《伤寒论》“悸”的辨治规律探讨

本文通过对《伤寒论》“心悸”、“心下悸”之病因病理及证治的探讨，认为其发病亦不外乎虚实二因：本脏虚损致悸者为虚，多为心阳不足、心阴心阳俱虚，气血两虚；水气上泛致悸者为实，多表现为本虚标实，由脾肾阳虚、水气凌心所致。另有邪郁少阳、阳郁不达而致悸，多属实证。其治疗，针对其病因病机，归纳为六法，分别给以补虚泄实，标本同治，对现代临床心系疾病的治疗有一定的实用价值。     

治疗肾性贫血的四个经验方

肾性贫血是指肾脏疾病发展到肾功能衰竭时出现的贫血，糖尿病肾病就是其中之一。单纯就肾性贫血而言，大致相当于中医学的血虚证。糖尿病肾病是糖尿病患病日久出现的慢性并发症，从“三消”辨证而言，病属下消，其病机为本虚标实，本虚主要为肝肾之虚，标实为痰瘀浊毒损伤肾络。     

王春林教授治疗冠心病临证经验总结

王春林教授认为冠心病辨证首先要辨明病位,其次要详审病机,冠心病的病机为本虚标实,本虚以气虚、气阴两虚或阳虚为主,标实以痰饮、瘀血、气滞、寒凝多见。治疗上应辨证施治,补虚泻实,标本兼顾。     

王安康活用温胆汤治疗脾胃病

温胆汤系《备急千金要方）｝治大病后胆寒、虚烦不得眠、惊悸不安之经方，由半夏、竹茹、帜实、陈皮、生姜、甘草组成。吾师王安康教授根据异病同治之治则，善长于以此方活用治疗多种脾胃病，所治病例极多，且疗效肯定，现将其经验略述于下。1慢性胆囊炎慢性胆囊炎多由急性胆囊炎发展而来，常与胆石症同时存在。王教授认为，胆囊炎发病日久，或失治或误治，发展为慢性病变。中医辨证为本虚标实之证。本虚表现胆气不足，气阴两虚；标实则表现为气滞血瘀，痰热留恋不去。因此，治疗上应该注意标本兼顾，在清胆和胃的同时，兼以疏肝理气，化瘀…     

脑老化的中医药实验研究进展

祖国医学认为脑老化的基本病机是髓减脑消，神机失用。其证候特征是本虚标实。本虚是精亏髓减、气血不足；标实为痰凝血瘀。近年来，国内学者对中医药延缓脑老化的机理进行了大量的实验研究，现作一概述。     

桥本病的中医辨证论治

桥本病是指甲状腺有弥漫性淋巴细胞浸润、纤维化、实质性萎缩、嗜酸变性，即慢性淋巴细胞性甲状腺炎。本病属于中医学“瘿病”“石瘿”及“气瘿”范畴。瘿病是由于情志内伤、饮食与水土失宜引起，且与体质因素密切相关。初起多属实，病久由实致虚，尤以阳虚、气虚为主，遂成虚实夹杂之证。本病本质为本虚标实，心肝阴虚及脾肾阳虚为本，气滞、血瘀、痰凝为标。     

从风论治心悸

陈晓虎教授认为气血不足、风邪扰心、血脉挛急是心悸病的基本病机,心悸属本虚标实之证,风邪贯穿心悸发病的全过程。初期风邪炽盛,病久风入心络,后期虚风内动。当辨证施治,巧用风药,以益气养血为本,祛风通络为标,兼祛他邪,令邪去正安,心悸则止。     

冠心病心绞痛的中医辨证分析

随着人口老龄化和劳动、饮食结构的改变,冠心病已成为威胁人类健康及导致死亡的主要疾病,其发病率逐年上升.根据临床表现,冠心病心绞痛当属中医学的"胸痹""心痛"范畴.其主要病机为心脉痹阻,基本病机为本虚标实.本虚包括气血阴阳之虚、五脏亏虚.标实为瘀血、痰浊、寒凝、气滞,病位在心.可因虚致实,亦可因实致虚,故临床上以虚中有实、实中有虚、虚实挟杂之证常见.冠心病心绞痛的中医分型包括心血瘀阻、气滞血瘀、痰浊闭阻、气阴两虚、阳气虚衰和寒凝血脉.其中血瘀证、痰浊证、寒凝证、阳脱证和气滞证为临床上常见的危险证型,应根据疼痛的部位和性质进行辨证分析,"急则治其标、缓则治其本",或先祛邪后补虚、或补中有通、或通中寓补、或通补兼施.在中医临床辨证治疗方面,应注重病证结合,以病为系统,病下系证,证下列方,方随证出.     

