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.

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.

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

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

We set up an animal model of acute hibernating myocardium isolated rat heart. which were perfused with human red blood cell-enhanced modified K-H buffer,were used. During ischemia,coronary flow were reduced to 20%. The results show: At 30 minutes of ischemia,left ventircular peak systolic pressure,+dp/dt max and - dp/dt max were decreased to 44% ,33% and 26% (P

Objective To assess the change of plasma adrenomedullin(ADM)and endothelin(ET)in patients with essential hypertensin. Methods Concentrations of plasma ADM and ET were measured in 18 healthy control subjects and 52 patients with essential hypertension, 36 patients of which had no target organ damage, while 16 patients of which were complicated with renal impair. Results The concentrations of ADM and ET were significantly higher in patients with renal impair than in patients without organ damage. Plasma concentrations of ADM and ET were strongly positively correlated with blood urea nitrogen levels and serum creatinine levels. A strong inverse correlation between GFR and plasma concentrations of ADM and ET was found. Conclusion The increase of plasma ET and ADM may have an intimate relation to the renal function. ADM and ET may play some important role in the pathophysiologic makeup of hypertension and hypertension with renal dysfunction. ADM may act against excessive vasoconstrictor ET increased in essential hypertension and may be part of a compensatory mechanism to offset further development of renal impair.

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.