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PubMed1992

Evaluation of quinapril on regional blood flow and cardiac function in patients with congestive heart failure.

Quinapril, a nonsulfhydryl ACE inhibitor, was evaluated in ten New York Heart Association (NYHA) functional class (FC) II-III CHF patients to determine its effects on regional blood flow [effective renal plasma flow (ERPF), renal blood flow (RBF), renal vascular resistance (RVR), hepatic blood flow (HBF), hepatic vascular resistance (HVR), segmental limb pressure (SLP), creatinine clearance (CRCL)] and cardiac function [left ventricular ejection fraction (LVEF)]. Previous vasodilator therapy was withdrawn 2 weeks before baseline measurements. Stable regimens of digoxin and diuretics were continued throughout the study. ERPF was assessed using p-aminohippurate (PAH), HBF by indocyanine green (ICG) clearance, and LVEF by radionuclide scintography. Segmental limb pressures were measured by Doppler flow detection. Measurements were performed at baseline (B) and after 4 weeks of quinapril therapy (10 mg BID). Quinapril increased renal (P less than 0.05) and hepatic blood flow (P = 0.06) and significantly reduced renal and hepatic vascular resistance. Glomerular filtration rate and left ventricular ejection fraction were unchanged. Mean arterial pressure and brachial segmental pressures decreased without change in heart rate. Noninvasive cardiovascular assessments indicate that quinapril improves regional blood flow while exhibiting no change in left ventricular ejection fraction, in patients with NYHA FC II-III CHF.

Antihypertensive Agents↗
PubMed1989

[Influence of microinjection of bicuculline into ventrolateral medulla on the suppression of cardiac function induced by diazepam in rabbits].

Experiments were carried out on 48 rabbits anaesthetized with urethane (1 g/kg). The animals were immobilized with gallamine triethiodide and ventilated artificially. Both intravenous injection of diazepam (0.5 mg/kg) and intracerebroventricular injection of flurazepam (2 mg in 50 microliters) or gamma-aminobutyric acid (GABA) (300 micrograms in 50 microliters) decreased the peak value of left ventricular pressure area of cardiac force loop and dp/dtmax. These suppressive effects of diazepam and flurazepam were prevented by intracerebroventricular injection of picrotoxin (15 micrograms in 50 microliters) or microinjection of bicuculline (3 micrograms in 0.5 microliter) into bilateral rostral ventrolateral medulla (gamma VLM). The results suggest that the inhibitory effects of diazepam on cardiac function may be mediated by activation of GABA receptor in gamma VLM.

Animals↗
PubMed1998

Nocturnal blood pressure in young patients with insulin-dependent diabetes mellitus: correlation with cardiac function.

Lack of a decline in nocturnal blood pressure is associated with an adverse effect on end organs in adults with insulin-dependent diabetes mellitus (IDDM). The role of the decline in nocturnal blood pressure in young patients with IDDM is not known. We studied 25 white subjects with IDDM (age = 20.8 +/- 3.7 years, mean +/- SD), 8 of whom were female. The duration of IDDM in these subjects was 12.9 +/- 5.4 years (mean +/- SD). We determined the values for glycosylated hemoglobin (HgbA1), 24-hour ambulatory blood pressure, diastolic cardiac function (the ratio of peak E wave to peak A wave velocity (E/A) and indexed peak filling rate ¿PFR/SV¿ by Doppler echocardiography), and albumin excretion rate. The HgbA1 level was 10.9% +/- 1.9% (mean +/- SD; normal range = 4.5%-8.5%). The HgbA1 concentration was inversely correlated (p < 0.005) with the decline in systolic (r = 0.57) and diastolic (r = -0.55) nocturnal blood pressure. Diastolic cardiac dysfunction ¿E/A ratio [r = 0.42, p < 0.03) and PFR/SV (r = 0.52, p < 0.01)¿ correlated with a smaller decrease in nocturnal diastolic blood pressure. An inverse correlation between decline in nocturnal systolic blood pressure and log albumin excretion rate (r = -0.37, p = 0.07) approached statistical significance. We conclude that poor glycemic control adversely affects nocturnal blood pressure and that the latter may play an important role in cardiac and possibly renal dysfunction in early IDDM.

Adolescent↗
PubMed2004

Overexpression of the catalytic subunit of protein phosphatase 2A impairs cardiac function.

