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Myocardial Contractility (myocardial + contractility)

Distribution by Scientific Domains

Medical Sciences	92%
Life Sciences	8%

Distribution within Medical Sciences

Cardiovascular Disease	39%
Anesthesia & Pain Management	26%
Pharmacology & Pharmaceutical Medicine	8%
5 Other Subdomains	27%

Selected Abstracts

Role of Myocardial Contractility and Autonomic Control in the Hypotensive Response to a Limited Access Ethanol Paradigm in SHRs

ALCOHOLISM, Issue 6 2007
Mahmoud M. El-Mas
Background: Previous experimental studies that evaluated the chronic hemodynamic effect of ethanol employed the continuous exposure protocol of ethanol, which does not mimic the pattern of alcohol consumption in humans. This study dealt with the long-term hemodynamic and cardiovascular autonomic effects of ethanol, in a limited-access regimen in telemetered spontaneously hypertensive rats (SHRs). Methods: Changes in blood pressure (BP), heart rate (HR), myocardial contractility (dP/dtmax), and spectral cardiovascular autonomic profiles during the ethanol exposure period (2.5 or 5% w/v, 8 h/d, 8:30 am till 4:30 pm) were followed for 12 weeks. Results: Compared with control pair-fed SHRs, body weight and urine output, osmolality, and potassium levels were decreased in SHRs receiving 5% but not 2.5% ethanol. Blood pressure showed progressive falls during ethanol-feeding periods with a maximum effect observed at week 5. The peak hypotensive effect was maintained thereafter in SHRs receiving 5% ethanol in contrast to steady rises in BP in the 2.5% ethanol group to near-control levels by the conclusion of the study. Heart rate was slightly but significantly increased by ethanol 5% whereas dP/dtmax showed persistent reductions. Power spectral analysis showed that ethanol attenuated the baroreflex gain of HR as suggested by the reductions in index ,, the spectral index of spontaneous baroreflex sensitivity (BRS). Conclusions: It is concluded that limited access ethanol drinking in SHRs elicited hypotension that was concentration dependent and mediated, at least partly, through reductions in myocardial contractility. Baroreflex sensitivity attenuation by ethanol appeared to have limited the tachycardic response to ethanol and perhaps its capacity to offset the evoked hypotension. [source]

Myocardial Contractility and Cardiac Filling Measured by Impedance Cardiography in Patients with Nitroglycerine-Induced Vasovagal Syncope

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2006
PETER MITRO
Objective: Increased myocardial contractility and inadequate cardiac filling leading to activation of the Bezold-Jarisch reflex were proposed as possible triggering mechanisms of vasovagal syncope (VVS). In the present study noninvasive hemodynamic measurements were performed in order to examine the role of myocardial contractility and cardiac filling in pathogenesis of VVS. Methods: Hemodynamic parameters were measured during head-up tilt test (HUT) by impedance cardiography in 46 patients with unexplained syncope. Myocardial contractility was measured as index of contractility (IC), acceleration index (ACI), and ejection fraction (EF). Afterload was measured as systemic vascular resistance index (SVRI) and preload was expressed as end-diastolic index (EDI). Serial measurements were done 1 minute before HUT, during HUT at 1-minute intervals, and 1 minute after completion of HUT. Results: HUT was positive in 30 patients (10 men, 20 women, mean age 36 ± 16 years) and negative in 16 patients (8 men, 8 women, mean age 31 ± 14 years). No significant differences were observed between HUT(+) and HUT(,) groups in hemodynamic parameters at supine rest and during HUT until the development of syncope. SVRI was lower in HUT(+) than in HUT(,) group at syncope (122.7 + 66.3 vs 185.6 + 51.4 dyn sec cm,5/m2, P = 0.002) and after syncope (117.0 + 61.1 vs 198.0 + 95.7 dyn sec cm,5/m2, P = 0.007). ACI, IC, EF, and EDI did not differ between groups at syncope. After syncope EF was higher in HUT(+) group compared to HUT(,) group (59.2 + 6.1 vs 52.7 + 9.4%, P = 0.02). Conclusion: The role of increased myocardial contractility and decreased cardiac filling is not confirmed in the present study. [source]

Does the pre-ischaemic administration of sevoflurane reduce myocardial stunning?

