1.Roles and mechanisms of ginseng in protecting heart.
Si-Dao ZHENG ; Hong-Jin WU ; De-Lin WU
Chinese journal of integrative medicine 2012;18(7):548-555
Ginseng, the root of Panax ginseng C. A. Mayer, has long been used clinically in China to treat various diseases. Multiple effects of ginseng, such as antitumor, antiinflammatory, antiallergic, antioxidative, antidiabetic and antihypertensive have been confirmed by modern medicine. Recently, the clinical utilization of ginseng to treat heart diseases has increased dramatically. The roles of ginseng in protecting heart are foci for research in modern medical science and have been partially demonstrated, and the mechanisms of protection against coronary artery disease, cardiac hypertrophy, heart failure, cardiac energy metabolism, cardiac contractility, and arrhythmia are being uncovered progressively. However, more studies are needed to elucidate the complex mechanisms by which ginseng protects heart. All such studies will provide evidence of ginseng's clinical application, international promotion, and new drug development.
Animals
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Cardiotonic Agents
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chemistry
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pharmacology
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Energy Metabolism
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drug effects
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Heart
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drug effects
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physiopathology
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Humans
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Myocardial Contraction
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drug effects
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Panax
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chemistry
2.The positive inotropic effect after washout of acetylcholine in isolated rabbit hearts.
Hai-Jian LUO ; Feng-Jie ZHANG ; Jun-Qiang SI ; Rui-Rui YANG ; Lei ZHAO ; Wei-Jian GAO
Chinese Journal of Applied Physiology 2008;24(2):197-200
AIMTo study the regular pattern and mechanism of positive inotropic effect after washout of ACh (rebound of myocardial contractile force) in isolated rabbit hearts.
METHODSThe changes of myocardial contractile force after perfusion and washout of ACh were observed in isolated Langendorff perfused rabbit hearts.
RESULTSMaximum rebound rate induced by ACh of 10(-8)-10(-3) mol/L were 2.20% +/- 1.70%, 6.71% +/- 3.40%, 9.18% +/- 3.54%, 14.16% +/- 3.27%, 4.37% +/- 5.86% and 1.03% +/- 6.86%, respectively. Compared with the ACh of 10(-5) mol/L in control group, adrenaline enhanced rebound of myocardial contractile force, maximum rebound rate in adrenaline group was 29.25% +/- 5.83% (P < 0.05), propranolol reduced rebound, and maximum rebound rate in propranolol group was 5.15% +/- 4.45% (P < 0.05), we had not detected rebound of myocardial contractile force in 800 s after addition ACh in verapamil group.
CONCLUSIONIn isolated rabbit heart, positive inotropic effect after washout of ACh has relevance to the activities of calcium current channel and beta-adrenergic receptor. Perhaps there are some different aspects in the mechanism of positive inotropic effect between perfusion of high concentration and after washout of ACh.
Acetylcholine ; pharmacology ; Animals ; Cardiotonic Agents ; pharmacology ; Heart ; drug effects ; In Vitro Techniques ; Myocardial Contraction ; drug effects ; physiology ; Rabbits
3.Effect of Panax Ginseng Alcohol Extract on Cardiovascular System.
Jong Sik HAH ; Bok Soon KANG ; Doo Hee KANG
Yonsei Medical Journal 1978;19(2):11-18
The effects of the alcohol extract of Panax ginseng on the myocardial contractility particularly with respect to Bowditch and Woodworth phenomena and the norepinephrine induced contraction of the vascular smooth muscle were studied in vitro. 1) In the isolated muscle preparation of guinea pig left auricle, the administration of ginseng-alcohol extract at concentrations of 10~50mg% resulted in a significant reduction of both Bowditch and Woodworth effects. 2) In the isolated Ca++ depleted heart of rabbit ginseng-alcohol extract inhibited the Ca++ uptake and the restoration of contractile force during perfusion with a Ca++ containing solution. 3) In the isolated muscle strip of the rabbit aorta noradrenaline (5 X 10-8 g/ml) induced contraction was inhibited by the ginseng-alcohol extract at concentrations of 10~50mg%. From these results it is speculated that the hypotensive effect of ginseng is accounted for by 1) the direct inhibition of myocardial contractility which is resulted from the reduction of Ca++ influx into cardiac cell, and 2) the inhibition of the catecholamine induced contractility of vascular smooth muscles.
Animal
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Aorta/drug effects
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Cardiovascular System/drug effects*
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Ethanol/pharmacology
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Female
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Guinea Pigs
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In Vitro
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Male
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Muscle Contraction/drug effects
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Muscle, Smooth/drug effects
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Myocardial Contraction/drug effects*
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Panax*
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Plant Extracts/pharmacology*
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Plants, Medicinal*
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Rabbits
4.Effects of scorpion toxins on the cardiovascular system.
China Journal of Chinese Materia Medica 2004;29(7):631-633
Being a biologic toxin, scorpion toxins have complicate physiologic and pharmalogic actions because of its intricate components. This text reviewed the effect of scorpion toxins on endothelial cell function, platelet function, microcirculation, atherosclerosis, ironic channel, and cardiac function.
