位、大小、数量和有关血流动力学改变与术中基本一致,而且可以发现有没有心脏基础的病变和是否出现并发症。结论超声心动图诊断感染性心内膜炎并赘生物的准确率高,可以对感染性心内膜炎的临床诊断及治疗提供可靠依据。     

感染性心内膜炎61例临床分析

目的了解笔者所在医院感染性心内膜炎的临床特点、病原菌及药敏情况,以指导临床治疗。方法回顾性分析笔者所在医院61例感染性心内膜炎患者的临床资料。结果 61例患者均有心脏基础疾病,其中先天性心脏病18例(29.51%),冠状动脉粥样硬化性心脏病、风湿性心瓣膜病各13例(各占21.31%),老年性心脏瓣膜病12例(19.67%),其他5例(占8.20%);人工瓣膜心内膜炎10例(16.39%)。发热、贫血和心功能不全为最常见的临床表现和首发症状。超声心动图检查发现心脏瓣膜病变51例(83.61%),最常见部位依次为二尖瓣、三尖瓣、主动脉瓣、肺动脉瓣;发现赘生物39例(63.93%),单一瓣膜受累的赘生物好发部位依次为二尖瓣(14例),主动脉瓣(13例);多个瓣膜同时受累中以二尖瓣和主动脉瓣最常见,有3例。61例血细菌培养阳性率为39.34%(24/61),其中革兰阳性细菌占绝对优势为83.33%(20/24),链球菌仍为主要致病菌。经验性抗菌治疗中,抗阴性菌为主者40例(65.57%),抗阳性菌为主者14例(22.95%)。本病死亡率高达14.75%,心功能不全和严重感染为常见原因。结论感染性心内膜炎瓣膜或心脏病变多样,临床表现特异性差,应引起足够重视。及时完善相关特殊检查,早明诊断,减少误诊;初始抗菌治疗仍以抗阳性菌的杀菌剂为主,及时的手术治疗亦同样重要。     

感染性心内膜炎 38 例分析

本文通过分析３８例感染性心内膜炎的临床资料，结果显示：以头病、偏瘫及胸痛、咳嗽、肺部急性炎症为突出表现者易掩盖本病诊断。超声心动图（ＵＣＧ）检查发现心瓣膜赘生物对诊断具有重要价值。治疗后其赘生物缩小和消失与否不能做为观察和判断疗效的可靠指标，应结合临床及其它实验室检查综合分析。     

感染性心内膜炎的外科治疗

目的 分析感染性心内膜炎的诊断、手术时机和疗效。方法 7例感染性心内膜炎均接受手术治疗。合并先天性心脏病1例,风湿性心脏病4例。术前均经抗菌治疗2周以上。血培养阳性2例,均为链球菌。超声心动图发现赘生物6例,脾脓肿1例。手术中清除所有病灶,同期瓣膜置换6例,心内畸形矫治1例。结果 术后死亡2例。术后并发症包括急性肾功能衰竭1例、脑出血1例及瓣周漏1例,其他患者随访至今无心内膜炎复发,心功能改善。结论 感染性心内膜炎早期诊断,适时外科手术和内外科联合治疗是治疗成功的关键。     

感染性心内膜炎的药物治疗

感染性心内膜炎为心血管临床常见病之一,临床在对症和抗感染治疗时应在掌握药物治疗原则的基础上,选择合适的药物施治,达到抗感染治愈心内膜炎的目的。本文通过归纳感染性心内膜炎临床药物治疗则,总结感染性心内膜炎的药物选用,从而给临床用药提供参考。感染性心内膜炎的药物治疗@廖志坚$广东省深圳市孙逸仙心血管医院!深圳518001     

阿司匹林对环磷酰胺大鼠皮质骨的影响

目的探讨环磷酰胺致大鼠骨质疏松模型中皮质骨的特点,观察中、低剂量阿司匹林的预防作用,并与碳酸钙维D进行比较。方法 3月龄SD大鼠灌服环磷酰胺4.5 mg.kg-1.d-1造模,同时给予中、低剂量阿司匹林和碳酸钙维D进行预防,用药时间为15 d。实验结束后,骨组织形态计量学观测左侧胫骨中段骨磨片的动静态参数。同时取大鼠右侧股骨进行骨生物力学检测,随后检测骨钙、磷、镁和羟脯氨酸含量。结果环磷酰胺通过抑制骨形成活性,使大鼠皮质骨骨髓腔扩大,管壁变薄,骨有机质和无机物等比例丢失,骨质量降低。中、低剂量的阿司匹林可有效促进骨形成,对抗环磷酰胺大鼠的骨丢失,效果与碳酸钙维D相当。低剂量的阿司匹林对于环磷酰胺大鼠骨质量的改善作用最佳。结论中、低剂量的阿司匹林均可有效地促进骨形成,预防环磷酰胺所诱导的大鼠低转换型骨质疏松。     

Effect of aspirin on adrenal weight in female rats.