Reversible protein phosphorylation is an essential regulatory mechanism in many cellular functions. In contrast to protein kinases, the role and regulation of protein phosphatases has remained ambiguous. To address this issue, we generated transgenic mice that overexpress the catalytic subunit alpha of protein phosphatase 2A (PP2A) (PP2Acalpha) in the heart driven by the alpha-myosin heavy chain promoter. Overexpression of the PP2Acalpha gene in the heart led to increased levels of the transgene both at RNA and protein levels. This was accompanied by a significant increase of PP2A enzyme activity in the myocardium. Morphological analysis revealed isles of necrosis and fibrosis. The phosphorylation state of phospholamban, troponin inhibitor, and eukaryotic elongation factor 2 was reduced significantly. The expression of junctional (calsequestrin) and free SR proteins (SERCA and phospholamban) was not altered. Whereas no increase in morbidity or mortality was noted, transgenic mice developed cardiac hypertrophy and reduced contractility of the heart, as well as cardiac dilatation as shown by biplane echocardiography. Taken together, these findings are indicative of the fundamental role of PP2A in cardiac function and imply that disturbances in protein phosphatases expression and activity may cause or aggravate the course of cardiac diseases.

Actins↗
PubMed2004

Crataegus special extract WS 1442 improves cardiac function and reduces infarct size in a rat model of prolonged coronary ischemia and reperfusion.

In Germany, hydroalcoholic extracts from hawthorn (Crataegus spp.) leaves with flowers are approved drugs for the treatment of mild forms of heart insufficiency. Besides cardiotonic effects these herbal remedies have been shown to possess cardioprotective properties. We now evaluated if treatment of rats with the Crataegus special extract WS 1442 also improves cardiac function and prevents myocardial infarction during prolonged ischemia and reperfusion lasting for 240 and 15 min, respectively. Oral administration of WS 1442 (10 or 100 mg x kg(-1) x day(-1)) for 7 days before ligation of the left coronary artery dose-dependently suppressed the decrease of the pressure rate product. WS 1442 treatment also attenuated the elevation of the ST-segment in the ECG, diminished the incidence of ventricular fibrillations (control: 67%; 10 mg x kg(-1): 64%; 100 mg x kg(-1): 27%) and reduced the mortality rate (control: 47%; 10 mg.kg(-1): 27%; 100 mg x kg(-1): 9%). Furthermore, the area of myocardial infarction within the ischemic zone was significantly smaller in treated rats (10 mg x kg(-1): 64.3 +/- 5.1%; 100 mg x kg(-1): 42.8 +/- 4.1%) when compared with controls (78.4 +/- 2.6%). It is suggested that these pharmacological effects are accounted for by the combined antioxidative, leukocyte elastase inhibiting and endothelial nitric oxide (NO) synthesis enhancing properties of WS 1442.

Analysis of Variance↗
PubMed2001

Improved cardiac function in patients with obstructive jaundice after internal biliary drainage: hemodynamic and hormonal assessment.

OBJECTIVE: To investigate myocardial function in patients with obstructive jaundice before and after internal biliary drainage. SUMMARY BACKGROUND DATA: Increased plasma levels of atrial natriuretic peptide (ANP) have been found in patients with biliary obstruction. METHODS: Thirteen patients with newly diagnosed obstructive jaundice and no previous heart, lung, or renal disease were studied using a Swan-Ganz catheter. Hemodynamic measurements were taken before and 4 days after internal biliary drainage. Levels of ANP and brain natriuretic peptide (BNP) were obtained and liver function tests were also determined. RESULTS: Plasma levels of ANP and BNP were increased twofold to fourfold in the basal state and declined after biliary drainage. Independent variables predicting left ventricular systolic work were total bilirubin concentrations, duration of jaundice, and BNP. In addition, bilirubin concentrations correlated with pulmonary vascular resistance, mean arterial pulmonary pressure, and right ventricular systolic work. Internal biliary drainage resulted in an improvement in left ventricular systolic work. A correlation was found between decreasing ANP concentrations and increasing cardiac output. CONCLUSIONS: Increased plasma levels of natriuretic peptides in patients with obstructive jaundice may reflect a subclinical myocardial dysfunction correlating with the degree of jaundice. After internal biliary drainage, there is a measurable improvement of cardiac function.

Adult↗
PubMed2004

Targeted cell delivery into infarcted rat hearts by retrograde intracoronary infusion: distribution, dynamics, and influence on cardiac function.

