OBJECTIVE: To evaluate the influence of papillary muscles and trabeculae on left ventricular (LV) cardiovascular magnetic resonance (CMR) analysis using three methods of cavity delineation (classic or modified inclusion methods, and the exclusion method) in patients with hypertrophic cardiomyopathy (HCM). MATERIALS AND METHODS: This retrospective study included 20 consecutive HCM patients who underwent 1.5-T CMR imaging with short-axis cine stacks of the entire LV. LV measurements were performed using three different methods of manual cavity delineation of the endocardial and epicardial contours: method A, presumed endocardial boundary as seen on short-axis cine images; method B, including solely the cavity and closely adjacent trabeculae; or method C, excluding papillary muscles and trabeculae. Ascending aorta forward flow was measured as reference for LV-stroke volume (SV). Interobserver reproducibility was assessed using intraclass correlation coefficients. RESULTS: Method A showed larger end-diastole and end-systole volumes (largest percentage differences of 25% and 68%, respectively, p < 0.05), compared with method C. The ejection fraction was 55.7 +/- 6.9% for method A, 68.6 +/- 8.4% for B, and 71.7 +/- 7.0% for C (p < 0.001). Mean mass was also significantly different: 164.6 +/- 47.4 g for A, 176.5 +/- 50.5 g for B, and 199.6 +/- 53.2 g for C (p < 0.001). LV-SV error was largest with method B (p < 0.001). No difference in interobserver agreement was observed (p > 0.05). CONCLUSION: In HCM patients, LV measurements are strikingly different dependent on whether papillary muscles and trabeculae are included or excluded. Therefore, a consistent method of LV cavity delineation may be crucial during longitudinal follow-up to avoid misinterpretation and erroneous clinical decision-making.
Adult ; Aged ; Cardiomyopathy, Hypertrophic/*pathology ; Female ; Heart Ventricles/physiopathology/*radiography ; Humans ; *Magnetic Resonance Imaging, Cine ; Male ; Middle Aged ; Papillary Muscles/*physiopathology ; Retrospective Studies ; Stroke Volume/physiology ; Systole/physiology

To study the antiarrhythmic effect of the newly developed alpha/beta-blocker TJ0711, a variety of animal models of arrhythmia were induced by CaCl2, ouabain and ischemia/reperfusion. Glass microelectrode technique was used to observe action potentials of right ventricular papillary muscle of guinea pig. The onset time of arrhythmia induced by CaCl2 was significantly prolonged by TJ0711 at 0.75, 1.5 and 3 mg x kg(-1) doses. TJ0711 (1.5 and 3 mg x kg(-1)) can significantly shorten the ventricular tachycardia (VT) and ventricular fibrillation (VF) duration, the incidence of VF and mortality were significantly reduced. On ischemia-reperfusion-induced arrhythmic model, TJ0711 (0.25, 0.5, 1 and 2 mg x kg(-1)) can significantly reduce the ventricular premature contraction (PVC), VT, VF incidence, mortality, arrhythmia score with a dose-dependent manner. At the same time, rats serum lactate dehydrogenase (LDH) and creatine kinase (CK) activities decreased significantly by TJ0711 (1 and 2 mg x kg(-1)). Ouabain could cause arrhythmia in guinea pigs, when TJ0711 (0.375, 0.75, 1.5 and 3 mg x kg(-1)) was given, the doses of ouabain inducing a variety of arrhythmia PVC, VT, VF, cardiac arrest (CA) were significantly increased with a dose-dependent manner. In the TJ0711 0.1-30 micromol x L(-1) concentration range, guinea pig right ventricular papillary muscle action potential RP (rest potential), APA (action potential amplitude) and V(max) (maximum velocity of depolarization) were not significantly affected. APD20, APD50 and APD90 had a shortening trend but no statistical difference with the increase of TJ0711 concentration. TJ0711 has antiarrhythmic effect on the sympathetic nerve excitement and myocardial cell high calcium animal arrhythmia model. Myocardial action potential zero phase conduction velocity and resting membrane potential were not inhibited by TJ0711. APD20, APD50 and APD90 were shortened by TJ0711 at high concentration. Its antiarrhythmic action mechanism may be besides the action of blocking beta1 receptor, may also have a strong selective blocking action on alpha1 receptor and reducing intracellular calcium concentration.
Action Potentials ; drug effects ; Adrenergic alpha-Antagonists ; administration & dosage ; pharmacology ; Adrenergic beta-Antagonists ; administration & dosage ; pharmacology ; Animals ; Anti-Arrhythmia Agents ; administration & dosage ; pharmacology ; Arrhythmias, Cardiac ; blood ; chemically induced ; etiology ; pathology ; physiopathology ; Calcium Chloride ; Creatine Kinase ; blood ; Dose-Response Relationship, Drug ; Female ; Guinea Pigs ; Heart Ventricles ; cytology ; Lactate Dehydrogenases ; blood ; Male ; Myocardial Reperfusion Injury ; complications ; Myocytes, Cardiac ; drug effects ; physiology ; Ouabain ; Papillary Muscles ; cytology ; Phenoxypropanolamines ; administration & dosage ; pharmacology ; Random Allocation ; Rats ; Rats, Sprague-Dawley

