The comparison of effects of different cell protective agents on reperfusion damage was performed on the model rabbit's ischemic shock intestine. The result showed that anisodamine, glutatbione, vitamin E and verapamil at a certain extent had protective effects on reperfusion damage; and that hydrocortisone, mannitol and sodium pentobarbitate did not tave any effects on it; although indomethacin and humic acid did not improve intestinal reperfusion damage, they significantly alleviated the subendocardial damage after ischemic intestinal reperfuison; and that in contrast to the above agents, ATR-MgCl_2 deteriorated the reperfusion injury. The possible mechanisms of reperfusion damage were discussed in this article.

Rat heart was perfused on Langendorff apparatus with Krebs-Henseteit buffer which contained Fluorescein Isothiocyanate-Lipopoly-saccharide (FITC-endotoxin, 25?g/ml) with or without 654-2 (25?g/ml), and the amount of endotoxin(ET) in the perfusion solution was measured before and after perfusion using fluorescence spectrometer. It was discovered that 654-2 decreased the binding of ET to myocardium by 47.7%. The difference between the 654-2 treated and the control group was significant (P

This work compared the preventive and therapeutic effect of verapamil and anisodamine on anoxia-reoxygenation injury (oxygen paradox) of isolated rat heart performed with Langendorff apparatus. Results showed that addition of anisodamine (1.64?10~(-4)M) or verapamil (5?10~(-8)M) to the perfusion fluid during anoxic period significantly ameliorated the anoxia-reoxygenation injury of the heart; e. g., the recovery of cardiac functions, the improvement of myocardial acidosis, the decrease in leakage of LDH from myocardium, and in the accumulation of lipid peroxides and calcium. When the drugs were given during the period of reoxygenation, anisodamine was very effective too, but verapamil had no effect. From these results it may be suggested that anisodamine has more extended anti-oxygen-paradox effect in ddition to calcium channel blocker action.

This work observed on isolated perfused rat hearts, that 10~(-9)mol/L endothelin (ET) induced myocardial contracture, decrease of heart function and coronary flow, intramyocardial Ca~(2+) accumulation and Mg~(2+) loss and etc. These cardiac action of ET were obviously more prominent when Mg~(2+) in the perfusion fluid was lowered to 0.12 mmol/L, and were significantly alIeviated when Mg~(2+) content was increased to 4.8mmol/L (normal plasma Mg~(2+) content is about 1.2 mmol/L). The mechanism of the Mg~(2+) effect on the cardiac action of ET may be related to its inhibition of Ca~(2+) influx into the myocytes. These results suggested that without magnesium defficiency, suitable replenishment of Mg~(2+) probably have practical clinical significance in the prevention and therapy of myocardial injury occurred during diseases with elevated circulatory ET level.

In oeder to investigate the pathogenetic role of mitochondria in the patho-genesis of intracellular calcium overload in septic rat. The present study observed the cal-cium content and calcium influx into myocardial mitochondria on the early and late sepsisof rat produced by cecal ligature and puncture. The results showed that mitochondrialcalcium contents increased markedly in both early (180%) and late (330%) sepsis. Thecalcium transport capacity of mitochondria in late sepsis decreased dramatically (uptakedecreased 34.6%, uptake velocity lowered 33.3%, p

The effects of adrenomedullin on infection, inflammation, immune regulation had been reviewed in this paper, suggesting that cardiovascular active peptides involve in defense reactions.

It is well established that renin-angiotensin system (RAS) is the major regulatory networkthat maintains blood pressure, fluid and electrolyte balance and the homeostasis of cardiovascular system.Most studies in the last decades centered on the pivotal members of RAS, that is, angiotensinⅡ (AngⅡ) and angiotensin converting enzyme (ACE). Recent identification of ACE-2, the homology of ACE,and the identification of the multiple products degraded from angiotensinⅠ, including AngⅢ, AngⅣ,Ang1 -9, Ang1 -7, Des-Asp-angiotensinⅠ(DAAⅠ), etc, have proved that AngⅡ is not the only bio-logical active compound of RAS. Peptides derived from angiotensinogen,that is, family of angiotensins,display independent and pleiotropic biological activitiesin vivo, and interact with each other both in me-tabolism pathway and the biologic effects. The imbalance of the network of angiotensin metabolites exhib-its significant pathophysiological role in cardiovascular disease.

Cardiovascular fibrosis is the common pathological manifestation of many heart diseases.Relaxin inhibits fibrosis through several mechanisms as follows relaxin inhibits fibroblast function,collagen synthesis/secretion and the influence of several profibrotic factors.Relaxin stimulates MMP expression.Relaxin rapidly inhibits cardiovascular fibrosis and has no effect on normal tissue.It is a potential and selective antifibrotic target of cardiovascular diseases.

Objective To explore the effect of hydrogen sulfide(H2S) on intercellular adhesion molecule-1(ICAM-1) in the pathogenesis of atherosclerosis in apoE knockout(apoE-/-) mice.Methods Six week-old C57BL/6J and apoE-/-mice were divided into control C57BL/6J group,apoE-/-group,apoE-/-+ sodium hydrosulfide(NaHS,a donor of H2S) group and apoE-/-+ DL-propargylglycine(PPG,an inhibitor of H2S synthase).There were 8 mice in each group.They were fed chow diet for 10 weeks.Serum H2S was measured by sulfide electrode-based method,serum ICAM-1 was determined by ELISA.Aortic ICAM-1 mRNA was detected by RT-PCR.The changes of atherosclerosis plaque size were observed by oil red O staining.Results Serum H2Slevel significantly decreased in apoE-/-mice(P

AIM: To explore the possible impact of hydrogen sulfide(H2S) donor-sodium hydrosulfide(NaHS) on endothelin-1(ET-1) and connective tissue growth factor(CTGF) expressions in rats with pulmonary hypertension induced by high pulmonary blood flow.METHODS: Thirty-two male SD rats were randomly divided into 4 groups: shunt group,shunt+NaHS group,sham group and sham+NaHS group.Rats in shunt group and shunt+NaHS group were subjected to an abdominal aorta-inferior vena cava shunt to create an animal model of high pulmonary flow.After 11 weeks of experiment,rat systolic pulmonary artery pressure(SPAP),lung tissue H2S,plasma ET-1 concentration and lung tissue ET-1mRNA expression,as well as pulmonary artery CTGF protein expression were detected.RESULTS: After 11 weeks of experiment,SPAP,lung tissue ET-1mRNA,plasma ET-1 as well as pulmonary artery CTGF expressions were increased markedly,respectively,whereas H2S in lung tissue decreased significantly in rats of shunt group as compared with that in sham group(all P