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2007
A porcine experimental model
Background:, In a porcine model, the cardioprotective effect of sevoflurane was studied with regard to the preservation of myocardial contractility (myocardial stunning) after a myocardial ischaemic insult. Methods:, Twenty-seven pigs were randomized to receive either a dual 4% sevoflurane inhalation period as a supplement to pentobarbital anaesthesia or pentobarbital anaesthesia only before a 15-min ischaemic insult on the left anterior descending coronary artery. The ischaemic period was followed by 180 min of reperfusion. Myocardial contractility was assessed by myocardial sonomicrometry. Results:, A significant difference was found between the sevoflurane group and the control group at 5 min of reperfusion. However, subsequently, there was no overall difference between the two groups. Conclusion:, Sevoflurane administered as a pre-ischaemic bolus does not provide long-term improvement of the myocardial contractility. However, it can be speculated that sevoflurane may induce an early improvement in contractility. [source]

Myocardial Contractility and Cardiac Filling Measured by Impedance Cardiography in Patients with Nitroglycerine-Induced Vasovagal Syncope

Central and peripheral cardiovascular adaptations to exercise in endurance-trained children

ACTA PHYSIOLOGICA, Issue 2 2002
S. NOTTIN
ABSTRACT Stroke volume (SV) response to exercise depends on changes in cardiac filling, intrinsic myocardial contractility and left ventricular afterload. The aim of the present study was to identify whether these variables are influenced by endurance training in pre-pubertal children during a maximal cycle test. SV, cardiac output (Doppler echocardiography), left ventricular dimensions (time,movement echocardiography) as well as arterial pressure and systemic vascular resistances were assessed in 10 child cyclists (VO2max: 58.5 ± 4.4 mL min,1 kg,1) and 13 untrained children (UTC) (VO2max: 45.9 ± 6.7 mL min,1 kg,1). All variables were measured at the end of the resting period, during the final minute of each workload and during the last minute of the progressive maximal aerobic test. At rest and during exercise, stroke index was significantly higher in the child cyclists than in UTC. However, the SV patterns were strictly similar for both groups. Moreover, the patterns of diastolic and systolic left ventricular dimensions, and the pattern of systemic vascular resistance of the child cyclists mimicked those of the UTC. SV patterns, as well as their underlying mechanisms, were not altered by endurance training in children. This result implied that the higher maximal SV obtained in child cyclists depended on factors influencing resting SV, such as cardiac hypertrophy, augmented myocardium relaxation properties or expanded blood volume. [source]

Left Ventricular Function in Male Patients with Secondary Hypogonadism

ECHOCARDIOGRAPHY, Issue 3 2007
Oben Baysan M.D.
Background: In addition to the effects on ventricular repolarization, testosterone could also affect left ventricular performance. The enhancement of left ventricular contractility in testosterone-deficient rats following testosterone replacement implies to the possible testosterone effect. Objectives: The aim of the current study is to reveal the alterations of left ventricular functions, if any, in secondary hypogonadal male patients. Methods: Thirty-four males with secondary hypogonadism comprised the study group. The control group consisted of 30 healthy subjects. Echocardiographic measurements including left ventricular dimensions, ejection fraction, mitral inflow, and left ventricular outflow parameters were obtained from all subjects. Tissue Doppler parameters were also measured from left ventricular lateral wall and interventricular septum. Results: Left ventricular diameters, wall thicknesses, and performance parameters were similar in both groups. Mitral inflow parameters showed a statistically insignificant difference. Pulse-wave tissue Doppler interpretation of hypogonadal and healthy subjects were similar in terms of lateral and septal basal segment Sm, Em, and Am wave velocities. Conclusions: Regarding the findings of previous studies that showed impaired myocardial contractility and lusitropy in testosterone deficient rats and our study results, further studies are needed for better understanding of testosterone's effects on human myocardium. [source]

Viable Myocardium: How Much Is Enough?

