55 cases of severe multiple organ failure above 60 years old were treated from April 1977 to January 1987. Each case suffered from 2 to 11 kinds of chronic diseases with an average of 3.8 kinds, and an average of 3.3 organ failures. The average mortality rate was 90.9%. The main precipitating factors were pulmonary infection(72.7%), metastatic carcinoma (14.6%), cardiac arrhythmia (7.3%) and improper medication (5.5%). Low organ infusion, endotoxin and immunological insufficiency probably contributed to their development. Diagnosis, prognosis, therapy and prevention of MOF in the elderly were discussed.

M-mode and pulsed Doppler echocardiography was used to evaluate the changes in structure and function of the left ventricle in 30 patients with chronic renal failure (CRF).The left ventricular mass index (LVMI) and systolic function were unchanged in the early stage of the CRF cases as compared with those of the controls (n = 30). However, the decrement in VE (early peak filling velocity) and the increase in VA/VE (late to early peak velocity ratio) indicated damage of the diastolic function. After 13 months follow-up, the LVMI of the CRF group elavated significantly and the VE diminished further.The ejection fraction (EF), shortening fraction (FS) and circumferencial muscular shortening velocity (mVcf) were decreased as compared with those before the follow up. 47.7% of the patients showed left ventricular heart failure.

Essential hypertension (EH) is an escalating problem for developed and developing countries.It is currently seen as a 'complex' genetic trait caused by multiple susceptibility genes which are modulated by gene-environment and gene-gene interactions.Over the past 10 years,mitochondrial defects have been implicated in a wide variety of degenerative diseases,aging,and cancer.Recently several studies showed that human essential hypertension has excess maternal transmission which suggests a possible mitochondrial involvement.However,the exact pathophysiology of mitochondrial DNA mutation (mtDNA) in essential hypertension still remains perplexing.With the application of a variety of imaging approaches and successive mouse model of mitochonddal diseases we convince that these problems will be resolved in the near future.(J Geriatr Cardiol 2008;5(1):60-64)

Objective To study acute toxicity of nanometer titanium dioxide to the liver and kidney of mice. Methods 20 KM mice (22-26 g) were randomly divided into two groups, the control group and the experimental group, TiO2 (20-30 nm) suspension (single dose of 5 g/kg body weight) was given to mice by a single oral gavage, the mice in the control group were given the physiologicalsaline. 14 days after the treatment, the mice were sacrificed and the serum were collected to evaluate the levels of ALT(alanine amino transferase), AST(aspartate aminotransferase), ALP(alkaline phosphatase), UA(uric acid), Cr(creatinine),BUN(blood urea nitrogen), CK(creatine kinase), LDH(lactate-dehydrogenase), ?-HBDH(alpha-hydroxybutyrate dehydrogenase), TBIL(total bilirubin levels). The tissues of the liver and kidney were excised and were embedded in paraffin blocks, hematoxylin-eosin (HE) staining for further histopathological diagnosis. Results The serum ALT, ALT/AST, BUN, LDH and ?-HBDH of the TiO2 group were statistically higher than those in the control group (P

To investigate the mechanism of aldosterone in the induction of hypertensive myocardial fibrosis, we compared the changes of the incorporation rate of 3H proline, the contents of cardiac tissue collagen, and the activities of the cardiac mitogen activated protein kinase (MAPK) in the spontaneous hypertensive rats (SHRs) untreated and treated with a competitive antagonist of the aldosterone receptorspironolactone (spiron), and also in normotensive rats. The results showed that the incorporation of 3H proline incubating with the myocardial tissue slices significantly increased at three time points (at 4,6,8 h), that the tissue collagen contents and the activities of tissue MAPK also increased in SHRs than in SHRs treated with spiron and in normotensive rats. It suggests that aldosterone stimulates the cardiac MAPK through specific recepter, thus increases the absorption of proline and synthesis of collagen in the cardiac fibroblasts, and in turn, is responsible for the myocardial fibrosis.