BACKGROUND: Intracoronary infusion for cell transplantation has potential advantages in disseminating cells globally into the myocardium with less injury over direct intramuscular injection. Arterial route, however, has a risk of coronary embolism and a limitation in cell delivery into ischemic or infarcted areas. We assessed the efficiency of retrograde intracoronary cell implantation into infarcted hearts using a novel rat model. METHODS AND RESULTS: After left coronary artery ligation in rat, a catheter was inserted into the left cardiac vein, which drains the left ventricular free wall. Through this, 1x10(6) skeletal muscle precursor cells expressing nuclear beta-galactosidase were infused retrogradely into the vein. In situ staining demonstrated that beta-galactosidase-expressing donor cells had disseminated throughout the left ventricular free wall, including both infarcted and surrounding border areas, at 10 minutes after infusion. At 28 days, in contrast, positively stained multinuclear myotubes were found in border zones, whereas no positive cells were seen in infarcted areas. Measurement of beta-galactosidase enzyme activity estimated that 29.8+/-6.9% of total infused cells were retained within the myocardium at 10 minutes and that this number decreased to 23.7+/-8.1% at 3 days but rapidly increased thereafter, reaching a plateau at 90.2+/-17.1% by 14 days. Echocardiography and Langendorff perfusion demonstrated that cell implantation improved cardiac function and dimensions by 28 days, compared with both sham-treated and phosphate-buffered saline-infused infarcted hearts, and this was associated with decreased collagen deposition. CONCLUSIONS: Retrograde intracoronary cell transplantation could provide an effective cell delivery into infarcted hearts and could be a useful strategy for treating myocardial infarction.

Animals↗
PubMed1992

Effect of flosequinan on exercise capacity and cardiac function in patients with chronic mild heart failure: a double-blind placebo-controlled study.

Although beneficial effects of a new vasodilating agent, flosequinan, have been demonstrated in patients with severe heart failure, its efficacy has not been studied in patients with a less severe form of chronic heart failure. In this study, the effects of 4 weeks' administration of flosequinan, 50 mg daily, and placebo on exercise capacity, cardiac function, and symptoms of heart failure were investigated in 24 patients with chronic mild heart failure (New York Heart Association functional class, mainly class II) in a double-blind clinical trial. When the parameter changes during the treatment period of the flosequinan and placebo groups were compared, no significant difference was found in any of the measurements except for left ventricular fractional shortening determined from M-mode echocardiograms; it was increased by 2.9 +/- 1.3% in the flosequinan group whereas it was decreased by 1.3 +/- 0.9% in the placebo group (P less than 0.05 vs flosequinan treatment). However, when compared to baseline values, flosequinan significantly increased exercise time in the symptom-limited maximal exercise test (704 +/- 103 to 763 +/- 107 s, P less than 0.05) and the oxygen uptake at the anaerobic threshold (13.8 +/- 1.3 to 16.7 +/- 1.4 ml/min kg, P less than 0.05), and improved symptoms assessed with a new heart failure severity classification (a median value of 2.0-1.5, P less than 0.05). These improvements were not observed in the placebo group. Serious adverse effects were not observed in either group. These results suggest that flosequinan is useful for the treatment of chronic mild heart failure as well as severe heart failure.

Adult↗
PubMedDate not supplied

[Effect on cardiac function of altered adenosine metabolism in rat brain structures in modelled hyperuricemia].

Experiments on 24 Wistar male rats were performed to clarify the role of central mechanisms in the onset of electrical instability of the heart due to disturbances in purine metabolism. The activity of the enzymes responsible for synthesis and conversion of adenosine-5-nucleotidase and adenosine deaminase in the sensomotor cortex, hypothalamus and hippocamp was studied. Changes in cardiac function were most severe in high levels of adenosine in the neurons of the sensomotor cortex, hypothalamus and hippocamp. Minimal changes occurred in low content of adenosine in the hypothalamus and hippocamp.

Adenosine↗
PubMed2004

Influence of long-term treatment of imidapril on mortality, cardiac function, and gene expression in congestive heart failure due to myocardial infarction.