ECHOCARDIOGRAPHY, Issue 1 2005
A Comparison of Viability by Comparative Imaging Techniques to Assess the Quantity, Functionality of Ischemic Myocardium
Left ventricular systolic dysfunction is mainly a result of coronary artery disease (CAD). Decrease in myocardial contractility results as a response to a chronic hypoperfusion state that produces a change in cardiac myocyte metabolism, resulting in a perfusion-contraction mismatch in which function is sacrificed for survival. If revascularization is performed in a timely fashion, metabolism can be restored leading to recovery of function. Through the use of noninvasive imaging modalities, assessing myocardial viability can be easily performed and will aid in selecting those patients who will benefit from revascularization. Viable myocardium can be identified by nuclear modalities that have a high sensitivity but a lower specificity, such as thallium-201 single photon emission computed tomography and positron emission tomography (PET); or by the use of dobutamine stress echocardiogram (DSE), which has a decreased sensitivity but a better specificity. A modality that is increasingly being used with an overall good sensitivity and specificity is contrast-enhanced magnetic resonance imaging. The purpose of this review is to explore the amount of myocardial viability that is relevant to pursue revascularization, since as myocardial function improves there is a decrease in morbidity and mortality from heart failure and arrhythmias. [source]

Treatment of congestive heart failure , current status of use of digitoxin

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue S2 2001
G. G. Belz
Digitalis glycosides exert a positive inotropic effect, i.e. an increase in myocardial contractility associated with a prolongation of relaxation period, and glycosides lower the heart rate (negative chronotropic), impede stimulus conduction (negative dromotropic) and promote myocardial excitability (positive bathmotropic). They seem to influence the activities of both the vagal and the sympathetic systems. Digitalis glycosides that belong to different substance classes are closely comparable concerning pharmacodynamics but differ substantially in regard to pharmacokinetics. Digoxin and its derivatives are less lipophilic, show lower protein binding and shorter half-life, are mainly eliminated via the kidney and accumulate rather rapidly in cases of insufficient kidney function. Digitoxin is highly lipophilic and extensively bound to plasma proteins, has a longer half-life, is mainly eliminated in the metabolized state via urine and faeces and does not accumulate in kidney dysfunction. As a result of a more stable pharmacokinetic profile, the incidence of toxic side effects seems to be lower with digitoxin than with digoxin. Since the beginning of the 1990s, the antagonists of the RAAS qualified as the standard treatment for congestive heart failure, often in combination with diuretics, vasodilators or ,-antagonists. However, the important role of digitalis glycosides as therapeutic comedication or alternative was never denied, especially in atrial fibrillation with tachycardia. The PROVED and RADIANCE trials proved a detrimental effect of the withdrawal of digoxin therapy on exercise capacity, left-ventricular ejection fraction and clinical symptoms. The DIG trial revealed that digoxin comedication in sinus rhythm patients with congestive heart failure was associated with a lower morbidity (as taken from death or hospitalization because of worsening heart failure) and an unchanged overall mortality , being a unique feature among the available inotropic drugs. Comparable studies for digitoxin have not yet been performed but, because of its higher pharmacological stability, it might well be associated with even more advantages in this regard than digoxin. [source]

Correlation of ,-skeletal actin expression, ventricular fibrosis and heart function with the degree of pressure overload cardiac hypertrophy in rats

EXPERIMENTAL PHYSIOLOGY, Issue 3 2006
Donatella Stilli
We have analysed alterations of ,-skeletal actin expression and volume fraction of fibrosis in the ventricular myocardium and their functional counterpart in terms of arrhythmogenesis and haemodynamic variables, in rats with different degrees of compensated cardiac hypertrophy induced by infra-renal abdominal aortic coarctation. The following coarctation calibres were used: 1.3 (AC1.3 group), 0.7 (AC0.7) and 0.4 mm (AC0.4); age-matched rats were used as controls (C group). One month after surgery, spontaneous and sympathetic-induced ventricular arrhythmias were telemetrically recorded from conscious freely moving animals, and invasive haemodynamic measurements were performed in anaesthetized animals. After killing, subgroups of AC and C rats were used to evaluate in the left ventricle the expression and spatial distribution of ,-skeletal actin and the amount of perivascular and interstitial fibrosis. As compared with C, all AC groups exhibited higher values of systolic pressure, ventricular weight and ventricular wall thickness. AC0.7 and AC0.4 rats also showed a larger amount of fibrosis and upregulation of ,-skeletal actin expression associated with a higher vulnerability to ventricular arrhythmias (AC0.7 and AC0.4) and enhanced myocardial contractility (AC0.4). Our results illustrate the progressive changes in the extracellular matrix features accompanying early ventricular remodelling in response to different degrees of pressure overload that may be involved in the development of cardiac electrical instability. We also demonstrate for the first time a linear correlation between an increase in ,-skeletal actin expression and the degree of compensated cardiac hypertrophy, possibly acting as an early compensatory mechanism to maintain normal mechanical performance. [source]