痹证用药浅析

痹者 ,闭也 ,其主要病理变化是邪阻经络 ,致使肢体、关节发生疼痛、酸楚、重着、麻木、屈伸不利 ,甚则关节肿大。其病机主要是本虚标实 ,机体气血亏虚 ,肝肾不足 ,不能抗邪 ,风寒湿热之邪稽留于关节经络 ,进一步影响到气血津液运行 ,形成痰瘀阻痹。治疗上必须针对病因病机用药     

从虚论治动脉粥样硬化

动脉粥样硬化引起的心脑血管疾病发病率居高不下,严重威胁着病人的生命安全。其基本病机为本虚标实,脏腑气血阴阳亏虚为本,痰瘀热毒之邪兼夹为标。其中,尤以肾虚、气虚、脾虚、阴虚等为关键,因此,临床治疗中应注重补肾健脾、益气养阴等补虚法的运用。现代研究及临床实践亦表明采用补虚治法方药治疗动脉粥样硬化可取得较好疗效。     

Gastric mucosal prostaglandin E2 levels in gastric non-ulcer and ulcer patients with chronic renal failure or without renal disease, and in healthy subjects

Investigations were carried out as to whether a disturbance in the formation of cytoprotective prostaglandin (PG) E2 in gastric mucosa is implicated in chronic renal failure. PGE2-like immunoactivity in gastric mucosal specimens was measured in individuals with chronic renal failure (creatine clearance less than 10 ml/min), in individuals without any renal disease, presenting either gastric ulceration or not, as well as in healthy subjects. Regardless of the group of patients, compared to normal mucosa a significant decrease in PGE2-like immunoactivity (about 50-70%) was found in mucosa from atrophic gastritis but not from superficial gastritis. Whenever patients of the control group or patients with kidney disease suffered from ulcers, PGE2-like immunoactivity showed a decrease of about 60-70% in the non-ulcerated mucosa compared to that of non-ulcer subjects. Moreover, ulcer patients showed the same frequency of gastritis and similar mucosal PGE2-like immunoactivity in their non-ulcerated mucosa. Furthermore, compared to the tissue from the ulcer edge, independent of the presence of renal disease, a relative deficiency of PGE2-like immunoactivity of about 50-60% was detected in the non-ulcerated mucosa of ulcer patients. We therefore conclude that chronic renal failure probably has no impact on PGE2 formation in the gastric mucosa. All told, relative mucosal PGE2 deficiency in gastric ulcer disease seems not to be correlated with chronic renal failure.     

Progression of gastric enterochromaffin-like cells growth in Zollinger-Ellison syndrome and atrophic body gastritis patients

BACKGROUND: Enterochromaffin-like cell hyperplasia of the gastric body mucosa occurs in hypergastrinaemic conditions such as atrophic body gastritis and Zollinger-Ellison syndrome. However, the time course of change or factors involved are not known. AIMS: To compare the rate of change of enterochromaffin-like cell proliferation in patients with atrophic body gastritis and Zollinger-Ellison syndrome. PATIENTS: From a consecutive series of atrophic body gastritis and Zollinger-Ellison syndrome patients, studied at the time of first diagnosis, 10 atrophic body gastritis (4 with pernicious anaemia) and 14 Zollinger-Ellison syndrome (4 with multiple endocrine neoplasia type 1) patients were followed-up for a median time of 48 months. METHODS: At entry and during follow-up patients underwent: plasma gastrin determination, endoscopic sampling of body mucosa for qualitative assessment of enterochromaffin-like cell hyperplasia pattern and degree of glandular atrophy, qualitative and morphometric analyses of body mucosa endocrine cells. RESULTS: At time of diagnosis, enterochromaffin-like cell lesions were more severe in atrophic body gastritis than in Zollinger-Ellison syndrome. During follow-up, no significant variations were observed in gastrin values, enterochromaffin-like cell patterns and grade of body mucosa atrophy in atrophic body gastritis. In contrast, gastrin levels were significantly increased [median 1200 (235-2625) vs 1947 (225-5200) pg/ml; p<0.001)] as was total volume density of enterochromaffin-like cells [median 1.60 (0.53-4.06) vs 3.18 (1.35-21.13)% of mucosal epithelial component; (p<0.005)] in Zollinger-Ellison syndrome. Micronodular hyperplasia of enterochromaffin-like cells, present in only one patient at diagnosis, was observed in 8 Zollinger-Ellison syndrome patients at follow-up. CONCLUSIONS: These data suggest that the progression of enterochromaffin-like cell growth in human gastric mucosa requires an increase of and/or a prolonged exposure to severe hypergastrinaemia.     

