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PubMedDate not supplied

Effects of the Na+/H+ exchange inhibitor cariporide (HOE 642) on cardiac function and cardiomyocyte cell death in rat ischaemic-reperfused heart.

1. Na+/H+ exchange has been implicated in the mechanism of reperfusion injury. We examined the effects of the cardiac-specific Na+/H+ exchange inhibitor cariporide (HOE 642) on postischaemic recovery of cardiac function and cardiomyocyte cell death (i.e. necrosis and apoptosis). 2. Rat isolated and buffer-perfused hearts were subjected to 25 min normothermic global ischaemia followed by 120 min reperfusion. Cariporide (10 micromol/L) or its vehicle (0.01% dimethylsulphoxide) was administered for 15 min before ischaemia and for the first 30 min after reperfusion. 3. Cariporide significantly improved the recovery of isovolumic left ventricular function (heart rate, left ventricular developed pressure and left ventricular end-diastolic pressure) and coronary flow throughout reperfusion. Creatine kinase release during reperfusion was significantly less in the cariporide-treated heart. In situ terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL)-positive cardiomyocytes were also significantly less in the cariporide-treated heart after 120 min reperfusion. Electron microscopy showed necrotic changes without typical apoptotic features in cardiomyocytes after reperfusion. Such necrotic changes were mitigated by cariporide. Simultaneous detection of necrotic and apoptotic cardiomyocytes using propidium iodide (PI) and Annexin V revealed that cardiomyocytes in the infarct area were stained with only PI or both PI and Annexin V. Cariporide did not alter the pattern of cardiomyocyte staining with PI and Annexin V, although the number of cardiomyocytes stained with PI or PI plus Annexin V was less than that in vehicle-treated hearts. 4. These results suggest that apoptosis is not a major manifestation of cardiomyocyte cell death in the ischaemic-reperfused myocardium and a cariporide-sensitive mechanism of reperfusion injury promotes both necrotic and apoptotic processes of cell death.

Animals↗
PubMed1986

A new approach to defining regional work of the ventricle and evaluating regional cardiac function: mean wall stress-natural logarithm of reciprocal of wall thickness relationship.

A new method of defining regional mechanical work done by a unit volume of myocardium of the ventricular wall and evaluating regional cardiac function is proposed. This method uses the relationship between mean wall stress (sigma) and the natural logarithm of the reciprocal of wall thickness (ln(1/H)). 1/H at a point on the epicardial surface is proportional to the regional area (A) of the ventricular wall containing that point. The value for regional work obtained from the relationship between the sigma and ln A or sigma and ln(1/H) has a true dimension of work, i.e., [J/m3]. The sigma-ln(1/H) relationship was studied in ten anesthetized dogs. Wall thickness and internal diameter of the left ventricle were measured with ultrasonic dimension gauges. Regional work per unit volume of myocardium multiplied by the total myocardial volume of the left ventricle correlated well with the total mechanical work of the entire left ventricle calculated from the pressure-volume relationship during pressure loading, contractility change, and volume loading. During pressure loading, the end-systolic sigma-ln(1/H) relationship showed linearity. After bolus injection of isoproterenol the sigma-ln(1/H) loop shifted to the left. We concluded that the sigma-ln(1/H) relationship provides a method of characterizing regional function normalized to the unit volume of myocardium. In addition, our methods have a potential for echocardiographic application.

Animals↗
PubMed2005

Modification of alterations in cardiac function and sarcoplasmic reticulum by vanadate in ischemic-reperfused rat hearts.

To study the cardioprotective effects of vanadate on ischemia-reperfusion (I/R) injury, isolated rat hearts perfused at constant flow were subjected to global ischemia for 30 min followed by reperfusion for 30 min. In this experimental model, I/R markedly decreased ventricular developed pressure and increased end-diastolic pressure. Pretreatment of hearts with 4 microM vanadate attenuated I/R-induced cardiac dysfunction. The reduction in sarcoplasmic reticulum (SR) Ca2+ uptake and Ca2+ release, as well as SR protein contents for Ca2+-pump ATPase and Ca2+-release channel, was also prevented by vanadate. Pretreatment of hearts with an antioxidant mixture containing superoxide dismutase + catalase exerted effects similar to those of vanadate in I/R hearts. Postischemic treatment of hearts with vanadate or superoxide dismutase + catalase also had beneficial effects on I/R-induced changes in cardiac performance and SR function. Alterations in cardiac function and SR Ca2+ transport due to an oxyradical-generating system (xanthine + xanthine oxidase) or an oxidant (H2O2) were attenuated by treatment with vanadate. These results suggest that vanadate may exert beneficial effects on cardiac performance and SR function in I/R hearts because of its antioxidant action.