Xenon and isoflurane improved biventricular function during right ventricular ischemia and reperfusion

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2010
M. HEIN
Background: Although anesthetics have some cardioprotective properties, these benefits are often counterbalanced by their negative inotropic effects. Xenon, on the other hand, does not influence myocardial contractility. Thus, xenon may be a superior treatment for the maintenance of global hemodynamics, especially during right ventricular ischemia, which is generally characterized by a high acute complication rate. Methods: The effects of 70 vol% xenon and 0.9 vol% isoflurane on biventricular function were assessed in a porcine model (n=36) using the conductance catheter technique, and the expression of the type B natriuretic peptide (BNP) gene was measured. The animals underwent 90 min of right ventricular ischemia followed by 120 min of reperfusion. A barbiturate-anesthetized group was included as a control. Results: Cardiac output was compromised in unprotected animals during ischemia by 33±18% and during reperfusion by 53±17%. This was mainly due to impaired contractility in the left ventricle (LV) and increased stiffness. Isoflurane attenuated the increase in stiffness and resulted in a higher preload. In contrast, xenon increased the right ventricular afterload, which was compensated by an increase in contractility. Its effects on diastolic function were less pronounced. Upregulation of BNP mRNA expression was impeded in the remote area of the LV by both isoflurane and xenon. Conclusions: Xenon and isoflurane demonstrated equipotent effects in preventing the hemodynamic compromise that is induced by right ventricular ischemia and reperfusion, although they acted through somewhat differential inotropic and vasodilatory effects. [source]

Validation of a New Noninvasive Device for the Monitoring of Peak Endocardial Acceleration in Pigs: Implications for Optimization of Pacing Site and Configuration

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2008
PIERRE BORDACHAR M.D.
Introduction: The peak of endocardial acceleration (PEA) is an index of myocardial contractility. We aimed to (1) demonstrate that the PEA measured by the noninvasive cutaneous precordial application of an accelerometer sensor is related to left ventricular (LV) dP/dt max and (2) assess the usefulness of PEA monitoring during graded ischemia and during different configurations of sequential biventricular pacing. Methods and Results: Measurements of invasive LV dP/dt max were compared with measurements of transcutaneous PEA in seven pigs at baseline and during acute drug infusions; increased heart rate; right, left, biventricular and sequential biventricular pacing before and after graded ischemia induced by the constriction of the left anterior descending coronary artery. A consistent PEA signal was obtained in all animals. PEA changes were highly related to LV dP/dt max changes (r= 0.93; P < 0.001). The changes of LV contractility induced by the different pacing configurations were detected by PEA analysis in the absence of ischemia (r= 0.94; P < 0.001) and in the presence of ischemic LV dysfunction (r= 0.91; P < 0.001). Conclusion: Noninvasive PEA measurement allows monitoring of left ventricular contractility and may be a useful tool to detect global effect of ventricular ischemia and to optimize the choice of both pacing site and pacing configuration. [source]

Xanthine oxidase inhibitor allopurinol attenuates the development of diabetic cardiomyopathy

