Cardiovascular diseases, like coronary heart disease and myocardial infarction, are the most common cause of death worldwide. Chinese medicines have demonstrated rich cardioprotective activities for clinical applications. Salvia miltiorrhiza, a very important component of traditional Chinese medicine, can promote blood circulation and relieve blood stasis. Salvia miltiorrhiza is widely used in treatment of cardiovascular and cerebrovascular disease such as coronary heart disease and cerebral infarction ( CI). Tanshinone II(A), the major lipophilic components extracted from the root of S. miltiorrhiza, possesses anti-atherosclerosis, anti-cardiac hypertrophy, anti-oxidant, anti-arrhythmia and so on. This paper discusses current research status of tanshinone II(A) in cardioprotective effects.
Animals ; Cardiovascular Diseases ; drug therapy ; genetics ; metabolism ; physiopathology ; Coronary Vessels ; drug effects ; physiopathology ; Diterpenes, Abietane ; therapeutic use ; Humans

This study was designed to clarify the dependency of hypoxic coronary vasodilation (HCD) on the endothelium and the role of the K+ channels on HCD in the rabbit coronary artery. HCD was investigated in an isolated left circumflex coronary artery precontracted with prostaglandin F2 alpha. Vascular rings were suspended for isometric tension recording in an organ chamber filled with Krebs-Henseleit (KH) solution. Hypoxia was induced by gassing the chamber with 95% N2 + 5% CO2 and was maintained for 15 approximately 25 min. Hypoxia elicited a vasodilation in the precontracted coronary artery with and without endothelium. There was no difference between the amplitude of the HCD induced by two consecutive hypoxic challenges and the effects of 20% O2 + 5% CO2 + 75% N2 and 95% O2 + 5% CO2 control K-H solution of subsequent responses to hypoxia. Inhibition of the cyclooxygenase pathway by treatment with indomethacin had no effect on HCD. Blockades of the tetraethylammonium chloride-sensitive K+ channel abolished HCD. Apamin, a blocker of the small conductance Ca(2+)-activated K+ (KCa) channel, and iberiotoxin, a blocker of the large conductance KCa channel had no effect on HCD, respectively. Glibenclamide, a blocker of the ATP-sensitive K+ (K+ATP) channel, reduced HCD. Cromakalim, an opener of the K+ATP channel, relaxed the coronary artery precontracted with prostaglandin F2 alpha. The degree of relaxation by cromakalim was similar to that by hypoxia while glibenclamide reduced both hypoxia- and cromakalim-induced vasodilatations. In conclusion, these results suggest that HCD is independent on endothelium and HCD is considered to be induced by activation of K+ATP channel.
Animal ; Anoxia/physiopathology* ; Coronary Vessels/physiopathology* ; Coronary Vessels/drug effects ; Cyclooxygenase Inhibitors/pharmacology ; Enzyme Inhibitors/pharmacology ; Female ; Indomethacin/pharmacology ; Male ; Nitroarginine/pharmacology ; Rabbits ; Tetraethylammonium/pharmacology ; Vasodilation/physiology*

OBJECTIVEPatient with myocardial bridging (MB) usually has a benign prognosis, but some MB patients might experience myocardial ischemia, infarction and sudden cardiac death, especially during active physical activities. The purpose of the study was to study the stress-induced blood flow changes of the mural coronary artery in MB patients determined by intracoronary Doppler.

METHODSIn 8 patients with MB, the basic average peak velocity (bAPV), hyperemic average peak velocity (hAPV) of blood flow, coronary flow reverse (CFR) proximal and distal to the mural coronary artery were measured before and during intravenously dobutamine (10 microg kg-1 min-1, then add 10 microg kg-1 min-1 at 3 min interval till 40 microg kg-1 min-1) by intracoronary Doppler.

RESULTSThe baseline mural coronary diameter reduction was (51.7+/-21.4)% and significantly increased to (90.0+/-12.7)% (P<0.01) during dobutamine infusion. bAPV on the segments proximal and distal to the mural coronary artery significantly increased from (19.83+/-5.84) cm/s and (20.75+/-4.91) cm/s to (31.52+/-10.93) cm/s and (30.46+/-9.01) cm/s (all P<0.05 vs. baseline) respectively post dobutamine infusion. CFR measured at proximal and distal to myocardial bridging also significantly decreased from (2.91+/-0.62) and (2.46+/-0.82) to (2.17+/-0.66) and (1.83+/-0.51) (all P<0.01).

CONCLUSIONStress can significantly increase the compression of intramural coronary artery and reduce CFR on coronary segments both proximal and distal to the MB. Thus, active exercise might induce myocardial ischemia in patients with myocardial bridging.