Animals
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Endothelial Cells
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metabolism
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Epoprostenol
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metabolism
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Ion Channels
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drug effects
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Microcirculation
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drug effects
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Myocardial Contraction
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drug effects
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Platelet Aggregation
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drug effects
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Scorpion Venoms
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pharmacology
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Tissue Plasminogen Activator
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metabolism
5.Protective Effects of Estradiol on Myocardial Contractile Function Following Hemorrhagic Shock and Resuscitation in Rats.
Chinese Medical Journal 2015;128(17):2360-2364
BACKGROUNDHemorrhagic shock (HS) results in myocardial contractile dysfunction. Studies showed that 17β-estradiol protects the myocardium against contractile dysfunction. The study investigated the cardioprotective effects of treatment with 17β-estradiol before resuscitation following 1 h of HS and resuscitation.
METHODSMale Sprague-Dawley rats were assigned to 2 sets of experimental protocols: Ex vivo and in vivo treatment and resuscitation. Each set had three experimental groups (n = 6 per group): Normotensive (N), HS and resuscitation (HS-R) and HS rats treated with 17β-estradiol (E) and resuscitated (HS-E-R). Rats were hemorrhaged over 60-min to reach a mean arterial blood pressure of 40 mmHg. In the ex vivo group, hearts were resuscitated by perfusion in the Langendorff system. In the 17β-estradiol treated group, 17β-estradiol 280 µg/kg was added for thefirst 5 min. Cardiac function was measured. Left ventricular generated pressure (LVGP) and +dP/dt were calculated. In the in vivo group, rats were treated with 17β-estradiol 280 µg/kg s.c. after 60-min HS. Resuscitation was performed in vivo by the reinfusion of the shed blood for 30-min to restore normotension.
RESULTSTreatment with 17β-estradiol before resuscitation in ex vivo treated and resuscitated isolated hearts and in the in vivo treated and resuscitated rats following HS improved myocardial contractile function. In the in vivo treated group, LVGP and +dP/dt max were significantly higher in 17β-estradiol treated rats compared to the untreated group (LVGP 136.40 ± 6.61 compared to 47.58 ± 17.55, and +dP/dt 661.85 ± 49.88 compared to 88.18 ± 0.85). Treatment with 17β-estradiol improved LVGP following HS.
CONCLUSIONSThe results indicate that treatment with 17β-estradiol before resuscitation following HS protects the myocardium against dysfunction.
Animals ; Estradiol ; therapeutic use ; Male ; Myocardial Contraction ; drug effects ; Myocardium ; pathology ; Rats ; Rats, Sprague-Dawley ; Resuscitation ; Shock, Hemorrhagic ; drug therapy
6.Melatonin protects against myocardial ischemia-reperfusion injury by inhibiting contracture in isolated rat hearts.
Lingheng KONG ; Na SUN ; Lanlan WEI ; Lijun ZHANG ; Yulong CHEN ; Li CHANG ; Xingli SU
Journal of Zhejiang University. Medical sciences 2020;40(7):958-964
OBJECTIVE:
To investigate the protective effect of melatonin against myocardial ischemia reperfusion (IR) injury in isolated rat hearts and explore the underlying mechanisms.
METHODS:
The isolated hearts from 40 male SD rats were randomly divided into 4 groups (=10): the control group, where the hearts were perfused with KH solution for 175 min; IR group, where the hearts were subjected to global ischemia for 45 min followed by reperfusion for 120 min; IR+melatonin (Mel+IR) group, where melatonin (5 μmol/L) was administered to the hearts 1 min before ischemia and during the first 5 min of reperfusion, followed by 115 min of reperfusion; and IR+2, 3-butanedione monoxime (IR+BDM) group, where the hearts were treated with BDM (20 mmol/L) in the same manner as melatonin treatment. Myocardial injury in the isolated hearts was assessed based on myocardial injury area, caspase-3 activity, and expressions of cytochrome C and cleaved caspase-3 proteins. Cardiac contracture was assessed using HE staining and by detecting lactate dehydrogenase (LDH) activity and the content of cardiac troponin I (cTnI) in the coronary outflow, measurement of left ventricular end-diastolic pressure (LVEDP) and electron microscopy. The content of ATP in the cardiac tissue was also determined.
RESULTS:
Compared with those in the control group, the isolated hearts in IR group showed significantly larger myocardial injury area and higher caspase-3 activity and the protein expressions of cytochrome C and cleaved caspase-3 with significantly increased LDH activity and cTnI content in the coronary outflow and elevated LVEDP at the end of reperfusion; HE staining showed obvious fractures of the myocardial fibers and the content of ATP was significantly decreased in the cardiac tissue; electron microscopy revealed the development of contraction bands. In the isolated hearts with IR, treatment with Mel or BDM significantly reduced the myocardial injury area, caspase-3 activity, and protein expressions of cytochrome C and cleaved caspase-3, obviously inhibited LDH activity, lowered the content of cTnI and LVEDP, reduced myocardial fiber fracture, and increased ATP content in the cardiac tissue. Both Mel and BDM inhibited the formation of contraction bands in the isolated hearts with IR injury.