To investigate changes in density of platelet glycoprotein (GP)Ⅱb/Ⅲa receptor during the perioperative period of hepatectomy in rats with myocardial infarction. 26 adult SD rats were randomly divided into 2 groups: the control group(1)( n =13) and the infarction group(2)( n =13). Myocardial infarction was produced by celiac injection (1 time/d) of isoproterenol (30mg/kg) for 3 days. All rats underwent hepatectomy after 3 weeks. Platelet surface density of GPⅡb/Ⅲ receptors was determined by flow cytometric analysis before and 6, 12, 24, 48, 72 hours after the operation. 12 hours after the operation, the density of GPⅡb/Ⅲa was transiently increased compared with preoperative period in control group ( P

To determine the effect of pulmonary lobectomy on myocardial blood supply and hemodynamics, 18 dogs were randomized into 3 groups. The dogs in group A and C were subjected to about 75% occlusion of the left anterior descending coronary artery. One week later, dogs in group C were sacrificed by arterial bleeding, while dogs in group A and B underwent right upper pulmonary lobectomy, and extremity ECG, blood routine, blood gas, hemodynamics and morphological changes of the myocardium were examined. The results showed that pulmonary lobectomy could result in or worsen myocardial ischemia. There was significant decrease in PO 2 , SaO 2 ; and CI, and significant elevation of LVEDP, PCWP and MPAP. There were more elevation of LVEDP and less decrease in CI after lobectomy in group A compared with group B. It suggested that pulmonary lobectomy could intensify myocardial ischemi and indace hemodynamic disturbances by lowering PO 2 and SaO 2 , especially where there was coronary artery stenosis before the operation.

Objective The aim of the study is to explore the relationship of lung infection(LI)and multiple organ failure in the elderly(MOFE).Methods Consecutive patients ,who were admitted to the Institute of Geriatric Cardiovascular Diseases of the PLA General Hospital and the Endocardial Department of the Air Force General Hospital,withage≥65 years old were enrolled into 5 groups retrospectively by following criteria:acute LI alone,LI with the first presentation of acute lung edema,chronic bronchitis complicated with LI,chronic heart failure complicated with LI,and nic bronchitis and heart failure complicated with LI.Results Sixty-eight patients were selected of(72.5?7.6)years old ( 38 male).There were 4 cases of pure LI(4%),12 cases of LI firstly presented with the symptoms of acute lung edema(18%),16 cases of LI complicated with chronic bronchitis(24%),15 cases of LI based on chronic heart failure(22%)and 22 cases of LI complicated with chronic bronchitis and heart failure(32%).LI initiated MOFE in 25 cases(37%).Most of them were developed on the basis of chronic bronchitis and/or heart failure(34%).Mortality of secondary LI was higher than that of the primary LI(7.4% VS 0%,P

During aging, cardiac contractile response to β-AR stimulation is decreased in humans and animal models. Recent studies demonstrate that the positive inotropic effects of both β1-AR and β2-AR stimulation are significantly decreased with aging.This is accompanied by decreases in both β-AR subtype densities and a reduction in membrane adenylyl cyclase activity. However,neither G protein-coupled receptor kinases (GRKs) nor inhibitory G proteins (Gi) appears to contribute to the age-associated reduction in the β-AR modulation of contraction. Thus, while both aging and chronic heart failure exhibit a diminution in cardiac β-AR responsiveness, only heart failure exhibits increased GRK-mediated desensitization ofβ-Ars and an upregulation of Gi proteins.

To investigate whether the calcium channel blocker amlodipine could inhibit macrophage matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) expression and secretion. Methods Peritoneal macrophages were isolated from BALB/C mice and incubated with low (5μg/L), middle (15μg/L) and high (305μg/L) concentrations of amlodipine, or in the medium alone (controls) for 24 hours, and the expression and secretion of MMP-2 and MM-9 of the cells were analyzed by RT-PCR and gelatin zymography. Results Compared with controls, amlodipine at low concentration had no significant effects on the expression and secretion of either MMP-2 and MMP-9 (P＞0.05);at middle concentrationit it could inhibited MMP-2 and MMP-9 expressions completely and significantly reduced the secretion of MMP-9 (P＜0.05); but it had no effect on the secretion of MMP-2. At high concentration it also inhibited MMP-2 and MMP-9 expression completely. Conclusion Amlodipine at 15 ìg/L inhibited the expression of MMP-2 and MMP-9 and reduced the secretion of MMP-9, suggesting that amlodipine may stabilize atherosclerotic plaque.