Blood Flow Velocity ; Cardiotonic Agents ; pharmacology ; Coronary Circulation ; drug effects ; Coronary Vessel Anomalies ; physiopathology ; Coronary Vessels ; drug effects ; Dobutamine ; pharmacology ; Female ; Humans ; Male ; Middle Aged

OBJECTIVETo study the effect of the Chinese medicine Qiangxin Fumai Granule (, QFG) on electrophysiological functions of the sinoatrial node during ischemia-reperfusion (IR) of the right coronary artery in rabbits.

METHODSThe right coronary artery IR model in rabbits was adopted. The modeled rabbits were randomly divided into 4 groups: the model group, the atropine group, the high-dose QFG group, and the low-dose QFG group, with 8 animals in each group. In addition, twelve rabbits were selected for the sham-operative group. The drugs were administered once via duodenal perfusion after modeling had been stabilized for 10 min. The changes in AA interval, the sinoatrial conduction time (SACT), the sinus node recovery time (SNRT), the corrected sinus node recovery time (CSNRT) and the index of sinus node recovery time (ISNRT) at different time points during ischemia and reperfusion were measured.

RESULTSThe AA interval was prolonged for more than 40 ms in the model group during ischemia. Compared with the model group, the four electrophysiological parameters abovementioned in the high-dose QFG group and the low-dose QFG group were decreased to different extents at each time point (P<0.01 or P<0.05), and no statistically significant differences were found between the QFG groups and the atropine group (P>0.05).

CONCLUSIONQFG is beneficial for accelerating the recovery of sinus node autorhythmicity and conduction function, so as to protect electrophysiological functions of the sinoatrial node. Accelerating the recovery of autorhythmicity and conduction function in the sinus node is considered its electrophysiological mechanism in the treatment of sinoatrial node injury induced by ischemia.

Animals ; Coronary Vessels ; drug effects ; physiopathology ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Electrophysiological Phenomena ; drug effects ; Heart Conduction System ; drug effects ; Myocardial Reperfusion Injury ; drug therapy ; physiopathology ; Phytotherapy ; Rabbits ; Sinoatrial Node ; drug effects ; physiopathology ; Time Factors

OBJECTIVETo investigate the impact of high-dose microbubbles induced by high mechanical index myocardial contrast echocardiography (MCE) on vascular permeability and its recovery time in rats.

METHODSThirty male Wistar rats were randomized into 4 MCE groups (groups A-D) and a control group. In the MCE groups, Evans blue was injected at 10 s before MCE (A), immediately after the end of MCE (B), and at 5 min (C) and 20 min after the end of MCE (D). In the control group, the microbubbles and Evans blue were injected at the end of a 5-min ultrasound exposure. All the rats were sacrificed 5 min after Evans blue injection, and the content of Evans blue in the myocardium and the percentage of Evans blue leakage area were determined.

RESULTSThe percentage of Evans blue leakage area in groups A, B and C were significantly higher than that in the control group (P<0.05), while the percentage was similar between group D and the control group (P>0.05). Evans blue contents in groups A and B were significantly higher than that in the control group (P<0.05), but groups C and D showed comparable contents with the control group E (P>0.05). No significant changes of the heart rates and premature beat number were observed during and after MCE in these groups (P>0.05).

CONCLUSIONHigh mechanical index MCE and a high contrast dose may induce increased microvascular leakage in rats, and the vascular permeability can recover in 20 min after MCE.

Animals ; Capillary Permeability ; drug effects ; Contrast Media ; pharmacology ; Coronary Vessels ; physiopathology ; Echocardiography ; Male ; Microbubbles ; Rats ; Rats, Wistar

Native coronary artery spasm after coronary artery bypass grafting (CABG) is scarce. It frequently causes disastrous circulatory collapse. We report a 72-yr-old male, who experienced native coronary artery spasm and grafted artery spasm following CABG, which was successfully treated with coronary angiography and intracoronary injection of nitroglycerine.
Aged ; Coronary Angiography ; Coronary Artery Bypass/*adverse effects ; Coronary Vasospasm/drug therapy/*etiology ; *Coronary Vessels/drug effects/physiopathology/surgery ; Humans ; Male ; Nitroglycerin/therapeutic use ; Treatment Outcome ; Vasodilator Agents/therapeutic use

OBJECTIVETo assess the effect and safety of intra-coronary administration of anisodamine on "slow-reflow" phenomenon of infarct related artery (IRA) following primary percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI).