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 8b 2009
Mohanraj Rajesh
Abstract In this study, we investigated the effect of the xanthine oxidase (XO) inhibitor, allopurinol (ALP), on cardiac dysfunction, oxidative-nitrosative stress, apoptosis, poly(ADP-ribose) polymerase (PARP) activity and fibrosis associated with diabetic cardiomyopathy in mice. Diabetes was induced in C57/BL6 mice by injection of streptozotocin. Control and diabetic animals were treated with ALP or placebo. Left ventricular systolic and diastolic functions were measured by pressure,volume system 10 weeks after established diabetes. Myocardial XO, p22phox, p40phox, p47phox, gp91phox, iNOS, eNOS mRNA and/or protein levels, ROS and nitrotyrosine (NT) formation, caspase3/7 and PARP activity, chromatin fragmentation and various markers of fibrosis (collagen-1, TGF-,, CTGF, fibronectin) were measured using molecular biology and biochemistry methods or immunohistochemistry. Diabetes was characterized by increased myocardial, liver and serum XO activity (but not expression), increased myocardial ROS generation, p22phox, p40phox, p47phox, p91phox mRNA expression, iNOS (but not eNOS) expression, NT generation, caspase 3/7 and PARP activity/expression, chromatin fragmentation and fibrosis (enhanced accumulation of collagen, TGF-,, CTGF and fibronectin), and declined systolic and diastolic myocardial performance. ALP attenuated the diabetes-induced increased myocardial, liver and serum XO activity, myocardial ROS, NT generation, iNOS expression, apoptosis, PARP activity and fibrosis, which were accompanied by improved systolic (measured by the evaluation of both load-dependent and independent indices of myocardial contractility) and diastolic performance of the hearts of treated diabetic animals. Thus, XO inhibition with ALP improves type 1 diabetes-induced cardiac dysfunction by decreasing oxidative/nitrosative stress and fibrosis, which may have important clinical implications for the treatment and prevention of diabetic cardiomyopathy and vascular dysfunction. [source]

Phosphodiesterase inhibition by naloxone augments the inotropic actions of ,-adrenergic stimulation

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2009
W. K. PARK
Background: In a shock state, naloxone generates the cardiovascular pressor effect by displacing the endogenous opiate-like peptide ,-endorphin, resulting in restoration of the normal response to catecholamines. In addition to this opioid antagonistic effect, the non-opiate receptor-mediated effect has also been proposed. The aim of this study was to define the mechanism of non-opiate receptor-mediated action of naloxone. Methods: In guinea-pig ventricular tissues, cumulative concentration,response curves for isoproterenol as well as for forskolin and 3-isobutylmethylxanthine (IBMX) were obtained by increasing the concentration stepwise. To assess the effect on the phosphodiesterase (PDE), the effects of naloxone on contractile forces induced by isoproterenol (0.05 ,M) in the presence of IBMX, cilostamide (a PDE III inhibitor), or rolipram (a PDE IV inhibitor) were observed. Naloxone-induced changes in cAMP production by isoproterenol both in the absence and in the presence of IBMX were measured. Naloxone-induced changes in cAMP production by forskolin in the presence of IBMX were also measured. Results: Naloxone (30 ,M) produced a leftward shift of the isoproterenol concentration,response curve (0.01,2 ,M) without changing the maximal response. Forskolin (0.5,10 ,M) produced a concentration-dependent increase in contractile forces. Naloxone increased the maximal inotropic response of forskolin. Naloxone showed no effect on the IBMX concentration,response curve. In the presence of IBMX (200 ,M), naloxone did not alter the contractions evoked by isoproterenol or forskolin. Whereas naloxone increased contractile forces significantly (approximately 25%) more than that of isoproterenol in the presence of rolipram, no alteration of contractile forces in the cilostamide-incubated muscles was observed. Naloxone caused a concentration-related increase of cAMP in the absence of IBMX, but caused no change in its presence. Conclusions: The enhancement of myocardial contractility by naloxone in the presence of stimulation of adenylyl cyclase activity appears to be mediated by inhibition of PDE, specifically PDE III. [source]

Effects of levosimendan on indocyanine green plasma disappearance rate and the gastric mucosal,arterial pCO2 gradient in abdominal aortic aneurysm surgery