Daily ingestion of Purina laboratory chow supplemented with 1% powdered aspirin for 25 days caused a marked depression in adrenal weight as well as decreased body weight and ovarian and uterine weight. The action of aspirin on adrenal weight did not appear to be mediated through pituitary-ovarian activity as measured by organ weight indices of sham and hemiovariectomized female rats.     

Effect of aminophylline on aspirin penetration into the central nervous system in rats

This study investigated with the effect of aminophylline on the penetration of aspirin through the blood-brain barrier (BBB) into the central nervous system (CNS) in rats. Acetylsalycylic was injected into the right axillary artery, to avoid the drug affecting the peripheral organs before it reached the CNS. The test animals received subcutaneously (s.c.) aminophylline 30 min before aspirin injection, while the control animals received an equimolar dose of physiological solution s.c. At time intervals of 30, 60, 90, 120, and 240 s after aspirin injection, the animals were decapitated and blood samples from the left jugular vein, as well as samples from the brainstem, cerebellum and left and right cerebral hemispheres, were taken to determine aspirin concentrations in all of them by a standard method. It was found that aspirin concentrations in the CNS were even 30 times lower than in the blood, with the concentrations being higher in the brainstem and cerebellum than in the left and right hemispheres. The presence of aminophylline did not alter aspirin concentrations either in the blood or the brain, and therefore did not affect significantly the aspirin penetration through the BBB into the CNS.     

Effect of Helicobacter pylori on delay in ulcer healing induced by aspirin in rats

Experiments were performed to characterize the pharmacology of SCH 206272 [(R,R)-1'[5-[(3,5-dichlorobenzoyl)methylamino]-3-(3,4-dichlorophenyl)-4(Z)-(methoxyimino)pentyl]-N-methyl-2-oxo-[1,4'bipiperidine]-3-acetamide] as a potent and selective antagonist of tachykinin (NK) NK(1), NK(2), and NK(3) receptors. SCH 206272 inhibited binding at human tachykinin NK(1), NK(2), and NK(3) receptors (K(i) = 1.3, 0.4, and 0.3 nM, respectively) and antagonized [Ca(2+)](i) mobilization in Chinese hamster ovary (CHO) cells expressing the cloned human tachykinin NK(1), NK(2), or NK(3) receptors. SCH 206272 inhibited relaxation of the human pulmonary artery (pK(b) = 7.7 +/- 0.3) induced by the tachykinin NK(1) receptor agonist, [Met-O-Me] substance P and contraction of the human bronchus (pK(b = 8.2 +/- 0.3) induced by the tachykinin NK(2) receptor agonist, neurokinin A. In isolated guinea pig tissues, SCH 206272 inhibited substance P-induced enhancement of electrical field stimulated contractions of the vas deferens, (pK(b = 7.6 +/- 0.2), NKA-induced contraction of the bronchus (pK(b) = 7.7 +/- 0.2), and senktide-induced contraction of the ileum. In vivo, oral SCH 206272 (0.1-10 mg/kg, p.o.) inhibited substance P-induced airway microvascular leakage and neurokinin A-induced bronchospasm in the guinea pig. In a canine in vivo model, SCH 206272 (0.1-3 mg/kg, p.o.) inhibited NK(1) and NK(2) activities induced by exogenous substance P and neurokinin A. Furthermore, in guinea pig models involving endogenously released tachykinins, SCH 206272 inhibited hyperventilation-induced bronchospasm, capsaicin-induced cough, and airway microvascular leakage induced by nebulized hypertonic saline. These data demonstrate that SCH 206272 is a potent, orally active tachykinin NK(1), NK(2), and NK(3) receptor antagonist. This compound may have beneficial effects in diseases thought to be mediated by tachykinins, such as cough, asthma, and chronic obstructive pulmonary disease.     

Antipyretic testing of aspirin in rats

A reproducible antipyretic test method has been developed to assay low doses of po administered aspirin in rats. Rectal temperatures recorded 19–24 hr after a sc injection of 20 ml/kg of an aqueous suspension of brewer's yeast were elevated 1.5 to 2.0°C. Statistically significant antipyresis was demonstrated 15 min after a po dose of 150 mg/kg of aspirin. Maximum effect occurred 120 min post drug. Aspirin, administered po at 5, 25, 50 and 100 mg/kg, exhibited antipyretic activity at all doses. The ED50 values calculated from these data ranged from 10.3 to 21.1 mg/kg. Untreated fevered controls showed no marked temperature variability during the test period.     