Animals↗
PubMedDate not supplied

[Destabilization of the cardiac function of an insect by a low-frequency electric field].

The effect of high-intensity low-frequency electric field on the functioning of the heart of an insect was estimated from electrocardiogram. It was found that electric field causes a disturbance of the cardiac function. Its stressing activity is mainly related to the excitation of the insect by induced currents whose exciting action is enhanced by vibration in trichoid sensillas and antennas.

Animals↗
PubMedDate not supplied

Cardiac function during protein malnutrition and refeeding in the isolated rat heart.

In an attempt to elucidate the effect of protein restriction and subsequent refeeding on cardiac muscle function, 133 rat hearts were studied on a Langendorff perfusion apparatus: 19 normal controls, 55 rats during 6 weeks of protein restriction, and 59 rats during 6 weeks of refeeding following starvation. During starvation animals lost 14.3% of body weight and 12.8% in heart weight, both to be gained upon refeeding. Both developed force and force velocity tended to decrease in starving rats compared to control or refeeding rats. This trend was present at time 0, but more so after 60 min of perfusion. Furthermore, these differences became even more obvious and significantly different at the higher heart rates of 300 and 400 beats/min, and less so at 100 or 200 beats/min. These protein malnutrition-associated cardiac function derangements reversed almost completely to normal upon refeeding.

Animals↗
PubMed1998

Effects of type IV phosphodiesterase inhibition on cardiac function in the presence and absence of catecholamines.

Type IV phosphodiesterase (PDE4) inhibitors may be useful in several diseases in which catecholamine infusions are commonly used, including asthma, sepsis, and multiple organ failure. To determine whether type IV phosphodiesterase inhibitors alter baseline or catecholamine-induced changes in cardiac function or both, we examined the effects of Ro 20-1724 (PDE4 inhibitor) on several cardiac-performance parameters in the absence and presence of norepinephrine, epinephrine, isoproterenol, and dobutamine infusions (3, 1, 0.1, and 3 microg/kg/min, respectively). Male Sprague-Dawley rats received either Ro 20-1724 (10 microg/kg/min; n = 7) or vehicle (n = 6). After a left ventricular catheter was placed and connected to a heart-performance analyzer, each animal received each of the four catecholamines in randomized order (10 min per catecholamine with a 30-min washout period between infusions). In the absence of catecholamines, Ro 20-1724 significantly but mildly (i.e., <10%) increased heart rate but did not alter significantly any other measured cardiac parameter. In addition, Ro 20-1724 did not significantly alter norepinephrine-, epinephrine-, or dobutamine-induced changes in cardiac-performance parameters. There was, however, a significant attenuation of the isoproterenol-induced increase in a single measure of cardiac contractility (maximum dP/dt normalized to pressure). PDE4 inhibition does not cause significant cardiac toxicities in rats, both in the absence and presence of catecholamines. Our data suggest that PDE4 inhibitors may be safely used in critically ill patients receiving catecholamines. A clinical trial of this family of drugs in patients with critical illness is now being planned.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed2004

Randomized clinical trial of the effect of pneumoperitoneum on cardiac function and haemodynamics during laparoscopic cholecystectomy.

BACKGROUND: Conventional laparoscopic cholecystectomy (CLC) with carbon dioxide pneumoperitoneum may cause major cardiovascular changes. The aim of this study was to evaluate the effect of carbon dioxide pneumoperitoneum and positional changes on haemodynamics and cardiac function in patients assigned randomly to CLC or gasless laparoscopic cholecystectomy (GLC). METHODS: Fifty patients with American Society of Anesthesiologists physical status I and II were randomly allocated to CLC (28 patients) or GLC (22). Left ventricular end-diastolic and end-systolic diameters, fractional shortening and cardiac output were determined by transoesophageal echocardiography. Measurements were performed before (phase 1) and 10 and 30 min (phases 2 and 3 respectively) after pneumoperitoneum or abdominal wall traction, and after desufflation or release of abdominal wall traction (phase 4) in supine, Trendelenburg and reverse Trendelenburg positions. RESULTS: Mean diastolic diameter, systolic diameter, mean arterial pressure and heart rate were significantly higher, and fractional shortening was significantly lower, with carbon dioxide pneumoperitoneum than with the gasless procedure during phases 2 and 3. There were no significant differences in cardiac output between the two groups. CONCLUSION: Carbon dioxide pneumoperitoneum was associated with increased preload and afterload in patients undergoing laparoscopic cholecystecomy. It also decreased heart performance (fractional shortening), but did not affect cardiac output.

