Cardiac contractility variability (CCV) is a new concept which is introduced in the research field of cardiac contractility in recent years, that is to say, there are some disparities between cardiac contractilities when heart contracts. The changing signals of cardiac contractility contain a plenty of information on the cardiovascular function and disorder. In order to collect and analyze the message, we could quantitatively evaluate the tonicity and equilibrium of cardiac sympathetic nerve and parasympathetic nerve, and the effects of bio-molecular mechanism on the cardiovascular activities. By analyzing CCV, we could further understand the background of human being's heritage characteristics, nerve types, the adjusting mechanism, the molecular biology, and the adjustment of cardiac automatic nerve. With the development of the computing techniques, the digital signal processing method and its application in medical field, this analysis has been progressing greatly. By now, the assessment of CCV, just like the analysis of heart rate variability, is mainly via time domain and frequency domain analysis. CCV is one of the latest research fields in human cardiac signals being scarcely reported in the field of sports medicine; however, its research progresses are of important value for cardiac physiology and pathology in sports medicine and rehabilitation medicine.
Autonomic Nervous System ; physiology ; Exercise ; physiology ; Humans ; Myocardial Contraction ; physiology ; Phonocardiography ; methods ; Signal Processing, Computer-Assisted

Phonocardiogram exercise testing(PCGET) is a recently developed method for evaluating cardiac contractility and the cardiac reserve of patients with heart disease and of healthy subjects. In order to test the reliability of PCGET method in physical sport, the present author conducted a clinical study. The ratio of the amplitude of the first heart sound after PCGET to that recorded at rest was defined as an indicator, i.e. cardiac contractility reserve index (CCRI). PCGET was performed on 30 athletes and 30 non-athletes. The results showed that the average of CCRI was 10.139 +/- 2.631 in 30 athletes and 6.612 +/- 3.104 in 30 non-athletes. There was a significant difference between CCRI of the two groups (P < 0.01). Thus, PCGET might be a noninvasive, convenient and inexpensive technique to evaluate the cardiac reserve quantitatively for athletes.
Adolescent ; Adult ; Exercise Test ; methods ; Feasibility Studies ; Humans ; Myocardial Contraction ; physiology ; Phonocardiography ; methods ; Sports ; physiology

In order to culture cardiomyocytes or to observe the contractile function of adult mouse cardiomyocytes, it is necessary to isolate high-yield and high-quality cardiomyocytes at first. The mouse was injected with heparin (5,000 IU/kg, i.p.) 20 min prior to the experimental protocol, then was sacrificed by cervical dislocation. The heart was excised and the aorta was cannulated rapidly. The cannulated heart was mounted on a Langendorff perfusion apparatus with constant flow and perfusion pressure was monitored. The initial perfusion pressure was maintained at 40 mmHg by regulating the flow rate. The heart was digested by 0.05 % crude collagenase I at 37 degrees C and the enzymatic digestion was terminated immediately when the perfusion pressure was lowered to 28 mmHg. The heart was then cut off the cannula and the atria and aorta dissected away. The ventricular tissue was chopped and the single myocyte was dispersed gently by a wide tipped pipette. The viability of freshly isolated cardiomyocytes was more than 70 %. The cardiomyocytes were kept in Joklik's minimum essential medium containing 1 % BSA and 10 mmol/L BDM, then extracellular calcium was restored step-wise to a final concentration of 1.25 mmol/L. The viability of cardiomyocytes reduced to (40-50) % after 4 h standing. More than 90 % of rod-shaped cardiomyocytes were quiescent and had visible cross striations and sharp edges. The amplitude of unloaded shortening in cardiomyocytes was (9.72+/-0.43) % during 1.0 Hz stimulation, (11.28+/-0.43) % at 2.0 Hz and (11.40+/-0.45) % at 5.0 Hz. These results indicate that high yield and high quality cardiomyocytes can be obtained. In addition, the standards of identifying cardiomyocyte quality are concise and are suitable to culture the cardiomyocytes or to study the physiological function of cardiomyocytes.
Animals ; Cell Separation ; methods ; Cells, Cultured ; Female ; Male ; Mice ; Myocardial Contraction ; physiology ; Myocytes, Cardiac ; cytology ; physiology