Effect of aspirin on prostanoids and nitric oxide production in streptozotocin-diabetic rats with ischemic retinopathy

The importance in experimental diabetic retinopathy of prostacyclin and nitric oxide (NO), as well as the possible effect of acetylsalicylic acid (ASA), are well known. To investigate the effect of two doses of aspirin in the prevention of retinal ischemia in streptozotocin-diabetic rats, we compared nondiabetic rats and diabetic rats after 1, 2 and 3 months of diabetes, and diabetic rats treated with 2 mg or 10 mg ASA/kg per day p.o. from the first day of diabetes.The parameters determined after 1, 2 and 3 months of development were platelet aggregation, thromboxane B(2) (TxB(2)) production, 6-keto-prostaglandin F(1)(alpha) (stable metabolite of prostacyclin), NO, plasma nitrites/nitrates, and percentage retinal surface occupied by horseradish peroxidase (HRP)-permeable vessels. In diabetic rats platelet aggregation and thromboxane concentration were increased, and prostacyclin, NO and area occupied by HRP-permeable vessels were decreased.Acetylsalicylic acid reduced platelet aggregation, and lowered thromboxane production by 82%-99%. Prostacyclin production was inhibited by 92%-95% with 10 mg ASA/kg per day, and by 8%-20% with 2 mg ASA/kg per day. In diabetic rats NO production increased after 2 and 3 months of treatment to levels seen in nondiabetic rats. The reduction in HRP-permeable retinal surface decreased from a maximum of 87% in DR to 51% after treatment with 2 mg ASA/kg per day, and to 62% after 10 mg ASA/kg per day. We conclude that ASA (2 mg/kg per day and 10 mg/kg per day) increased NO production in streptozotocin-diabetic rats and reduced the degree of retinal ischemia.     

阿斯匹林对Alzheimer病大鼠学习记忆影响及其分子机制

目的　观察阿斯匹林 (aspirin ,As)对喹啉酸损伤海马所致痴呆大鼠学习记忆影响及其分子机制。方法　用立体定位技术对海马CA1区微量注射喹啉酸 (quinolinicacid ,QA)造成Alzheimer病 (AD)大鼠模型 ;Y形迷宫检测大鼠学习记忆能力 ;电子显微镜、流式细胞仪检测海马细胞凋亡 ;原子吸收分光光度计检测海马组织钙离子浓度。结果　阿斯匹林可明显提高喹啉酸所致痴呆大鼠学习记忆水平 ;显著降低其海马细胞凋亡率 ;减少海马组织钙离子浓度。结论　阿斯匹林对AD大鼠的保护作用与钙拮抗、抑制QA诱导海马细胞凋亡有关。     

Effect of verapamil on gastric acid secretion and ulceration by pyloric-ligation and aspirin in albino rats

Verapamil at doses 5, 10, 20 and 40 mg/kg, intraperitoneally (ip) and 40 mg/kg, orally reduced incidence of ulceration by Pyloric-ligation. Similarly verapamil inhibited aspirin-induced ulceration at a dose 40 mg/kg, orally and ip. Effect of verapamil on gastric acid secretion was also studied. At low dose it increased acid secretion significantly (5 mg/kg, ip) and at high dose (40 mg kg, ip and orally) it significantly decreased volume of secretion. This indicates that reduction of acid secretion contributes little to the antiulcer activity of verapamil because antiulcer effect was seen even at doses which did not decrease acid secretion.     

Effects of aspirin on 14C-pirprofen disposition in rats.

The effects of aspirin on 14C-pirprofen disposition in the rat were studied. An oral 60-mg/kg dose of aspirin significantly reduced plasma radioactivity during the 1--8-hr interval after an intravenous 5-mg/kg injection of 14C-pirprofen. The aspirin-treated group had only 69% as much area under the radioactivity curve as the control group. The radioactive material in plasma consisted almost entirely of 14C-pirprofen, as shown by GLC. The plasma clearance of 14C-pirprofen was 7.4 ml/hr for the aspirin-treated group and 5.1 ml/hr for the control group, while the volumes of distribution were 0.32 and 0.20 liter/kg, respectively. The apparent elimination half-life was unchanged at 5.9 hr. 14C-Pirprofen was approximately 98.6% bound to plasma proteins, and the binding decreased to an average of 97.2% in the presence of salicylate. Binding to blood cellular constituents was insignificant. Rats give 14C-pirprofen by intravenous injection without aspirin secreted 36.0--42.8% of the dose radioactivity into bile during 4 hr while a comparable group given 60 mg of aspirin/kg secreted 46.4--70.8%. TLC and GLC demonstrated that the radioactivity in rat bile was 80--90% conjugated 14C-pirprofen. The increased radioactive material secretion into bile was compensated in the intact rat by reabsorption, since the total radioactive material excreted in urine was not changed by aspirin administration.