Adult↗
PubMed2006

Long-term administration of pirfenidone improves cardiac function in mdx mice.

Duchenne muscular dystrophy, an X-linked recessive neuromuscular disorder due to lack of the protein dystrophin, manifests as progressive muscle degeneration and cardiomyopathy with increased fibrosis. The exact mechanisms involved in fibrosis are unknown, but a cytokine, transforming growth factor-beta (TGF-beta), is a likely mediator. This study tested whether the TGF-beta antagonist, pirfenidone, could reduce cardiac fibrosis. Eight-month-old mdx mice were treated for 7 months with 0.4%, 0.8%, and 1.2% pirfenidone in drinking water; untreated water was given to control mdx and C57 mice. Mice treated with 0.8% and 1.2% pirfendone had lowered cardiac TGF-beta mRNA and improved in vitro cardiac contractility (P < 0.05) to levels consistent with C57 mice, yet without a change in cardiac stiffness or fibrosis. These results show that the TGF-beta antagonist, pirfenidone, can improve cardiac function in mdx mice, potentially providing a new avenue for developing cardiac therapies for patients with Duchenne muscular dystrophy.

Animals↗
PubMed1996

Diastolic abnormalities in systemic sclerosis: evidence for associated defective cardiac functional reserve.

OBJECTIVE: To investigate the pattern of diastolic abnormalities in patients with systemic sclerosis (SSc) and the relationship between impaired ventricular filling and systolic function. METHODS: Twenty four patients with SSc underwent M-mode and two dimensional echocardiography using echo-Doppler and gated blood pool cardiac angiography, both at rest and after exercise. RESULTS: An impaired diastolic relaxation of the left ventricle was detected in 10 of the 24 patients with SSc. Left ventricular ejection fraction at rest in these 10 patients with impaired ventricular filling did not differ from that in the remaining 14 patients, but eight of the 10 failed to increase their ejection fraction during exercise, compared with two of the 14 with normal ventricular filling (p = 0.003). CONCLUSION: Impaired relaxation of the left ventricle is a recently described feature of scleroderma heart disease. Diastolic dysfunction in SSc could depend on myocardial fibrosis or myocardial ischaemia, or both. It was found to be associated with a defective cardiac functional reserve. However, its prognostic significance remains to be clarified.

Adult↗
PubMed1988

Cardiac function after alcohol ingestion in patients with ischemic heart disease and cardiomyopathy: a controlled study.

Thirty male patients with ischemic heart disease and cardiomyopathy entered a controlled study of the acute effects of alcohol on cardiac function evaluated by right heart catheterization. Twenty patients, nine with angina pectoris and 11 with congestive heart failure, were studied during alcohol intoxication, and ten patients, five with angina pectoris and five with heart failure, served as a control group. The mean serum ethanol concentration in the alcohol group was 93 mg/100 ml (S.D. 17). The systemic arterial blood pressure was reduced by 6% in the alcohol group, P less than 0.05 compared with the control group. No significant changes occurred in the central venous pressure, the pulmonary artery pressure, the pulmonary capillary wedge pressure, or in cardiac output, stroke volume and total peripheral resistance. Alcohol intake in moderate doses has no measurable effect on pulmonary blood pressures or cardiac output in patients with ischemic heart disease and cardiomyopathy. Such an effect may, however, be masked by a reduction of afterload.

Aged↗
PubMed1983

Homologous radio-immunoassay of human plasma dopamine-beta-hydroxylase: analysis of homospecific activity, circulating plasma pool and intergroup differences based on race, blood pressure and cardiac function.

We used a homologous human dopamine-beta-hydroxylase (DBH) radio-immunoassay (RIA) to explore reported differences in plasma DBH enzymatic activity among patient groups stratified for race, blood pressure and cardiac function, as well as to determine plasma immunoreactive DBH protein pool and the relative activity of the enzyme in plasma versus human chromaffin tissue storage vesicles. Plasma DBH activity was lower in patients with congestive heart failure than in control subjects (19.9 +/- 4.0 versus 34.4 +/- 5.9 iu/l, P less than 0.05), paralleled by lower immunoreactive plasma DBH protein concentration (3.50 +/- 0.73 versus 6.34 +/- 1.05 micrograms/ml, P less than 0.05). All subject groups had similar plasma DBH homospecific activity (plasma DBH enzymatic activity/immunoreactive plasma DBH protein), ranging from 5.03 +/- 0.28 to 5.84 +/- 0.44 iu/mg. For the entire subject group, there was a significant relationship between plasma DBH activity and plasma DBH immunoreactive protein (r = 0.89, n = 78, P less than 0.01) from which no subgroup deviated systematically. Black hypertensives had lower plasma DBH activity than white hypertensives (23.0 +/- 5.2 versus 42.9 +/- 4.8 iu/l, P less than 0.01), though their plasma DBH homospecific activities and activity/immunoreactive protein plots were indistinguishable. Total circulating plasma DBH pools were large (from 13.1 +/- 3.7 to 27.5 +/- 4.8 mg).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Prolonged stability of brain natriuretic peptide: importance for non-invasive assessment of cardiac function in clinical practice.

