衰老心脏的临床意义

心血管疾病是老年人死亡的主要原因。本文综述老年人心血管疾病的发病情况,讨论衰老心脏的临床意义。已知随年龄增长静息输出量每年下降1％,最大耗氧量每10年下降5～10％。老年人对药物比年轻人更敏感和更容易出现副作用。本文对老年人心血管药物的应用,老年人冠心病的手术适应症及其并发症,以及与衰老心脏有关的高血压性心脏病、心脏淀粉样变、心肌病、瓣膜钙化、衰老的心电图改变等作了深入的阐述。     

呼吸困难的病理生理

呼吸困难为呼吸费力或喘不过气的感觉,是病人的通气反应能力不能满足需求时产生的呼吸不适、胸部紧束、呼吸费劲和空气不足或窒息的痛苦感觉。因此,呼吸困难不同于呼吸急促或通气增加而是一个主观症状。实际上呼吸困难也有其客观变化,可根据病人的呼吸频率、深度和节律变化,以及是否用力呼吸和动用呼吸辅助肌,观察是否存在呼吸困难。不过正常人只有在剧烈运动时,或缺乏锻炼者在中度活动时有可能发生呼吸困难,而病人则在休息时或轻度活动时就会感觉呼吸困难。一、呼吸困难的病因呼吸困难可发生于不同系统疾病,最常见于心、肺疾病患者。(1)循环系疾病:如充血性心衰、心包积液、卵园孔未闭等。(2)呼吸系疾病:可发生于呼     

休克的病理生理

休克是一种很常见的临床综合征。微循环学说认为:休克是急性循环障碍使组织血液灌流量严重不足,以致各重要生命器官机能代谢发生严重障碍的全身性病理过程。但是,临床实践证明,微循环学说仍不能完全解决休克的防治问题,尤其是机制较为复杂的败血性休克,目前其死亡率仍高达30～80%,而且在有些病情非常严重、甚至已接近死亡的败血性休克的病人其血流仍然正常。因此,八十年代,人们以细胞作为功能单位,对休克的本质及其发生,发展规律进行了大量的研究。提出:休克是在     

排便的生理和便秘的病理生理

慢性便秘可以看作是不同病理生理过程的最终症状表现 ,其胃肠运动主要出现以下病理生理变化 :( 1)结肠运动功能异常 :表现为运动亢进、减弱、不协调。结肠非推进性收缩幅度、频率增加 ,肠传输时间延长 ,肠内容物水分吸收过多 ,粪便干燥 ;结肠推进性收缩的幅度频率减少、结肠蠕动无力 ,肠传输时间增加 ,粪便无法正常推送至直肠 ;不协调运动 ,结肠某一部分收缩增强、逆向蠕动 ,影响传输时间 ;( 2 )直肠运动异常 :直肠张力下降 ,顺应性增加 ,感觉功能下降 ;( 3 )肛门括约肌功能异常 ;( 4 )盆底肌群收缩功能下降 ,持续收缩、不协调收缩或松弛。本文对排便的生理和便秘的病理生理进行综述     

肺栓塞的病理生理

肺栓塞是内源性或外源性栓子堵塞肺动脉或其分支引起肺循环障碍的临床和病理生理综合征。目前对肺栓塞的病理生理学改变已有广泛研究 ,其病理生理学变化复杂多变 ,主要是影响呼吸系统、血流动力学[1 4 ] 及血管内皮功能[5,6 ] ,从而产生一系列心肺功能异常及血管内皮功能改变。影响程度主要取决于既往是否患有心肺血管疾病、肺动脉堵塞的范围及速度。一、血流动力学改变及血管内皮功能影响发生急性肺栓塞时 ,栓子堵塞肺动脉 ,造成机械性肺毛细血管前动脉高压 ,肺血管床减少 ,肺循环阻力增加 ,肺动脉压力上升 ,右心室负荷增加 ,心输出量下降…     

昼夜节律和血压控制：生理和病理生理因素

本文综述了影响血压变异的生理，行为和病理生理因素，高血压和其他疾病时血压变异的临床和预后意义，抗高血压治疗对于血压变异的影响和靶器官的保护。     

糖尿病肾病的病理生理和病理

糖尿病肾病（ＤＮ）是糖尿病的主要长期并发症之一,其发病机理复杂,遗传易感性和长期高血糖状态导致的一些细胞因子及（或）生长因子的增多等因素可能参与其病理生理的改变。高血糖引起肾小球细胞外基质（ＥＣＭ）生成增多,降解减少及ＥＣＭ积聚导致的肾小球损伤,即为...     

