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.

The endoplasmic reticulum (ER) serves several important functions, mainly post-translational modification, folding and assembly of newly synthesized secretary proteins, synthesizing lipids and cellular calcium storage. Various factors can disrupt ER homeostasis and disturb its functions, which leads to the accumulation of unfolded and misfolded proteins and to potential cellular dysfunction and pathological consequences, collectively termed ER stress. Recent progress suggests that ER stress plays a key role in the immune response, diabetes, tumor growth, and some neurodegenerative diseases. In particular, ER stress is involved in several processes of cardiovascular diseases, such as ischemia/reperfusion injury, cardiomyopathy, cardiac hypertrophy, heart failure, and atherosclerosis. Further research on the relation of ER stress to cardiovascular diseases will greatly enhance the understanding of these pathological processes and provide novel avenues to potential therapies.

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

A lot of reports suggested that inducible nitric oxide synthase (iNOS) has a very different nature from constitutive NOS including endothelial NOS (eNOS) and neural NOS (nNOS). When exposed to cytokines or bacterial products, iNOS could be greatly activated and produces hundreds or thousands fold more NO than it does usually. Whether iNOS activation is arterial pressure related is not clear. In the present experiment, we studied three groups(n=6) of Sprague Dawley (SD) rats with implanted aorta and venous catheters that were maintained on 1 mEq/d, 12.5 mEq/d and 25 mEq/d of sodium intake respectively. Pulsatile arterial pressure signals from the amplifier were sent to a digital computer and the urine samples were taken every other day for nitrate/nitrite excretion (UNOx) assay using Greiss Reaction. After 6 days infusion, the rats were euthanized with an overdose of sodium pentobarbital, and the renal medullas were rapidly removed and frozen on dry ice for iNOS activity assay. Morever separate groups of hypertensive rats including spontaneously hypertensive rat (SHR, n=6) and High NaCl-induced hypertensive rat (NaHR, n=6) were used to measure renal iNOS protein by Western Blotting. The results showed that the mean arterial pressure (MAP) were significantly increased with the increase intake of sodium, the MAP (mmHg) at day 6 were 99.6±3.5,116.65±4.2 and 125.43±4.5, and the iNOS activity (nmol*g-1 protein*min-1) were 122.3±23.4, 342.4±35.6 and 623.9±65.4 in 1 mEq/d, 12.5 mEq/d and 25 mEq/d of sodium intake-rats respectively. At the same time, UNOx at day 6 were also increased, in turn, to 5 865.6±343.0 (for 12.5 mEq/d intake-rats) and (9 642.8±1 045.3) (for 25 mEq/d sodium intake-rats) nmol/d from (3 834.9±234.8) nmol/d of 1 mEq/d sodium intake-rats respectively. Western blotting showed that the renal medullary iNOS protein in SHR and NaHR were increased by 178%±13% and 104%±9% of normal Wistar rats. The data indicates that elevated arterial pressure could be an effective stimulus for iNOS activation.