1.BNP and ANP are important research indices of severity of heart failure. However, uncertainty regarding the stability of these peptides at room temperature has limited their use to assess cardiac function in routine clinical practice. 2. We assessed the stability of BNP and ANP in blood samples left for 2 h or 2 days at room temperature compared with levels in blood processed immediately (initial). These times were chosen to reflect possible times for samples to be processed in a hospital outpatient clinic (2 h) or a blood sample posted to a laboratory from general practice (2 days). Samples were obtained from eight heart transplant recipients. Blood was separated and plasma stored immediately after collection (initial) and after 2 h or 2 days at room temperature respectively. 3. Initial plasma BNP and ANP values measured by radioimmunoassay after Sep-Pak extraction were 38.9+/-11.1(S.E.M.) pg/ml and 113.6+/-28.1 pg/ml, respectively. After 2 h at room temperature there was no significant fall in either peptide level (35.5+/-9.9 pg/ml, BNP; 104. 9+/-30.6 pg/ml, ANP). However, after 2 days at room temperature there was a significant fall in ANP to 38.1+/-12.6 pg/ml (P<0.005 versus initial level). In contrast, there was no significant fall in BNP after 2 days (32.0+/-8.4 pg/ml). After 2 days at room temperature only 30.4+/-4.3% of the ANP remained, but 86.0+/-5.0% of BNP compared with the initial ANP and BNP measurements. 4. Our study clearly showed that ANP is stable for 2 h and thus could be useful as a screening test for heart disease in hospital. In contrast, BNP remained stable for 2 days. Measuring BNP may thus be practical as a test of heart function both for routine use in hospital and by general practitioners in the community.

Adult↗
PubMedDate not supplied

Cardiac function, inflammatory mediators and mortality in critical limb ischemia.

Patients with critical limb ischemia (CLI) have a high frequency of concomitant coronary heart disease and congestive heart failure. The aim of the study was to evaluate cardiac function in relation to inflammatory markers and 1-year mortality rate among patients with CLI. The authors investigated 232 consecutive patients with CLI by means of electrocardiogram (ECG), and measurements of endothelin (ET)-1, tumor necrosis factor alpha (TNF)alpha, interleukin (IL)-6, neopterin, CD40 ligand, and 8-epi-prostaglandin (PG)F2alpha in plasma. Echocardiography (echo) was performed in 88 (38%) patients. One-year mortality rate was assessed after prospective follow-up. One hundred and eighty-six (80%) patients had sinus rhythm (SR), 36 (16%) had atrial fibrillation or flutter (AF), and 10 (4%) pacemaker rhythm. Ischemic ECG changes occurred in 143 (62%) patients. Patients with AF showed higher IL-6 (p = 0.0296) and neopterin (p = 0.0494) concentrations. Patients with ischemic ECG changes showed higher ET-1 (p = 0.0303), 8-epi-PGF2alpha (p = 0.0027), neopterin (p = 0.0004) concentrations and 1-year mortality rate (p = 0.0105). The difference in ET-1 remained in logistic regression (p = 0.0152). Internal diameter of the left ventricle on echo correlated with IL-6 (r = 0.345, p = 0.0017), TNFalpha (r = 0.240, p = 0.0273), and neopterin (r = 0.327, p = 0.0028). Internal diameter of the left atrium correlated with TNFalpha (r = 0.384, p = 0.0092) and neopterin (r = 0.526, p = 0.0004), and ejection fraction (EF) correlated inversely with IL-6 (r = -0.380, p = 0.0015) and neopterin (r = -0.346, p = 0.0038). Patients with EF <40% showed higher (p = 0.0462) 1-year mortality rate than patients with EF >40%. In conclusion, in critical limb ischemia, cardiac rhythm disturbances and ischemic ECG changes were related to inflammatory mediators and predicted 1-year mortality rate. The inflammatory mediators correlated with echocardiographic signs of congestive heart failure.