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2008
H. LEPPIKANGAS
Background: Levosimendan has a dual mechanism of action: it improves myocardial contractility and causes vasodilatation without increasing myocardial oxygen demand. In a laboratory setting, it selectively increases gastric mucosal oxygenation in particular and splanchnic perfusion in general. The aim of our study was to describe the effects of levosimendan on systemic and splanchnic circulation during and after abdominal aortic surgery. Methods: Twenty abdominal aortic aneurysm surgery patients were randomized to receive either levosimendan (n=10) or placebo (n=10) in a double-blinded manner. Both the mode of anaesthesia and the surgical procedures were performed according to the local guidelines. Automatic gas tonometry was used to measure the gastric mucosal partial pressure of carbon dioxide. Systemic indocyanine green clearance plasma disappearance rate (ICG-PDR) was used to estimate the total splanchnic blood flow. Results: The immediate post-operative recovery was uneventful in the two groups with a comparable, overnight length of stay in the intensive care unit. Cumulative doses of additional vasoactive drugs were comparable between the groups, with a tendency towards a higher cumulative dose of noradrenaline in the levosimendan group. After aortic clamping, the cardiac index was higher [4(3.8,4.7) l/min/m2 vs. 2.6(2.3,3.6) l/min/m2; P<0.05] and the gastric mucosal,arterial pCO2 gradient was lower in levosimendan-treated patients [0.9(0.6,1.2) kPa vs. 1.7(1.2,2.1) kPa; (P<0.05)]. However, the total splanchnic blood flow, estimated by ICG-PDR, was comparable [29(21,29)% vs. 20(19,25)%; NS]. Organ dysfunction scores (sequential organ dysfunction assessment) were similar between the groups on the fifth post-operative day. Conclusion: Levosimendan favours gastric perfusion but appears not to have a major effect on total splanchnic perfusion in patients undergoing an elective aortic aneurysm operation. [source]

Role of Myocardial Contractility and Autonomic Control in the Hypotensive Response to a Limited Access Ethanol Paradigm in SHRs

Ischaemic heart disease in the dog: a review of 65 cases

JOURNAL OF SMALL ANIMAL PRACTICE, Issue 3 2000
T. Falk
Sixty-five dogs are reviewed with histopathologically confirmed intramural arteriosclerosis. Clinical data (clinical signs, electrocardiographic findings and ultrasound parameters) on these animals were collected from nine small animal clinics in Sweden: 16 dogs had died suddenly, with few or no previous clinical signs; 13 dogs died or were euthanased during or shortly after general anaesthesia or sedation; 30 dogs developed acute (14) or chronic (16) congestive heart failure; and six dogs died or were euthanased for causes unrelated to cardiac disease. Electrocardiography of 23 of the dogs revealed several types of arrhythmias, with atrial fibrillation and sinus tachycardia being most commonly detected. Ultrasonographic examinations of 24 dogs found a relatively high number (19) with decreased indices of contractility. Dogs that had died suddenly and in relation to general anaesthesia or sedation had a higher incidence (25 of 29) of purely arteriosclerotic changes in the myocardial vessels, whereas just over half the dogs with congestive heart failure (16 of 30) had other concomitant heart lesions (in most cases endocardiosis). The incidence of myocardial infarcts was high (51 of 65 cases). It is postulated that arteriosclerosis in the dog may be an important reason for sudden death and death during general anaesthesia. Coronary arterial disease should also be a consideration in the clinical evaluation of dilated cardiomyopathy and may contribute to the decreased myocardial contractility when it is present in dogs with mitral regurgitation. [source]

Does the pre-ischaemic administration of sevoflurane reduce myocardial stunning?