OBJECTIVEThe clinical diagnosis and treatment of ischemia mitral regurgitation (IMR) remained difficult because of its unclear mechanisms. This paper reviews studies on the mechanisms of IMR during the last 20 years, and discusses the relevance of the various mechanisms.

DATA SOURCESData used in this review were mainly from CNKI and Pubmed in English. The search terms were "ischemia mitral regurgitation mechanism", "myocardial infarction" AND "mitral regurgitation".

STUDY SELECTIONArticles were selected if they involved mechanisms of IMR.

RESULTSIMR is one of the common complications of coronary artery disease. But currently, the clinical diagnosis and treatment of IMR remained difficult because of its unclear mechanisms.

CONCLUSIONSFor now, dominating theory of ischemic mitral regurgitation mechanisms are left ventricular remodeling, imbalance of leaflet tethering and the closing force, left ventricular dysfunction, changes in spatial structure of the annulus and the dyssynchrony of the left ventricular electromechanical activity.

Animals ; Humans ; Mitral Valve Insufficiency ; etiology ; Myocardial Ischemia ; complications ; Papillary Muscles ; physiology ; Systole ; Ventricular Dysfunction, Left ; complications ; Ventricular Remodeling

It is proved that polydatin has cardioprotection against ischemia-induced arrhythmia, but the electrophysiological mechanism is not clear. The aim of the present study was to investigate the effect of polydatin on action potential (AP) in ventricular papillary muscle and the underlying ionic mechanism in rat using intracellular recording and whole-cell patch clamp techniques. The results showed: (1) In normal papillary muscles, polydatin (50 and 100 µmol/L) shortened duration of 50% repolarization (APD(50)) and duration of 90% repolarization (APD(90)) in a concentration-dependent manner (P<0.01). But polydatin had no effects on resting potential (RP), overshoot (OS), amplitude of action potential (APA) and maximal rate of depolarization in phase 0 (V(max)) in normal papillary muscles (P>0.05). (2) In partially depolarized papillary muscles, polydatin (50 µmol/L) not only shortened APD(50) and APD(90) (P<0.05), but also decreased OS, APA and V(max) (P<0.05). (3) After pretreatment with glibenclamide (10 µmol/L), an ATP-sensitive K(+) channel blocker, the electrophysiological effect of polydatin (50 µmol/L) was partially inhibited. (4) Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 1 mmol/L), a nitric oxide (NO) synthase inhibitor, failed to abolish the effect of polydatin (50 µmol/L) on AP. (5) Polydatin (25, 50, 75 and 100 µmol/L) decreased L-type Ca(2+) current in ventricular myocytes in a concentration-dependent manner (P<0.05). (6) Polydatin (50 µmol/L) increased ATP-sensitive K(+) current in ventricular myocytes (P<0.05). The results suggest that polydatin can shorten the repolarization of AP in normal papillary muscle and inhibit AP in partially depolarized papillary muscle, which might be related to the blocking of L-type Ca(2+) channel and the opening of ATP-sensitive K(+) channel.
Action Potentials ; drug effects ; Animals ; Calcium Channels, L-Type ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Glucosides ; pharmacology ; Heart Ventricles ; cytology ; KATP Channels ; metabolism ; Male ; Papillary Muscles ; metabolism ; physiology ; Rats ; Rats, Sprague-Dawley ; Stilbenes ; pharmacology

OBJECTIVETo study the effect of Ginkgo biloba extract 50 (GBE50), a new multicomponent drug with a polyvalent action extracted from the leave of Ginkgo biloba, on the action potentials in normal and simulated ischemic guinea pig papillary muscles.