Aged↗
PubMed2003

Effect of human urotensin-II infusion on hemodynamics and cardiac function.

Recent studies have shown that the vasoactive peptide urotensin-II (U-II) exerts a wide range of action on the cardiovascular system of various species. In the present study, we determined the in vivo effects of U-II on basal hemodynamics and cardiac function in the anesthetized intact rat. Intravenous bolus injection of human U-II resulted in a dose-dependent decrease in mean arterial pressure and left ventricular systolic pressure. Cardiac contractility represented by +/-dP/dt was decreased after injection of U-II. However, there was no significant change in heart rate or diastolic pressure. The present study suggests that upregulation of myocardial U-II may contribute to impaired myocardial function in disease conditions such as congestive heart failure.

Animals↗
PubMed1997

Analysis of cardiac function by MRI and stereology.

Design-based stereology and phase contrast magnetic resonance imaging (MRI) were combined to monitor changes in the volume of the four chambers of the human heart during the cardiac cycle. The data set consisted of 18 adjacent slices (or 'scanning levels') of 0.5 cm thickness, perpendicular to the long axis of the body, and encompassing the whole heart of a healthy volunteer. At each scanning level, a cardiac gated MR image was obtained at each of 16 equally spaced time frames within the cardiac cycle. Given stationarity with respect to time, absence of image artefacts and appropriate definition of chamber boundaries, for each time frame unbiased estimates of total blood volume in the relevant heart chambers were efficiently obtained using the Cavalieri method and point counting. Combined with a proper MRI acquisition, modern stereological methods constitute an efficient and reliable tool to quantify cardiac function noninvasively.

Blood Volume↗
PubMed2000

Influence of inhibition of nitric oxide synthesis on cardiac function in the newborn lamb after hypoxic-ischemic injury.

The aim of the present study was to investigate the effect of immediate post-hypoxic-ischemic (HI) inhibition of nitric oxide synthesis by N(omega)-nitro-L-arginine (NLA) on cardiac function and reactive oxygen species production. Fifteen newborn lambs were subjected to severe HI. Upon resuscitation 5 received 10 mg NLA/kg, 4 40 mg NLA/kg and 6 a placebo. Left ventricular (LV) contractility, cardiac output (CO), non-protein-bound iron (NPBI), ratio of reduced/oxidized ascorbic acid, alpha-tocopherol, sulfhydryl groups and malondialdehyde were measured before and 15, 60 and 120 min after resuscitation. There was a significant decrease in CO in all 3 groups at 60 min post-HI (p < 0.05). Reactive oxygen species production was also highest at 60 min post-HI (significantly increased NPBI and decrease in sulfhydryl groups in control lambs; p < 0.05). These results suggest neither a positive nor a negative effect of nitric oxide synthesis inhibition on post-HI myocardial performance but may suggest a positive effect of NLA on reactive oxygen species-mediated post-HI damage.

Animals↗
PubMed2001

Effects of 15 months of 17 beta-estradiol and dydrogesterone on systolic cardiac function according to quantitative and Doppler echocardiography in healthy postmenopausal women.

OBJECTIVE: Our goal was to investigate the short-term and intermediate effects of low-dose hormone replacement therapy on echocardiographic parameters of cardiac function in healthy postmenopausal women. STUDY DESIGN: In a prospective, controlled study 30 healthy postmenopausal women (mean age, 52 +/- 3 years) were randomly assigned to 2 groups. Women in the hormone replacement therapy group (n = 15) received 1 mg micronized 17 beta-estradiol daily sequentially combined with 5 or 10 mg dydrogesterone for 14 days of each 28-day cycle during 12 months and thereafter 2 mg 17 beta-estradiol combined with 10 mg dydrogesterone for a period of 3 months. The control group (n = 15) received no treatment. M-mode, quantitative 2-dimensional, and Doppler echocardiographic measurements were performed at baseline and within the 17 beta-estradiol phase at 3, 12, and 15 months. RESULTS: After 12 months significant differences in change between the 2 groups were found for left ventricular end-diastolic and left ventricular end-systolic diameters, left ventricular mass index, and stroke volume index. These differences were caused by changes in the control group rather than in the hormone replacement therapy group, in which no significant within-group changes were found. All other parameters measured showed no effect. CONCLUSION: Within 15 months of 17 beta-estradiol and dydrogesterone treatment no clinically relevant differences were found in the M-mode, quantitative 2-dimensional, and Doppler echocardiographic parameters measured in this study. It is suggested that 15 months of treatment probably is too short a period for detection of direct effects on the heart itself.

Double-Blind Method↗