Atrophic gastritis: deficient complex I of the respiratory chain in the mitochondria of corpus mucosal cells

Background  Mitochondrial dysfunction is one of the most characteristic properties of the cancer cell. However, it is not known whether oxidative energy metabolism has already become altered in conditions of atrophic gastritis, a precancerous state of gastric disease. The purpose of our study was to comparatively characterize oxidative phosphorylation (OXPHOS) in the atrophic and nonatrophic gastric corpus mucosa. Methods  Mucosal biopsies were taken from 12 patients with corpus dominant atrophic gastritis and from 12 patients with nonatrophic mucosa (controls). One part of the tissue samples was permeabilized with saponin for analysis of the function of the respiratory chain using high-resolution respirometry, and another part was used for histopathological examination. The serum level of pepsinogen I (S-PGI) was determined with a specific enzyme immunoassay (EIA). Results  Compared to the control group, the maximal capacity of OXPHOS in the atrophy group was almost twofold lower, the respiratory chain complex I-dependent respiration, normalized to complex II-dependent respiration, was reduced, and respiratory control by ADP in the presence of succinate was increased in the atrophic corpus mucosa. In the whole cohort of the patients studied, serum S-PGI level correlated positively with complex I-dependent respiration or complex Idependent to complex II-dependent respiration ratio. Conclusions  Corpus dominant atrophic gastritis is characterized by decreased respiratory capacity and relative deficiency of the respiratory complex I of mitochondria in the mucosa, the latter defect probably limiting mitochondrial ATP production and energetic support of the secretory function of the zymogenic mucosal cells.     

ATROPHIC GASTRITIS IN THE AGED

The incidence of gastritis and the correlation of this finding with the presence of circulating parietal cell antibodies and gastric secretory function was studied in 24 asymptomatic subjects aged over 6o years. A gastric biopsy examination, a maximal histamine-stimulation test, a test for parietal cell antibody and a Schilling test were performed on each subject. The biopsy specimens were examined by histological and histochemical methods. The gastric juice was assayed for acid and intrinsic factor content, and the serum iron and vitamin B₁₂ levels were measured. All but one subject showed some degree of chronic atrophic gastritis. Close correlation was found between gastric secretory function, the histological changes in the gastric mucosa and the reduction in specialized cells demonstrated on histochemical examination. Two subjects presented a “pre-pernicious anæmia” picture with gross reduction in intrinsic factor secretion, a degree of malabsorption of vitamin B₁₂ but no evidence of vitamin B₁₂ deficiency; a very similar case not included in the series is described to illustrate the diagnostic problem which may occur with hæmatological evidence of vitamin B₁₂ deficiency as a result of atrophic gastritis. Serum iron levels were reduced in some cases with severe atrophic gastritis. Antibodies to parietal cells occurred with increasing frequency as the changes in the gastric mucosa became more marked. Atrophic gastritis is a common finding in the “normal” aged male even in the absence of gastrointestinal symptoms, and a clinical picture simulating early pernicious anæmia may occur as a result of “normal ageing” of the gastric mucosa.     

小儿慢性胃炎辨证分型与内镜象及幽门螺杆菌感染的相关性研究

[目的]探讨小儿慢性胃炎中医证型与胃黏膜改变及幽门螺杆菌感染之间的内在关系.[方法]将符合入选条件的404例慢性胃炎患儿中医辨证分型后进行胃镜检查及尿素13C-呼气试验(13 C-UBT)检查,并登记造表,进行统计学处理.[结果]肝胃不和型胃炎主要表现为胃黏膜充血和微小结节形成,脾胃湿热型胃炎表现以黏膜斑和黏膜糜烂为主,胃络瘀血型胃炎则以胃黏膜出现出血斑点为主,脾胃虚弱型胃炎以胃黏膜水肿为主,胃阴不足型胃炎以胃黏膜花斑为主.13 C-UBT阳性率实证高于虚证,与证型无相关性;13C-UBT值实证高于虚证,尤以肝胃不和型和脾胃湿热型为最高.[结论]小儿慢性胃炎中医辨证分型与胃黏膜改变及幽门螺杆菌感染之间存在实质性联系,为辨证施治提供了理论基础.     

大鼠胃黏膜萎缩过程中的组织学变化和p16、Bcl-2、增殖细胞核抗原表达

慢性萎缩性胃炎尤其是胃窦萎缩性胃炎与胃癌关系密切。胃黏膜恶变过程中，细胞增殖与凋亡异常发挥重要作用。目的：研究大鼠胃黏膜萎缩过程中的组织学变化，以及p16、Bcl-2、增殖细胞核抗原（PCNA）表达情况．探讨这些调控因子的改变对萎缩性胃炎形成的影响。方法：以氨水、脱氧胆酸钠和乙醇三种损伤因素联合作用诱导慢性萎缩性胃炎。大鼠分为正常对照组和模型组，分别于2、4、6个月后处死。取胃黏膜行大体观察和组织学检查，以免疫组化方法检测胃窦黏膜p16、Bcl-2、PCNA表达。结果：模型组胃黏膜炎症细胞浸润明显；胃窦小凹增生．腺体层厚度和腺体数目明显减少；胃体病变较轻，仅于后期出现壁细胞数目减少。在胃窦黏膜萎缩过程中，p16表达逐渐降低，Bcl-2和PCNA表达逐渐升高。萎缩组p16表达较非萎缩组显著降低，Bcl-2、PCNA表达较非萎缩组显著升高。结论：多因素长期慢性刺激可致大鼠胃黏膜萎缩。模型大鼠胃黏膜细胞处于高增殖状态．抑癌基因p16蛋白表达低下．凋亡抑制基因Bcl-2蛋白高表达，萎缩性胃炎的发病与细胞增殖与凋亡失衡相关。     