METHODStandard intracellular microelectrode technique was used to examine the effects of GBE50 on the action potential parameters [action potential amplitude (APA), overshoot, rest potential, action potential amplitude at 20%, 50%, 90% of repolarization (APD20, APD50, APD90)].

RESULTIn normal guinea pig cardiac papillary muscles, GBE50 (20, 50, 100 mg x L(-1)) shortened APD50 and APD90, and did not affect the rest potential parameters. In simulated ischemic guinea pig cardiac papillary cells, action potential duration was significantly shortened, resting potential and action potential amplitude were reduced. 100 mg x L(-1) GBE50 partly attenuated the change induced by ischemia.

CONCLUSIONGBE50 shortened APD of normal guinea pig cardiac papillary cells in a concentration-dependent manner. Under ischemia, all action potential parameters were reduced . GBES0 could alleviate the electrophysiological heterogeneity of ischemic myocardium, which may attenuate myocardial ischemia and block the onset of arrhythmia.

Action Potentials ; drug effects ; Animals ; Disease Models, Animal ; Ginkgo biloba ; chemistry ; Guinea Pigs ; Humans ; Male ; Myocardial Ischemia ; drug therapy ; physiopathology ; Papillary Muscles ; drug effects ; physiology ; physiopathology ; Plant Extracts ; administration & dosage ; Random Allocation

The cardiac electrophysiological effects of hydrogen sulfide (H2S) were examined in guinea pig papillary muscles in vitro using intracellular microelectrode technique. The results obtained were as follows: (1) the duration of action potential (APD) in the normal papillary muscles was decreased by NaHS (H(2)S donor, 50, 100, 200 micromol/L) in a concentration-dependent manner; (2) in partially depolarized papillary muscles, 100 micromol/L NaHS not only reduced APD, but also decreased the amplitude of action potential (APA), overshoot (OS) and maximal velocity of depolarization at phase 0 (V(max)); (3) pretreatment with ATP-sensitive K(+) (K(ATP)) channel blocker glibenclamide (20 micromol/L) partially blocked the effects of NaHS (100 micromol/L); (4) pretreatment with L-type Ca(2+) channel agonist Bay K8644 (0.5 micromol/L) also partially blocked the effects of NaHS (100 micromol/L); (5) pretreatment with Ca(2+)-free Krebs-Henseleit solution containing glibenclamide (20 micromol/L) completely blocked the effects of NaHS (100 micromol/L); (6) APD in the normal papillary muscles was increased by DL-propargylglycine (PPG, an inhibitor of cystathionine gamma-lyase, 200 micromol/L). All these results suggest that the electrophysiological effects of H(2)S on papillary muscles in our study are due to an increase in potassium efflux through the opening of K(ATP) channels and a decrease in calcium influx. Endogenous H(2)S may act as an important regulator in electrophysiological characters in papillary muscles.
Action Potentials ; physiology ; Animals ; Calcium ; metabolism ; Female ; Guinea Pigs ; Hydrogen Sulfide ; pharmacology ; In Vitro Techniques ; KATP Channels ; metabolism ; Male ; Papillary Muscles ; metabolism ; physiology

OBJECTIVETo investigate the effects and underlying mechanisms of interferon-alpha (IFN-alpha) on the isolated Langendorff perfused rat hearts and the isolated papillary muscles.

METHODSThe left ventricular developed pressure (LVDP), maximal rise/fall rate of left ventricular pressure (+/-dP/dt(max)), left ventricular end-diastolic pressure (LVEDP), heart rate (HR) and coronary flow (CF) were recorded in isolated Langendorff perfused rat hearts. The average contractile force was measured in the isolated papillary muscles of rat right ventricle.

RESULTIFN-alpha (10 - 10,000 U/ml) induced a concentration-dependent decrease of LVDP and +/-dP/dt(max), and increase of LVEDP and CF in the isolated perfused rat heart (P < 0.05), and decrease of the average contractile force of the papillary muscle (P <0.05). Pretreatment with L-NAME (10(-4) mol/L), an inhibitor of nitric oxide synthase, attenuated the effect of IFN-alpha in the isolated rat hearts and the isolated papillary muscles (P <0.05). Isoproterenol (ISO, 10(-9) - 10(-6)mol/L) increased the contractile force of the rat papillary muscles in a concentration-dependent manner. Perfusion for 10 min with IFN-alpha at 1,000 U/ml attenuated the enhancing effect of ISO. Pretreatment with L-NAME reduced the effects of IFN-alpha on the isolated papillary muscles.

