Weak beta-adrenoceptor-mediated relaxation in the human internal mammary artery

The function of beta-adrenoceptors in the human internal mammary artery was studied in vitro to predict the way in which the internal mammary artery graft would respond to beta-adrenergic agonists and antagonists given in the perioperative period. Ring segments of the distal internal mammary artery obtained from patients not receiving beta-blocker therapy were mounted in organ baths and isometric wall force was measured. For comparison, similar experiments were conducted on segments of canine coronary artery, a vessel known to have powerful beta-adrenoceptor function. All arteries were precontracted with potassium or the thromboxane mimetic agent, U46619, before isoproterenol cumulative concentration-relaxation curves were constructed. In the human internal mammary artery, the maximum relaxation induced by isoproterenol was only 14% of the potassium-induced contraction and 24% of the U46619-induced contraction. These responses were weak compared with 54% and 86% for beta-adrenoceptor relaxation measured in corresponding experiments in the canine coronary artery. In all experiments, propranolol antagonized the relaxation induced by isoproterenol. These studies suggested that the human internal mammary artery has only a small number of beta-adrenoceptors. We conclude that beta-adrenoceptors would contribute little to the reactivity of the human internal mammary artery graft to sympathomimetic drugs.     

Comparison of the metabolic response of the hypertrophic and the normal heart to hypothermic cardioplegia. The effect of temperature

The aim of this study was to test for metabolic differences in the response of hypertrophic and normal hearts to hypothermic cardioplegia. Hypertrophic dog hearts and normal control hearts were subjected to 6 hours of hypothermic cardioplegia with the St. Thomas' Hospital solution. Levels before arrest of subepicardial and subendocardial adenosine triphosphate, creatine phosphate, and lactate in eight hypertrophic hearts were the same as those levels in 12 normal hearts. In hypertrophic hearts, but not in normal hearts, the induction of arrest was slow and was associated with an 11% increase in adenosine triphosphate levels, a 59% decrease in creatine phosphate levels, and a 12-fold increase in lactate levels. Seven hypertrophic hearts and eight normal hearts were studied during 6 hours of arrest and showed no further differences in metabolic response. Reducing the myocardial temperature from 20 degrees C to 12 degrees C slowed the rate of depletion of adenosine triphosphate and the rate of accumulation of lactate in both groups. We conclude that in the nonfailing, severely hypertrophic heart, levels before arrest of high-energy phosphates and lactate are normal, but that marked biochemical changes may occur if the induction of arrest is prolonged because of underdosing with cardioplegic solution. Cooling from 20 degrees C to 12 degrees C improves myocardial preservation in both hypertrophic and normal hearts.     

体表高频超声技术评价家兔血管成形术后再狭窄模型与病理学结果的相关性

目的:分析体表高频超声检测家兔血管内球囊成形术后再狭窄程度与组织病理学分析的相关性。评估体表超声检测的可行性、可靠性及应用价值。方法:实验于2002-03/2003-12在北京中医药大学中医内科学重点学科实验室完成。①日本大耳白兔26只,随机分为正常组10只、假手术组6只、模型组10只。②模型组电刺激兔颈总动脉,电流1.2mA,刺激12～15min,术后第2天喂饲高脂饲料共8周,假手术组仅剥离颈总动脉,不做电刺激,喂高脂饲料,正常组不施加任何干预因素。③模型组和假手术组根据B超选择颈总动脉有斑块或血流明显改变者行球囊血管内成形术。分别于电刺激后8周、血管成形术后4周行超声检查动脉内径和动脉内膜厚度。④所有动物于血管成形术后4周处死取材,进行病理学半定量分析,并与超声测量结果进行相关分析。结果:进入结果分析数量24只,正常组中途死亡1只,原因为牙齿畸型影响进食。模型组1只因电刺激8周时超声评价颈动脉未形成斑块及血流无明显改变而剔出实验。①超声检测电刺激8周时正常组内膜厚为(0.028±0.004)cm,模型组管壁明显增厚(0.043±0.014)cm,差异有显著性(P<0.05),至血管成形术后膜厚增加更明显(0.064±0.002)cm,内径稍有扩大,但差异不显著。②超声检测模型组颈动脉内径与膜厚的测量结果与病理学测量结果呈正相关关系(OR=0.361,P<0.05;OR=0.526,P<0.01),病理狭窄率与超声是否检测到斑块呈正相关关系(OR=0.796,P<0.01)。结论:体表高频超声在评价家兔颈动脉狭窄诊断中有一定应用价值,与病理学半定量分析结果相关性良好。     