CONCLUSIONS
Mel can alleviate myocardial IR injury in isolated rat hearts by inhibiting cardiac contracture, the mechanism of which may involve the upregulation of ATP in the cardiac myocytes to lessen the tear of membrane and reduce cell content leakage.
Animals
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Heart
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drug effects
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Male
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Melatonin
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pharmacology
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therapeutic use
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Muscle Contraction
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drug effects
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Myocardial Reperfusion Injury
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drug therapy
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Myocytes, Cardiac
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drug effects
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Rats
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Rats, Sprague-Dawley
9.Effects of oxyphenamone on myocardial ischemia in cats and rats.
Li-li FAN ; Jun MA ; Ya-fang WANG ; Ying-mao RUAN ; Xian-ke ZENG
Acta Pharmaceutica Sinica 2005;40(2):122-126
AIMTo study the therapeutic effects of oxyphenamone, a novel inodilator, on myocardial ischemia.
METHODSThe cardiac hemodynamic variables in cats with acute myocardial infarction induced by occlusion of the left anterior descending coronary artery (LAD) were recorded with a physiological polygraph and electromagnetic flowmeter. A model of myocardial necrosis induced by subcutaneous injection of isoproterenol was used for evaluating the effects of drugs on myocardial enzymes and morphological change.
RESULTSIntravenous injection of oxyphenamone (2 - 8 mg x kg(-1)) dose-dependently decreased heart rate, mean arterial pressure, vascular resistance and the parameters of myocardial oxygen consumption (tension time index, TTI) in cats with myocardial infarction. It increased myocardial contractile force and cardiac output transiently but showed no influence on the left ventricular pressure and cardiac work. The changes of myocardial morphology, creatine phosphate kinase (CPK), malodialdehyde (MDA) and serum glutamic-oxaloacetic transaminase (GOT) induced by isoproterenol in rats were diminished by intraperitoneal injection of oxyphenamone (4 - 8 mg x kg(-1)).
CONCLUSIONBy the examination of the cardiac hemodynamics, myocardial enzymes and morphology, it showed that the myocardial damage induced by ischemia or beta-agonist can be antagonized markedly by oxyphenamone, indicating that oxyphenamone may be beneficial for the treatment of myocardial infarction.
Animals ; Blood Pressure ; drug effects ; Cardiac Output ; drug effects ; Cardiotonic Agents ; pharmacology ; Cats ; Heart ; physiopathology ; Heart Rate ; drug effects ; Male ; Myocardial Contraction ; drug effects ; Myocardial Infarction ; pathology ; physiopathology ; Myocardium ; metabolism ; pathology ; Organic Chemicals ; pharmacology ; Rats ; Rats, Wistar ; Vasodilator Agents ; pharmacology
10.Effects of genistein on contractility of isolated right ventricular muscles in guinea pig.
Jin-xia WU ; Hong-fang LI ; Chong-bin LIU ; Zhi-feng TIAN
Chinese Journal of Applied Physiology 2008;24(4):406-409
AIMTo study the effect of genistein (GEN) on contractility of isolated right ventricular muscles in guinea pig and its mechanisms.
METHODSIsolated guinea pig ventricular muscles were suspended in organ baths containing K-H solution.After an equilibration period, the effect of GEN on contraction of myocardium was observed.
RESULTSGEN and isoprenaline hydrochloride had the positive inotropic effects on contractity of myocardium. Meanwhile, the effect of GEN (1-100 micromol x L(-1)) was in dose-dependent manner. Propranolol (1 micromol x L(-1)) and verapamil hydrochloride (0.5 micromol x L(-1)) attenuated the positive inotropic effect of isoprenaline hydrochloride (1 micromol x L(-1)), but did not change the effect of GEN (50 micromol x L(-1)). Further more, the enhancement of the contraction induced by elevation of extracellular Ca2+ concentration in ventricular muscles had no change after pretreatment with GEN (1.10 micromol x L(-1)). In addition,the positive inotropic effect of GEN was inhibited partially by tamoxifen (1 micromol x L(-1)) and SQ22536 (1 micromol x L(-1)), also, could be attenuated by bpV (1 micromol x L(-1)).
CONCLUSIONGEN has the positive inotropic effect on guinea pig ventricular muscles, which is not related to the activation of beta adrenoceptor, Ca2+ channel on cell membrane,but may involve in cAMP of intracellular signal transduction and tyrosine kinase pathway.
Animals ; Cardiotonic Agents ; pharmacology ; Cyclic AMP ; metabolism ; Genistein ; pharmacology ; Guinea Pigs ; Heart Ventricles ; drug effects ; In Vitro Techniques ; Male ; Myocardial Contraction ; drug effects ; Protein-Tyrosine Kinases ; metabolism