Nuclear factor-,B inhibition improves myocardial contractility in rats with cirrhotic cardiomyopathy

LIVER INTERNATIONAL, Issue 5 2008
Hongqun Liu
Abstract Background/Aims: Cytokines such as tumour necrosis factor (TNF-,) contribute to the pathogenesis of cirrhotic cardiomyopathy. Nuclear factor-,B (NF-,B) is crucial for cytokine regulation, and induces cardiac dysfunction in several heart disease models. We aimed to elucidate possible NF-,B involvement in cirrhotic cardiomyopathy. Methods: Rats were bile duct ligated (BDL) to produce cirrhosis; controls received sham operation. Animals were studied 4 weeks later. Two NF-,B inhibitors were used: pyrrolidine dithiocarbamate (PDTC) and Bay 11-7082. Four groups were studied in most protocols: sham control, sham+PDTC, BDL and BDL+PDTC. Additional contractility studies were performed with Bay 11-7082. Myocardial NF-,B and TNF-, expression was measured by Western blot and ELISA. The contractility of isolated cardiomyocytes was observed under direct microscopy. Results: Nuclear factor-,B and TNF-, levels were increased in cirrhotic hearts compared with controls. PDTC significantly reduced NF-,B activity and TNF-, expression in cirrhotic hearts; controls were unaffected. Cirrhotic cardiomyocytes showed decreased systolic and diatolic velocity compared with sham controls. Both PDTC and Bay 11-7082 restored contractile function in cirrhotic cardiomyocytes, but did not affect controls. Conclusions: Inhibition of the increased NF-,B activity in cirrhotic hearts was associated with improvement of attenuated cardiomyocyte contractility. NF-,B, via effects on cytokine expression, may contribute to the pathogenesis of cirrhotic cardiomyopathy. [source]

Myocardial Contractility and Cardiac Filling Measured by Impedance Cardiography in Patients with Nitroglycerine-Induced Vasovagal Syncope

Clinical Use of Intracardiac Impedance: Current Applications and Future Perspectives

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4 2001
WAYNE ARTHUR
ARTHUR, W., et al.: Clinical Use of Intracardiac Impedance: Current Applications and Future Perspectives. For over 40 years the measurement of intracardiac impedance has been proposed as a method of assessing the contractile state of the heart muscle. This technique requires the positioning of one or more intracavitary electrodes and the generation of an electric field from an alternating current source. Variations in the calculated impedance signal reflect changes in the ventricular blood pool volume adjacent to the electrodes. Intracardiac impedance measurement has been successfully developed as a research tool to assess myocardial contractility, and from this, clinical uses have evolved. Commercial rate responsive pacing systems use intracardiac impedance to assess the inotropic state of the heart. Further development of this technology might allow hemodynamic discrimination of cardiac arrhythmias. [source]

The effects of mild induced hypothermia on the myocardium: a systematic review

ANAESTHESIA, Issue 5 2010
F. E. Kelly
Summary Mild induced hypothermia improves neurological outcome and reduces mortality among initially comatose survivors of out-of-hospital cardiac arrest. Similar pathological processes occur in the heart and the brain, namely ischaemia followed by reperfusion injury. Animal data indicate that mild induced hypothermia results in improved myocardial salvage, reduced infarct size, reduced left ventricular remodelling and better long-term left ventricular function. Several small human studies suggest that infarct size may be reduced by mild induced hypothermia, although this has not reached significance in any human study to date. There are variable reports of harm to the myocardium caused by mild induced hypothermia, including reduced myocardial contractility and cardiac output, electrocardiographic changes and arrhythmias, especially bradycardia. These harmful effects are reversible with rewarming. [source]

Different sensitivity of isoprenaline-induced responses in ventricular muscle to sodium nitroprusside in normotensive and spontaneously hypertensive rats 1

AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 2 2000
A. M. Manso
1 The aim of the present work was to study the possible modulatory role of nitric oxide (NO) on the positive inotropic effect induced by the ,-adrenoceptor agonist isoprenaline in myocardial contractility, and whether this modulation is altered by hypertension. 2 The study was performed using right ventricular strips from the hearts of 6-month-old male Wistar,Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The contractile force of electrically-stimulated ventricular strips was measured by a force-displacement transducer. 3 Isoprenaline (from 10 nmol l,1 to 10 ,mol l,1) induced a concentration-dependent increase in cardiac contractility in strips from both rat strains. This positive inotropic effect to isoprenaline was reduced by the NO donor sodium nitroprusside (SNP, 0.1 mmol l,1) in muscles from WKY rats and slightly increased in those from SHR. The SNP-induced increase in strips from SHR was abolished by superoxide dismutase (100 U ml,1). 4 NG-nitro-arginine-methyl ester (L-NAME, 0.1 mmol l,1) and 1H-[1,2,4]oxadiazolo[4,3]quinoxalin-1-one (ODQ, 10 ,mol l,1), respective inhibitors of NO synthase and guanylate cyclase, increased the response to isoprenaline in muscles from WKY rats, whereas it was unaltered in strips from SHR. 5 In strips from WKY rats, the combination of ODQ and SNP produced an increase in the response elicited by isoprenaline, which was similar to that observed with ODQ or L-NAME. 8-Br-cyclicGMP (8-Br-cGMP, 0.1 mmol l,1), a permeable and structural cGMP analogue, decreased the effect induced by isoprenaline only in muscles from WKY rats. 6 These results suggest that the positive inotropic response to isoprenaline in ventricular strips from WKY rats is negatively modulated by NO, and positively by superoxide anions in those from SHR. The lack of a modulatory response to NO in ventricular strips from SHR is probably a result of an alteration of mechanisms in NO-signalling pathway downstream of cGMP formation in SHR hearts. [source]

Transcoronary transplantation of autologous mesenchymal stem cells and endothelial progenitors into infarcted human myocardium

CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 3 2005
Demosthenes G. Katritsis MD PhD
Abstract The aim of the study was to investigate whether a combination of mesenchymal stem cells (MSCs) capable of differentiating into cardiac myocytes and endothelial progenitors (EPCs) that mainly promote neoangiogenesis might be able to facilitate tissue repair in myocardial scars. Previous studies have shown that intracoronary transplantation of autologous bone marrow stem cells results in improvement of contractility in infracted areas of human myocardium. Eleven patients with an anteroseptal myocardial infarction (MI) underwent transcoronary transplantation of bone marrow-derived MSCs and EPCs to the infarcted area through the left anterior descending artery. Eleven age- and sex-matched patients served as controls. Wall motion score index was significantly lower at follow-up in the transplantation (P = 0.04) but not in the control group. On stress echocardiography, there was improvement of myocardial contractility in one or more previously nonviable myocardial segments in 5 out of 11 patients (all with recent infarctions) and in none of the controls (P = 0.01). Restoration of uptake of Tc99m sestamibi in one or more previously nonviable myocardial scars was seen in 6 out of 11 patients subjected to transplantation and in none of the controls (P = 0.02). Cell transplantation was an independent predictor of improvement of nonviable tissue. Intracoronary transplantation of MSCs and EPCs is feasible, safe, and may contribute to regional regeneration of myocardial tissue early or late following MI. © 2005 Wiley-Liss, Inc. [source]

Operative contractility: A functional concept of the inotropic state

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2005
Roberto Curiel
SUMMARY 1.,Initial unsuccessful attempts to evaluate ventricular function in terms of the ,heart as a pump' led to focusing on the ,heart as a muscle' and to the concept of myocardial contractility. However, no clinically ideal index exists to assess the contractile state. The aim of the present study was to develop a mathematical model to assess cardiac contractility. 2.,A tri-axial system was conceived for preload (PL), afterload (AL) and contractility, where stroke volume (SV) was represented as the volume of the tetrahedron. Based on this model, ,operative' contractility (,OperCon') was calculated from the readily measured values of PL, AL and SV. The model was tested retrospectively under a variety of different experimental and clinical conditions, in 71 studies in humans and 29 studies in dogs. A prospective echocardiographic study was performed in 143 consecutive subjects to evaluate the ability of the model to assess contractility when SV and PL were measured volumetrically (mL) or dimensionally (cm). 3.,With inotropic interventions, OperCon changes were comparable to those of ejection fraction (EF), velocity of shortening (Vcf) and dP/dt-max. Only with positive inotropic interventions did elastance (Ees) show significantly larger changes. With load manipulations, OperCon showed significantly smaller changes than EF and Ees and comparable changes to Vcf and dP/dt-max. Values of OperCon were similar when AL was represented by systolic blood pressure or wall stress and when volumetric or dimensional values were used. 4.,Operative contractility is a reliable, simple and versatile method to assess cardiac contractility. [source]