慢性乙型肝炎患者及其配偶心理状况

目的:认识慢性乙型肝炎患者及其配偶心理健康、生活质量及心理治疗的相关研究现状。资料来源:检索维普期刊全文数据库和中国医院知识仓库(CHKD期刊全文库)1985-01/2006-01有关乙型肝炎与心理方面的文献,检索词为"生活质量,乙型肝炎,心理健康,心理干预,配偶",并限定语言种类为中文;检索Pubmed数据库同期相关文献检索词为"CHB,quality of life,psychology health",并限定语言种类为英语。其他文章查找具体书籍或杂志获得原文。资料选择:对资料进行初审,选择与乙型肝炎患者及配偶心理健康、生活质量及心理治疗等相关的文章。纳入标准:阐述详细,文章内容较新,有助于说明问题的文章。排除标准:去除重复性研究和一般了解性的文章。资料提炼:共收集到204篇文章及2本相关书籍,符合纳入标准的文章48篇,排除158篇。资料综合:慢性乙型肝炎是一种身心疾病,其发病机制复杂,除与病原和免疫因素有关外,心理社会因素起重要作用。同时,与之共同生活的慢性乙型肝炎患者配偶承受了巨大的心理压力,存在许多心理障碍,即夫妇的心理症状可交互影响。心理治疗对于乙型肝炎患者是必要的。结论:慢性乙型肝炎患者及其配偶存在严重的心理问题,心理治疗能取得一定的疗效。     

Can mupirocin prevent methicillin-resistant <Emphasis Type="Italic">Staphylococcus aureus</Emphasis> infections?

In a retrospective study, Dr Muller and colleagues have assessed the efficacy of mupirocin nasal ointment alongside hygienic measures in methicillin-resistant Staphylococcus aureus (MRSA)-positive patients admitted to the intensive care unit (ICU). Their findings, which suggest that intranasal mupirocin can prevent ICU-related MRSA infections, need confirmation in a well-designed clinical trial. In general: early identification, isolation and treatment of all MRSA carriers, including health care workers, and disinfection of contaminated environments, are the main 'ingredients' of an effective MRSA 'search and destroy' program.     

The impaired tolerance of the recently infarcted rat heart to cardioplegic arrest: the protective effect of orotic acid

After myocardial infarction, a reduced mass of non-infarcted myocardium remains to maintain cardiac output. This acutely stressed, non-infarcted myocardium exhibits many metabolic disturbances, and undergoes a process of acute hypertrophy. These stress-induced disturbances may reduce the tolerance of the heart to the global ischaemia of cardioplegic arrest and may explain the increased mortality and morbidity associated with cardiac surgery in patients with recent myocardial infarction. We postulated that orotic acid, a pyrimidine precursor which augments the rate of protein synthesis during hypertrophy, might improve the response of the recently infarcted heart to cardioplegic arrest. Myocardial infarction was induced in rats by coronary ligation, and after 2 days or 3 days the hearts were excised and perfused on the working heart apparatus. After measurement of work capacity, the hearts underwent 1 hour of hypothermic cardioplegic arrest. Post-arrest function was then measured and expressed as a percentage of the pre-arrest value. A group of sham-operated, non-infarcted hearts served as controls. There were two distinct findings: (1) when subjected to hypothermic cardioplegic arrest 2 days after myocardial infarction, hearts recovered only 49% of pre-arrest function, compared with 80% recovery in non-infarcted controls (P less than 0.001). Three days after infarction, recovery had improved to 68% (P less than 0.01 vs. 2 days, P less than 0.05 vs. non-infarcted). (2) Treatment with oral orotic acid following infarction augmented recovery from cardioplegic arrest to 83%, 2 days after infarction (P less than 0.001 vs. untreated) and to 87%, 3 days after infarction (P less than 0.01 vs. untreated).(ABSTRACT TRUNCATED AT 250 WORDS)