METHODSTwenty-five patients with slow-reflow phenomenon screened out from 153 AMI patient with post-PCI reflow IRA were enrolled. They were 17 males and 8 females; aged (62.3 +/- 9.3) years; 10 with focal artery at left anterior descendens, 5 in circumflux and 10 in right coronary artery; PCI was successfully performed on them about 7.11 +/- 2.31 h after the onset of angina pectoris and the post-operation mean TIMI flow was 1.75 +/- 0.42 grade. Nitroglycerin (200 microg) was injected into coronary previously for confirming the slow-reflow phenomenon as control, then the injection of anisodamine 500 microg 10 min later. Coronary arteriography (CAG) was performed at the 1 st, 3 rd and 10 th min after the medication. Gibson's TIMI frame count method and quantitative computer angiography (QCA) system was used to quantitatively detect the frames of blood flow and the diameter of arterial lumen at different time points after nitroglycerin or anisodamine administration. Hemodynamics and changes of electrocardiogram were determined.

RESULTS(1) No significant change in frames of blood flow was found between before and 1 min after intra-coronary administration of nitroglycerin (82.79 +/- 9.30 frames vs 78.43 +/- 9.37 frames, P >0. 05) after operation; but 1, 3 and 10 min after injection of anisodamine, it was decreased 46.25 +/- 4.55, 44.52 +/- 4.52 and 43.09 +/- 4.18, respectively, all P <0. 01, and the average coronary blood flow increased from TIMI grade 1.75 +/- 0.42 to grade 2.70 +/- 0.45 (t = 0. 34, P < 0.05). (2) The diameter of middle segment of reopened coronary artery slightly increased from 3.2 +/- 0.3 mm to 3.3 +/- 0.4 mm 3 min after anisodamine injection, but without statistical significance (P >0. 05). (3) Successive monitoring at 10 min after anisodamine injection showed that all the parameters, including intra-coronary pressure, peripheral blood pressure, P-R interval, Q-T interval and QRS duration were not changed significantly (P > 0.05), only the heart rate increased for 15-19 beats/min, but did not induce tachycardia or other malignant arrhythmia.

CONCLUSIONIntra-coronary administration of anisodamine 500 microg could improve the post-PCI slow-reflow phenomenon, it is safe and convenient, and may be taken as an effective approach for treatment of the illness.

Acute Disease ; therapy ; Adult ; Aged ; Angioplasty, Balloon, Coronary ; Coronary Vessels ; drug effects ; physiopathology ; Female ; Humans ; Injections ; Male ; Middle Aged ; Myocardial Infarction ; drug therapy ; physiopathology ; surgery ; Regional Blood Flow ; drug effects ; Solanaceous Alkaloids ; administration & dosage

OBJECTIVETo assess the effect of beta blocker on blood flow velocity and reserve on the intramural coronary artery of patients with myocardial bridging.

METHODSIn 8 patients with myocardial bridge, intracoronary Doppler was performed before and after esmolol was given intravenously. The basic average peak velocity (bAPV), hyperaemic average peak velocity (hAPV) of blood flow, and coronary flow reserve (CFR) proximal and distal to the mural myocardial bridging was measured and compared.

RESULTSAfter esmolol injection, the mural coronary diameter systolic reduction decreased from (58.0 +/- 14.7)% to (26.0 +/- 9.8)% (P < 0.01); the bAPV proximal and distal to myocardial bridging separately decreased from (19.4 +/- 4.9) cm/s and (18.4 +/- 3.6) cm/s to (4.7 +/- 3.9) cm/s (P < 0.01) and (15.1 +/- 1.5) cm/s (P < 0.05). Under hyperemization, esmolol changed the hAPV of proximal and distal to myocardial bridging separately from (54.1 +/- 14.9) cm/s and (44.7 +/- 9.4) cm/s to (49.7 +/- 16.4) cm/s and (48.9 +/- 10.1) cm/s (all P > 0.05); thus, the value of CFR both proximal and distal to myocardial bridge increased separately from 2.8 +/- 0.3 and 2.5 +/- 0.5 to 3.4 +/- 0.5 and 3.2 +/- 0.6 (all P < 0.01).

CONCLUSIONEsmolol can decreased the compression of the intramural coronary artery and increased the CFR to normal level of it.

Adrenergic beta-Antagonists ; pharmacology ; therapeutic use ; Coronary Circulation ; drug effects ; physiology ; Coronary Vessels ; diagnostic imaging ; drug effects ; physiopathology ; Female ; Humans ; Male ; Middle Aged ; Myocardial Bridging ; drug therapy ; physiopathology ; ultrastructure ; Propanolamines ; pharmacology ; therapeutic use ; Ultrasonography, Interventional

OBJECTIVETo study the effect of shensongyangxin capsule on myocardial remodeling and ventricular fibrillation characteristics in rat with coronary artery ligation.

METHODTwenty-three male rats were randomly divided into sham-group (n = 5), model group (n = 6), anmiodarone group (n = 6) and shensongyangxin capsule group (n = 6). Drugs were administrated after modeling of 2 days, lasting four weeks. Two dimensional and Doppler images were acquired by a 15 MHz high-frequency linear ultrasound transducer at 4 weeks after operation, and chest was opened to detect ventricular fibrillation threshold value and persistent time.