This study evaluated the application of quantitative tissue velocity imaging (QTVI) in assessing regional myocardial systolic and diastolic functions in dogs with acute subendocardial ischemia. Animal models of subendocardial ischemia were established by injecting microspheres (about 300 microm in diameter) into the proximal end of left circumflex coronary artery in 11 hybrid dogs through cannulation. Before and after embolization, two-dimensional echocardiography, QTVI and real-time myocardial contrast echocardiography (RT-MCE) via intravenous infusion of self-made microbubbles, were performed, respectively. The systolic segmental wall thickening and subendocardial myocardial longitudinal velocities of risk segments before and after embolization were compared by using paired t analysis. The regional myocardial video intensity versus contrast time could be fitted to an exponential function: y=A.(1-exp(-beta.t)), in which the product of A and beta provides a measure of myocardial blood flow. RT-MCE showed that subendocardial normalized A.beta was decreased markedly from 0.99+/-0.19 to 0.35+/-0.11 (P<0.05) in 28 left ventricular (LV) myocardial segments after embolization, including 6 basal and 9 middle segments of lateral wall (LW), 8 middle segments of posterior wall (PW) and 5 middle segments of inferior wall (IW). However, there was no statistically significant difference in subepicardial layer before and after embolization. Accordingly, the ratio of A.beta of subendocardial myocardium to subepicardial myocardium in these segments was significantly decreased from 1.10+/-0.10 to 0.31+/-0.07 (P<0.05). Although the systolic wall thickening did not change 5 min after the embolization in these ischemic segments (29%+/-3% vs 31%+/-5%, P>0.05), the longitudinal peak systolic velocities (Vs) and early-diastolic peak velocities (Ve) recorded by QTVI were declined significantly (P<0.05). Moreover, the subendocardial velocity curves during isovolumic relaxation predominantly showed positive waves, whereas they mainly showed negative waves before the embolization. This study demonstrates that QTVI can more sensitively and accurately detect abnormal regional myocardial function and post-systolic systole caused by acute subendocardial ischemia.
Contrast Media ; Echocardiography/*methods ; Endocardium/physiopathology ; Microbubbles ; Myocardial Contraction/physiology ; Myocardial Ischemia/etiology ; Myocardial Ischemia/*physiopathology ; Myocardial Ischemia/*ultrasonography ; Myocardium/pathology ; Ventricular Function, Left/*physiology

Autonomic nervous system plays an important role in the regulation of mammalian heart, and it is divided into the sympathetic and parasympathetic (vagal) subsystems. The parasympathetic (vagal) control of the atria involves modulation of chronotropic, dromotropic and inotropic activities, but the role of the parasympathetic innervation of the ventricles is still unclear. There is a common misconception that the sympathetic nerves innervate all over the heart; while the parasympathetic nerves only innervate the superventricular part of the heart, but not the ventricles. Recent evidence indicates that the cholinergic innervation of the left ventricle is functionally very important in some mammalian species. The present article reviews the evidence of vagal control in the ventricles from the anatomy and histochemistry, molecular biology, and function areas. Additionally we overview the vagal (muscarinic) regulation of cardiac contractile function and its signal transduction.
Animals ; Heart Ventricles ; anatomy & histology ; innervation ; metabolism ; Humans ; Myocardial Contraction ; physiology ; Receptors, Muscarinic ; metabolism ; Signal Transduction ; physiology ; Vagus Nerve ; physiology

