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.

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.

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.

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.

Objective To observe the changes of plasma urotensinⅡ(UⅡ)、PAMP(proadrenomedullin N-terminal peptide)and ANP(atrial natriuretic peptide)levels in patients with congestive heart failure (CHF) and to illustrate clinical significance of these changes.Methods 52 patients with CHF and 20 age and gender-matched control subjects were studied.Plasma UⅡ.PAMP and ANP levels of 52 patients with CHF and 20 control subjects were measured by radioimmunoassay.Heart function of all study subjects were mensurated by ultrasound cardiography.Results The plasma UⅡ levels were significantly lower in patients with CHF than that in control subjects [(1.48?1.05) vs (4.28?1.21) pg?mL -1,P

Objective: To investigate alteration and cross link of the aortic intima and platelet endogenous L-Arg/NOS/NO pathway induced by water immersion restraint (WIR) stress. Methods: After 7 h of WIR stress, the aortic intima was isolated and prepared the platelet, then NO_2- production released from aortic intima and platelet was measured with Greiss regent, NOS activity and L-arginine transport activity were detected by isotope tracer method. Results: After 7 h of WIR stress, the levels of NO_2- from platelet and aortic intima obviously decreased by 57% and 46% respectively as comparied with the control rats (P

In the isolated adult rat's ventricular myocytes and artificial bio-membrane-liposomes, the lipid peroxidation caused by generating system of free radicals (FeCl2 & ascorbic acid ) was significantly inhibited by Co Q10, and the inhibition effect of Co Q10 was both dose-and time-dependent. The results showed that Co Q10 had an antioxi-dation effect and served as a scavenger of free radicals at the level of membrane .