Advanced gastric cancer of the antrum: Anatomic-functional correlation between chief cell mass and serum pepsinogen I

Chief cell mass and type I serum pepsinogen (PGI) were calculated in 19 advanced antral gastric cancer of intestinal type. Comparisons were also made with parietal cell mass and acid secretion. In gastric cancer of the antrum there is a significant decrease of the chief cell mass and of serum pepsinogen I. The patients were subdivided according to the histological findings of the fundic mucosa. In cases of antral gastric cancer with superficial fundic gastritis there is normozymogenism with hyperpepsinogenemy; with preatrophic fundic gastritis there is hypozymogenism with normopepsinogenemy; with atrophic fundic gastritis there is hypozymogenism with hypopepsinogenemy. Similar behavior of the chief cell mass between antral gastric cancer and fundic atrophic gastritis without cancer has become recognized and while the validity of PGI as a marker of fundic atrophic gastritis has emerged it does not allow discrimination between atrophic fundic gastritis and atrophic fundic gastritis associated with gastric cancer of the antrum.     

Chronic gastritis

Abstract

Prevalence of chronic gastritis has markedly declined in developed populations during the past decades. However, chronic gastritis is still one of the most common serious pandemic infections with such severe killing sequelae as peptic ulcer or gastric cancer. Globally, on average, even more than half of people may have a chronic gastritis at present. Helicobacter pylori infection in childhood is the main cause of chronic gastritis, which microbial origin is the key for the understanding of the bizarre epidemiology and course of the disease. A life-long and aggressive inflammation in gastritis results in destruction (atrophic gastritis) of stomach mucosa with time (years and decades). The progressive worsening of atrophic gastritis results subsequently in dysfunctions of stomach mucosa. Atrophic gastritis will finally end up in a permanently acid-free stomach in the most extreme cases. Severe atrophic gastritis and acid-free stomach are the highest independent risk conditions for gastric cancer known so far. In addition to the risks of malignancy and peptic ulcer, acid-free stomach and severe forms of atrophic gastritis may associate with failures in absorption of essential vitamins, like vitamin B12, micronutrients (like iron, calcium, magnesium and zinc), diet and medicines.     

Hp相关性慢性胃炎中医证型分布及血清胃泌素-17水平的相关性分析

目的:探讨Hp相关性慢性胃炎中医证型分布及各证型间胃泌素-17(G-17)水平的相关性.方法:收集Hp相关性慢性胃炎患者400例,按慢性胃炎中医辨证分为脾胃湿热证、脾胃虚寒证、寒热错杂证、肝胃不和证、胃阴不足证、胃络瘀阻证6个证型,并测各证型内患者G-17水平.结果:Hp相关性慢性胃炎各证型例数由高到低分别为:脾胃湿热...     

Phospholipid composition of human gastric mucosa: a study of endoscopic biopsy specimens.

Gastric mucosal phospholipids, and in particular those of the surface layer, play an important part in mucosal barrier function. This study examined whether the phospholipid composition of the full thickness gastric mucosa is changed in peptic ulcer disease and gastritis. The phospholipid composition of gastric mucosa from endoscopic biopsy specimens in 28 subjects (eight healthy controls, 12 patients with duodenal ulcer, and eight with chronic atrophic gastritis) was studied. In addition, the phospholipid composition of gastric mucosa was compared with that of duodenal mucosa in 10 patients with duodenal ulcer. As expected phosphatidylcholine and phosphatidylethanolamine prevailed in all three groups. Lysolecithin was the smallest component in the duodenal ulcer and chronic atrophic gastritis groups. The phosphatidylethanolamine value was higher in duodenal ulcer and lower in chronic atrophic gastritis compared with the control group. In chronic atrophic gastritis there was an appreciable amount of phosphatidylglycerol that was not present in patients with duodenal ulcer or in the control group. There was no significant difference in phospholipid composition between antral and duodenal sites in duodenal ulcer patients. In conclusion, the phospholipid composition of gastric mucosa changes in human gastrointestinal diseases but its relation to cellular functions needs further study.