The aim of the present study was to investigate the influence of osmotic pressure on myocardial contractility and the possible mechanism. Electrical stimulation was used to excite papillary muscles of the left ventricle of Sprague-Dawley (SD) rats. The contractilities of myocardium in hyposmotic, isosmotic, and hyperosmotic perfusates were recorded. The influences of agonist and antagonist of the transient receptor potential vanilloid 4 (TRPV4) on the contractility of myocardium under hyposmotic, isosmotic and hyperosmotic conditions were observed. The results were as follows: (1) Compared with that under isosmotic condition (310 mOsm/L), the myocardial contractility was increased by 11.5%, 21.5% and 25.0% (P<0.05) under hyposmotic conditions when the osmotic pressure was at 290, 270 and 230 mOsm/L, respectively; and was decreased by 16.0%, 23.7% and 55.2% (P<0.05) under hyperosmotic conditions when the osmotic pressure was at 350, 370 and 390 mOsm/L, respectively. (2) When ruthenium red (RR), an antagonist of TRPV4, was added to the hyposmotic perfusate (270 mOsm/L), the positive inotropic effect of hyposmia was restrained by 36% (P<0.01); and when RR was added to the hyperosmotic perfusate (390 mOsm/L), the inhibitory effect of hyperosmia on myocardial contractility was increased by 56.1% (P<0.01). (3) When 4-α-phorbol-12,13-didecanoate (4α-PDD), an agonist of TRPV4, was added to the isosmotic perfusate (310 mOsm/L), the myocardial contractility did not change; and when 4α-PDD was added to the hyperosmotic perfusate (390 mOsm/L), the inhibition of myocardial contractility by hyperosmia was increased by 27.1% (P<0.01). These results obtained indicate that TRPV4 is possibly involved in the osmotic pressure-induced inotropic effect.
Animals ; Heart ; physiology ; Myocardial Contraction ; physiology ; Osmotic Pressure ; Phorbol Esters ; pharmacology ; Rats ; Rats, Sprague-Dawley ; TRPV Cation Channels ; physiology

AIMTo investigated the effect of estrogen on global myocardial ischemia/reperfusion (I/R) injury in ovariectomized (Ovx) rats.

METHODSSprague-Dawley rats were randomly repartitioned into three groups including sham-operated(Sham), ovariectomized (Ovx), or ovariectomized and then given 17beta-estradiol (Ovx + E2). Hearts were excised, mounted on the Langendorff. After the initial stabilization period, all of the three group hearts were randomly divided into normal perfusion subgroup (Control) and I/R perfusion subgroups. Control, perfused for 60 min after stabilization. I/R perfusion subgroups divided into 10 min I + 30 min R, 20 min I + 30 min R, 30 min I + 0 min R, 30 min I + 5 min R, 30 min I + 15 min R and 30 min I + 30 min R. And then, every group hearts were isolated into the single cardiomyocyte. The cardiomyocytes basal contraction and isoproterenol(ISO) stimulation contraction were measured. The viability and yield of cardiomyocytes were counted. LDH and CK concentrations in coronary effluent were assayed with assay kit.

RESULTSThe viability and yield of cardiomyocytes were significantly decreased in the conditions of 30 min ischemia followed by different times of reperfusion. The releases of LDH and CK in coronary effluent were significantly increased in the conditions of 30 min ischemia followed by different times of reperfusion. Except the 10 min and 20 min ischemia, the releases of LDH and CK were significantly increased in Ovx during I/R. Ovx + E2 could abate the heart injury through decreasing the releases of LDH and CK. Besides the control and the 10 min I + 30 min R groups, the myocardial basal and ISO stimulation contraction were higher from Ovx than Sham, and the effect was reversed by Ovx + Ez.

CONCLUSIONThe results indicate estrogen plays a cardioprotective role in global myocardial ischemia/reperfusion injury in ovariectomized (Ovx) rats.