Although it is generally accepted that the efficacy of imidapril, an angiotensin-converting enzyme inhibitor, in congestive heart failure (CHF) is due to improvement of hemodynamic parameters, the significance of its effect on gene expression for sarcolemma (SL) and sarcoplasmic reticulum (SR) proteins has not been fully understood. In this study, we examined the effects of long-term treatment of imidapril on mortality, cardiac function, and gene expression for SL Na+/K+ ATPase and Na+ -Ca2+ exchanger as well as SR Ca2+ pump ATPase, Ca2+ release channel (ryanodine receptor), phospholamban, and calsequestrin in CHF due to myocardial infarction. Heart failure subsequent to myocardial infarction was induced by occluding the left coronary artery in rats, and treatment with imidapril (1 mg.kg(-1).day(-1)) was started orally at the end of 3 weeks after surgery and continued for 37 weeks. The animals were assessed hemodynamically and the heart and lung were examined morphologically. Some hearts were immediately frozen at -70 degrees C for the isolation of RNA as well as SL and SR membranes. The mortality of imidapril-treated animals due to heart failure was 31% whereas that of the untreated heart failure group was 64%. Imidapril treatment improved cardiac performance, attenuated cardiac remodeling, and reduced morphological changes in the heart and lung. The depressed SL Na+/K+ ATPase and increased SL Na+-Ca2+ exchange activities as well as reduced SR Ca2+ pump and SR Ca2+ release activities in the failing hearts were partially prevented by imidapril. Although changes in gene expression for SL Na+/K+ ATPase isoforms as well as Na+-Ca2+ exchanger and SR phospholamban were attenuated by treatments with imidapril, no alterations in mRNA levels for SR Ca2+ pump proteins and Ca2+ release channels were seen in the untreated or treated rats with heart failure. These results suggest that the beneficial effects of imidapril in CHF may be due to improvements in cardiac performance and changes in SL gene expression.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Mechanism of overshoot in cardiac function during recovery from submaximal exercise in man.

BACKGROUND: A sudden increase (overshoot) in the left ventricular ejection fraction during the recovery from maximal exercise has been reported in patients with coronary artery disease, but its mechanism has not been fully clarified. We investigated whether this phenomenon may occur in normal subjects, and whether it depends on the intensity of exercise. METHODS: Thirteen normal subjects (mean [+/- SD] age, 59 +/- 8 years old) performed two levels (25 W and 50 W) of mild-intensity, constant-work-rate exercise for 6 min on a cycle ergometer. Left ventricular function was monitored continuously during the recovery from exercise using a computerized cadmium telluride detector. RESULTS: An overshoot was observed in the ejection fraction during the first minute of recovery compared with the end-exercise value. The overshoot in the ejection fraction during recovery after the 50-W exercise was greater than that seen after the 25-W exercise. An overshoot phenomenon in stroke volume was also observed during the recovery from 50-W exercise. CONCLUSIONS: The overshoot in cardiac function observed during the early phase of recovery, which was caused mainly by an immediate decrease in end-systolic volume, occurred even after exercise of mild intensity. This phenomenon appears to suggest the existence of a transient mismatch between cardiac contractility and afterload reduction during the recovery from mild-intensity exercise, even in normal subjects.

Aged↗
PubMed2005

Ethyl pyruvate enhances ATP levels, reduces oxidative stress and preserves cardiac function in a rat model of off-pump coronary bypass.

BACKGROUND: Off-pump coronary artery bypass grafting is associated with transient periods of myocardial ischemia during revascularization resulting in myocardial contractile dysfunction and oxidative injury. The purpose of this study was to investigate the efficacy of ethyl pyruvate as a myocardial protective agent in a rat model of off-pump coronary artery bypass grafting associated with transient myocardial dysfunction without infarction. METHODS: Wistar rats were subjected to transient ischemia via 10 min occlusion of the LAD coronary artery followed by 10 min of reperfusion. Animals received an IV bolus of Ringer's solution as a control (n=10) or Ringer's ethyl pyruvate (n=10) immediately before the initiation of ischemia and reperfusion. Myocardial ATP and lipid peroxidation levels were quantified for an estimation of energetics and oxidative stress, respectively. In vivo cardiac function was assessed throughout the ischemia and reperfusion periods. RESULTS: Ethyl pyruvate significantly increased myocardial ATP levels compared to controls (2650+/-759 nmol/g versus 892+/-276 nmol/g, p=0.04). Myocardial oxidative stress was significantly reduced in animals treated with ethyl pyruvate compared to controls (70.4+/-2.6 nmol/g versus 81.8+/-2.4 nmol/g, p=0.04). dP/dt max and cardiac output were significantly greater in the ethyl pyruvate group compared to controls during ischemia and reperfusion. CONCLUSIONS: Ethyl pyruvate enhances myocardial ATP levels, reduces oxidative stress, and preserves myocardial function in a model of transient ischemia/reperfusion injury not subject to myocardial infarction.

Adenosine Triphosphate↗
PubMed1982

The effect of digoxin on exercise capacity and exercising cardiac function in cystic fibrosis.