CONCLUSIONIFN-alpha may induce a negative inotropic effect in normal and beta-adrenergic activated cardiac muscles and this effect at least partly be mediated by nitric oxide.

Animals ; Heart ; drug effects ; physiology ; Heart Rate ; drug effects ; In Vitro Techniques ; Interferon-alpha ; pharmacology ; Male ; Myocardial Contraction ; drug effects ; Myocardium ; metabolism ; NG-Nitroarginine Methyl Ester ; pharmacology ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; antagonists & inhibitors ; metabolism ; Papillary Muscles ; drug effects ; metabolism ; physiology ; Perfusion ; Rats ; Rats, Sprague-Dawley

A change in pH can alter the intracellular concentration of electrolytes such as intracellular Ca2+ and Na+ ([Na+]i) that are important for the cardiac function. For the determination of the role of pH in the cardiac magnesium homeostasis, the intracellular Mg2+ concentration ([Mg2+]i), membrane potential and contraction in the papillary muscle of guinea pigs using ion-selective electrodes changing extracellular pH ([pH]o) or intracellular pH ([pH]i) were measured in this study. A high CO2-induced low [pH]o causes a significant increase in the [Mg2+]i and [Na+]i, which was accompanied by a decrease in the membrane potential and twitch force. The high [pH]o had the opposite effect. These effects were reversible in both the beating and quiescent muscles. The low [pH]o-induced increase in [Mg2+]i occurred in the absence of [Mg2+]o. The [Mg2+]i was increased by the low [pH]i induced by propionate. The [Mg2+]i was increased by the low [pH]i induced by NH4Cl-prepulse and decreased by the recovery of [pH]i induced by the removal of NH4Cl. These results suggest that the pH can modulate [Mg2+]i with a reverse relationship in heart, probably by affecting the intracellular Mg2+ homeostasis, but not by Mg2+ transport across the sarcolemma.
Animals ; Cations, Divalent ; Female ; Guinea Pigs ; Heart Ventricles/metabolism ; Hydrogen-Ion Concentration ; Ion Transport/physiology ; Ion-Selective Electrodes/veterinary ; Magnesium/*metabolism ; Male ; Membrane Potentials/physiology ; Papillary Muscles/*metabolism ; Propionates/pharmacology ; Sodium/*metabolism

Action Potentials ; drug effects ; Animals ; Estradiol ; pharmacology ; Female ; Guinea Pigs ; Heart Ventricles ; cytology ; Myocardial Contraction ; drug effects ; Papillary Muscles ; drug effects ; physiology ; Progesterone ; pharmacology

The purpose of this study was to investigate the effects of resveratrol on delayed afterdepolarization (DAD) and triggered activity (TA) induced by ouabain in guinea pig papillary muscles and the underlying mechanism. Action potentials were recorded using intracellular microelectrode technique. The results obtained are as follows: (1) DAD and TA induced by ouabain (1 micromol/L) were inhibited by pretreatment with resveratrol (30, 60, and 120 micromol/L) in a concentration-dependent manner; (2) Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 1 mmol/L), a nitric oxide (NO) synthase inhibitor, failed to abolish the above effect of resveratrol (60 micromol/L ); (3) 5 micromol/L 17beta-estradiol (E(2)) or 30 micromol/L resveratrol had no effects on DAD and TA, however, resveratrol combined with E(2) at the same doses exerted significant inhibitory effects on DAD and TA; (4) Pretreatment with tamoxifen (TAM, 10 micromol/L), an inhibitor of estrogen receptor, also did not blocked the effects of resveratrol (60 micromol/L) on DAD and TA induced by ouabain. All these results indicated that resveratrol exerted an inhibitory effects on DAD and TA induced by ouabain, possibly by reducing calcium influx, which might not be mediated by NO and estrogen receptor. The antiarrhythmic effects of resveratrol may contribute to its cardioprotective action.
Action Potentials ; drug effects ; Animals ; Anti-Arrhythmia Agents ; pharmacology ; Calcium Channel Blockers ; pharmacology ; Dose-Response Relationship, Drug ; Guinea Pigs ; Male ; Microelectrodes ; Ouabain ; antagonists & inhibitors ; Papillary Muscles ; physiology ; Stilbenes ; pharmacology