Animals ; Estradiol ; pharmacology ; Estrogens ; pharmacology ; Female ; Myocardial Contraction ; physiology ; Myocardial Ischemia ; physiopathology ; Myocardial Reperfusion Injury ; prevention & control ; Myocytes, Cardiac ; metabolism ; physiology ; Ovariectomy ; Random Allocation ; Rats ; Rats, Sprague-Dawley

To evaluate the possibility and accuracy of Doppler tissue image (DTI) on assessment of normal and abnormal ventricular activation and contraction sequence, 9 open chest canine hearts were analyzed by acceleration mode, M-mode, and spectrum mode DTI. Our results showed that: (1) Acceleration mode DTI could show the origin of activation and conduction sequence on line; (2) M-mode DTI revealed that the activation in mid-interventricular septum was earlier than that in mid-left ventricular posterior wall at sinus activation; (3) Spectrum DTI showed the ventricular endocardium was activated earlier than the ventricular epicardium in all segments at sinus rhythm. The earliest site of activation of the normal ventricular wall was at middle interventricular septum; the latest site was at basal-posterior wall; the contraction sequence was different at the different walls; (4) During abnormal ventricular activation, mid-left ventricular posterior wall was activated earliest in accordance with the pacing sites. Abnormal ventricular activation was slower than sinus activation, and the contraction sequence varied at different sites of ventricular wall. It is concluded that DTI can be used to localize the origin of normal or abnormal myocardial activation and to assess the contraction sequence conveniently, accurately and non-invasively.
Animals ; Dogs ; Echocardiography, Doppler ; instrumentation ; methods ; Heart Ventricles ; diagnostic imaging ; Myocardial Contraction ; physiology ; Sinoatrial Node ; physiology ; Tachycardia ; diagnostic imaging ; physiopathology

OBJECTIVETo precisely visualize cardiac anatomic structures and simultaneously depict electro-mechanical events for the purpose of precise underblood intervention.

METHODSIntracardiac high-resolution tissue Doppler imaging was used to map real time myocardial contractions in response to electrical activation within the anatomic structure of the cardiac conductive system using a canine open-chest model.

RESULTSThe detailed inner anatomic structure of the cardiac conductive system at different sites (i.e., sino-atrial, atrial wall, atrial-ventricular node and ventricular wall) with the inside onset and propagation of myocardial velocity and acceleration induced by electrical activation was clearly visualized and quantitatively evaluated.

CONCLUSIONThe simultaneous single modality visualization of the anatomy, function and electrical events of the cardiac conductive system will foster target pacing and precision ablation.

Animals ; Dogs ; Echocardiography, Doppler ; Electrocardiography ; Heart Conduction System ; diagnostic imaging ; physiology ; Myocardial Contraction ; Sinoatrial Node ; diagnostic imaging ; physiology

OBJECTIVETo investigate the effects of exhaustive exercise on contraction mediated by beta-adrenoceptor (beta-AR) in rat cardiac myocytes and to analyze the mechanism by which cardiac systolic dysfunction is caused after exhaustive exercise.

METHODSSixteen SD rats were divided randomly into sedentary group and trained group. Cardiac myocytes were isolated from sedentary group and trained group after five times of exhaustive exercise in one week. Shortening response to norepinephrine (NE), time-to-peak contraction (TTP) and time-to-95% relaxation (R95) were measured after alpha1-AR were blocked. Also shortening responses to different levels of NE were observed.

RESULTSShortening amplitudes in trained rat cardiomyocytes were lower than that in sedentary group. Compared with sedentary group, shortening amplitudes induced by beta-AR stimulation were significantly decreased, meanwhile TTPs and R95 were prolonged when beta-AR were activated in trained rat cardiomyocytes. beta-AR responsiveness to NE was weakened in trained group compared with that in sedentary group.

CONCLUSIONDecreased shortening cardiomyocyte systolic function stimulating by beta-AR could result in cardiac systolic dysfunction after exhaustive exercise.

Animals ; Male ; Myocardial Contraction ; Myocytes, Cardiac ; physiology ; Physical Conditioning, Animal ; physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta-1 ; blood