RESULTAfter administration of four weeks, echocardiogram was detected. Compared with model group, shensongyangxin capsule group diastasis interventricular septum thickness (IVSTd) and left ventricle diameter (LVDd) were significiently different between them (1.20 +/- 0.49) vs (0.78 +/- 0.08) mm and (6.77 +/- 1.34) vs (7.95 +/- 0.92) mm, (P < 0.01 and 0.05); echocardiogram result had no difference in amiodarone and model groups (P > 0.05). LVMI measured by practicion was different between shensongyangxin capsule and model groups: (17.12 +/- 1.91) vs (18.95 +/- 1.41) g x m(-2), (P < 0.05), while amiodarone group had no difference compared with model group. Electrophysiology was used to detect ventricular fibrillation threshold value and 1-5, 6-10, 11-15 V three stages' ventricular fibrillation threshold persistent time were significiently different among each group (P < 0.01), 16-20 V stage's ventricular fibrillation persistent time were also different among each group (P <0.05). Sample "average ranks" showed ventricular fibrillation threshold value of amiodarone group and shensongyangxin capsule group were four times than model group; and amiodaron group had best effect of holding-back ventricular fibrillation persistent time.

CONCLUSIONThe coronary artery ligation can result in myocardial remodeling by increasing volume load, and at the same time influencing electrophysiology function of heart. Amiodaron elevated ventricular fibrillation threshold of heart, this effect maybe relate to influencing many ion channels of myocardial cellular membrane; shensongyangxin capsule also elevate ventricular fibrillation threshold of heart, this effect maybe also relate to influencing many ion channels of myocardial cellular membrane, and on the other hand this effect maybe relate to hold-back ventricular remodeling after coronary artery was ligated, accordingly improve electrophysiological base material of heart.

Animals ; Capsules ; therapeutic use ; Coronary Vessels ; drug effects ; physiopathology ; surgery ; Disease Models, Animal ; Drugs, Chinese Herbal ; administration & dosage ; Heart ; drug effects ; physiopathology ; Humans ; Ligation ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Ventricular Fibrillation ; drug therapy ; surgery ; Ventricular Remodeling ; drug effects

The present study aimed to explore whether the stretch of ischemic myocardium could modulate the electrophysiological characteristics via mechanoelectric feedback (MEF), as well as the effect of phalloidin on the electrophysiological changes. Thirty-two Wistar rats were randomly divided into 4 groups: control group (n=9), phalloidin group (n=7), myocardial infarction (MI) group (n=9), MI + phalloidin group (n=7). The acute myocardial infarction (AMI) was conducted by ligation of the left anterior descending (LAD) coronary artery for 30 min in isolated rat heart. The volume alternation of a water-filled latex balloon in the left ventricle produced the stretch of myocardium. After perfused on Langendorff, the isolated hearts were stretched for 5 s by an inflation of 0.1, 0.2 and 0.3 mL separately and the effect of stretch was observed for 30 s, including the left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), ±dp/dt(max), monophasic action potential duration at 90% repolarization (MAPD90), and occurrence of premature ventricular beats (PVB) and ventricular tachycardia (VT). The stretch caused an increase of MAPD(90) in both control and MI rats (P<0.05, P<0.01). Moreover, MAPD(90) in MI group increased more significantly than that in the control group at the same degree of stretch (P<0.05, P<0.01). Phalloidin (1 μmol/L) had no effect on MAPD(90) in basal state. After stretch, MAPD(90) in phalloidin group slightly increased but was not significantly different from that in the control group. However, phalloidin reduced MAPD(90) in infarcted myocardium, especially when ΔV=0.3 mL (P<0.05). The incidence rates of PVB and VT in MI group were higher than that in the control group (both P<0.01). And there was no significant difference in the incidence rates of PVB and VT between phalloidin group and control group. Phalloidin inhibited the occurrence of PVB and VT in infarcted hearts (both P<0.01). LVSP and +dp/dt(max) in MI group obviously decreased (P<0.01 vs control). With application of phalloidin, LVSP slightly, but not significantly increased in infarcted hearts, while -dp/dt(max) significantly increased (P<0.05). It is suggested that MI facilitates the generation and maintenance of malignant arrhythmias, while phalloidin obviously inhibits the occurrence of arrhythmias.
Action Potentials ; Animals ; Arrhythmias, Cardiac ; prevention & control ; Coronary Vessels ; Heart ; drug effects ; physiopathology ; Heart Ventricles ; Myocardial Infarction ; physiopathology ; Phalloidine ; pharmacology ; Rats ; Rats, Wistar