充血性心力衰竭的病理生理研究进展

充血性心力衰竭(CHF)是临床上常见的综合征,在其发生及发展的过程中,由于心排血量下降,组织氧供不足,促使机体动员各种储备力量进行代偿。这些代偿机制在一定程度上可使受损的心功能得以补偿,但是代偿过度往往又加重心脏负荷使心排血量反而下降,形成恶性循环。对于CHF的极其复杂的病理生理过程的研究从未间断过。近十年来,在这一领域中取得了较大的进展,不少的研究成果已对临床提高防治CHF的水平起着重要的指导作用。以下就几个重要方面的研究进展作一简要的介绍。一、心脏工作性能的研究现况心脏的功能传统上用每搏血量、心排血量及血压等血流动力学指标进行衡量,而这些血流动力学效应乃是心肌收缩过程的表现。心脏在执行其泵血     

核因子κB在脑缺血病理生理过程中的作用

核因子κB(NF—κB)是一种广泛存在、功能多样的核转录因子，国内外对其在缺血性脑血管病中作用的研究方兴未艾。文章就近几年关于NF—κB在脑缺血病理生理过程中的作用作了综述。     

Pathophysiology of the aging kidney

It is the alterations in renal function associated with age that necessitate physicians treating geriatric patients to have an understanding of the fragile senescent kidney. This article examines the physiologic impact of the aging kidney on homeostasis and includes a discussion of altered pharmacodynamics occurring with impaired renal function. We also discuss the limitations of various quantitative methods of measuring renal function and present several "bedside techniques" for the assessment of renal function.     

Pathophysiology of the atherogenic process

Atherosclerosis is conceptually defined as the result of a multiplicity of interactive cascades among injurious stimuli and the healing responses of the arterial wall, occurring concurrently within a hyperlipidemic environment. In this discussion, the inflammatory nature of the disease is emphasized. Four aspects of the pathophysiology of atherogenesis are addressed: (1) The role(s) of fluid mechanical or hemodynamic stresses in the focal initiation and/or augmentation of lesions is discussed in terms of the influence of shear stress on endothelial cellular geometry, compliance, membrane anisotropy (r), low-density lipoprotein (LDL)-receptor expression, intracellular potential and replication; (2) mechanisms of blood monocyte recruitment to the arterial intima, including the roles of chemoattractants such as smooth muscle cell-derived chemotactic factor and oxidized LDL; (3) the alternate or "scavenger" receptor pathway of the macrophage and its pivotal roles in foam cell formation and plaque pathogenesis; and (4) the emerging significance of various lipoprotein modifications, and in particular, the oxidative modification of LDL, which facilitates the uptake of the cytotoxic oxidized LDL via the scavenger receptor, thus providing a non-down-regulating mechanism for foam cell formation and plaque development. Evidence indicates that the antioxidant drug probucol prevents the oxidative modification of LDL, thereby retarding atherogenesis independently of cholesterol reduction.     

Reducing equivalents in the aging process

Reducing equivalents may play a major role in the aging process. These metabolites are responsible for the endogenous redox potential in the living cell which is kept under tight regulation. Among their various roles is the ability to donate electrons to reactive oxygen species and by doing so to scavenge them. Most of the reducing equivalents in the cell are molecules with low molecular weights, such as glutathione and NADH which are synthesized by the cell. Other members of this group, such as uric acid are produced as waste products, while others, such as ascorbic acid and tocopherol, are derived from the diet. We studied the role of these equivalents in the aging process in various rat tissues. We demonstrated that the reducing power of a tissue may reflect its antioxidant activity. We used cyclic voltammeter methodology in order to evaluate the overall reducing power of tissue homogenates and other biological fluids. It was found that reducing power changes during the aging process in a bell-shaped manner in liver, lungs and kidneys, but not in heart and brain. We also showed that skin possesses strong reducing power which decreases dramatically with age. A non-invasive procedure to evaluate the oxidation status and the antioxidant activity of skin was developed. Using this method we demonstrated that there is an accumulation of organic peroxide in old skin compared to young skin, supporting the free radical hypothesis of aging.     

Telomerase and the aging process

The level of telomerase activity is important in determining telomere length in aging cells and tissues. Here evidence on the importance of telomerase activity is reviewed with respect to aging rates of mammalian species and the health and life span of individuals within a species. The significance of telomerase reactivation for both cancer development and for immortalizing cells for therapeutic processes is assessed.     

The aging process

The intricate cause of the aging process in humans and animals, at present a matter of intense speculation, has given rise to many theories. Despite its uncertain cause, aging constitutes the most significant and universal problem confronting physicians today. Age-related physiologic deterioration and age-associated diseases are of immense concern to physicians because of the "old-age boom" anticipated in the first part of the twenty-first century. Biomedical research achievements in the twentieth century have permitted more persons to approach the fixed upper limit of the human lifespan. We discuss the functional decline of the aging heart and the underlying mechanisms of that decline; quantitative and qualitative changes in the immune system; and normal aging of the human brain contrasted to the brain changes seen in Alzheimer disease. With our growing geriatric population, we greatly need to increase our understanding of both the causes of human aging and the goals of gerontology and geriatrics and to expand research into the significant problem of Alzheimer disease.     

Enteral resorption kinetics in the aging process

With growing age functional and morphological changes in the alimentary tract appear. The age dependence of the intestinal absorption was investigated with the help of the modified D-xylose absorption test. By means of a graphic-mathematical evaluation of the blood level kinetics of D-xylose after oral and intravenous application the absorption rapidity (constant k12), the temporary position of the relative maximum of the D-xylose concentrations in the blood serum after oral application (time tm) and the size of the relative absorption of the small intestine were established depending on the time RR (t). Within the age range of 3 to 96 years it has been proven that a slowing down of the enteral absorption occurred with growing age. By prolonging the period during which the food components are absorbed in the small intestine (shift of tm towards later times) the old organism is just as capable of complete absorption as is the young one, even though the absorption processes take place at a slower rate. Absorption disorders in old age are due to morbidity and not, sui generis, to involution.