The ability of digoxin to increase exercise capacity and stroke volume (SV) during exercise was evaluated in ten patients with cystic fibrosis (CF) ages 12 to 20 years with moderate to severe degrees of airway obstruction but no history of heart failure. A double-blind crossover trial of digoxin versus placebo was carried out. An evaluation of exercise performance was undertaken upon entry into the study, and after each of the one-week periods in which digoxin 0.25 mg/day or placebo was taken. Exercise testing consisted of a progressive exercise test on a cycle ergometer to measure maximum work capacity (Wmax) and a steady state test at 2/3 of the baseline Wmax. During the steady state test, the oxygen consumption and carbon dioxide production were measured and cardiac output (Q) was calculated by the indirect Fick (CO2) method. From Q and heart rate (HR), SV was derived. After digoxin, Wmax was unchanged. On steady state exercise HR was unchanged, but there was a slight but significant fall in Q due to a fall in SV. The decrease in SV was associated with exercising hypoxemia. We conclude that digoxin did not increase exercise capacity or improve exercising cardiac function in patients with moderate to severe airway obstruction due to CF.

Adolescent↗
PubMed2005

Influence of cardiac function and failure on sleep-disordered breathing: evidence for a causative role.

Heart failure is an increasingly common public health problem that is strongly linked to both central and obstructive sleep apnea, collectively referred to as sleep-disordered breathing. Much attention has been given to the deleterious effects of sleep-disordered breathing on the failing heart and potential mechanisms by which treatment of sleep-disordered breathing may result in improved cardiac performance and long-term outcomes. However, there is compelling evidence that cardiac dysfunction may contribute to sleep-disordered breathing. Although there is recognized overlap between pathophysiological mechanisms in central sleep apnea and obstructive sleep apnea, data supporting the role of cardiac function are certain forms of central sleep apnea are well established, whereas investigation into the relationship with obstructive sleep apnea is less mature but continues to evolve. This review will examine experimental and observational data that explore possible pathophysiological mechanisms and potential targets for therapy in heart failure and sleep-disordered breathing.

Animals↗
PubMed1998

Improved cardiac function after catheter ablation in a patient with type B Wolff-Parkinson-White syndrome with an old myocardial infarction.

A 67-year-old man was admitted to hospital for the treatment of exertional dyspnea. He suffered from congestive heart failure due to an old inferior myocardial infarction with type B Wolff-Parkinson-White syndrome. Asynchronous wall motion caused by pre-excitation through a right-side bypass tract caused his cardiac function to deteriorate. Catheter ablation of the bypass tract increased the ejection fraction, and improved his symptoms, prior to surgical revascularization.

Aged↗
PubMed1992

Combined invasive and noninvasive study of left ventricular systolic and diastolic function following acute administration of cicloprolol to subjects with normal cardiac function.

Cicloprolol is a new beta-blocking agent with high selectivity for beta 1 receptors and high intrinsic sympathomimetic activity. We studied the acute hemodynamic effects of cicloprolol in nine subjects with no evidence of left ventricular dysfunction who underwent cardiac catheterization for the evaluation of chest pain. All patients had normal coronary angiography and left ventriculography. Left ventricular pressure was determined throughout the cardiac cycle using a Millar 8Fr Minotip catheter; an echocardiogram, phonocardiogram, and ECG were simultaneously recorded to obtain left ventricular pressure-diameter loops. All the measurements were repeated before and after the intravenous administration of cicloprolol. Cicloprolol was administered at increasing doses of 0.05, 0.10, and 0.25 mg/kg until a cardiac output increase of at least 15% over basal values was achieved. A decrease of mean arterial pressure or cardiac output after cicloprolol was not observed in any patient. Cicloprolol administration significantly increased cardiac output (24%), stroke volume (22%), and peak positive dP/dt (25%); no significant changes in heart rate, systemic blood pressure, right atrial pressure, or pulmonary artery pressures were observed. No significant change in the echocardiographic parameters occurred. Among the indices of left ventricular diastolic function, the time constant of isovolumetric relaxation was significantly decreased (-43%) after cicloprolol; moreover, the left ventricular pressure-diameter loop in the protodiastolic phase was shifted to the left following cicloprolol infusion. This study confirms that in subjects with normal left ventricular function cicloprolol can improve resting left ventricular systolic function, and it shows that this action can also be attended by a more rapid isovolumetric relaxation, similar to what has been observed with other sympathomimetic amines.

Adrenergic beta-Agonists↗
PubMed1999

Quantification of myocardial perfusion with FAST sequence and Gd bolus in patients with normal cardiac function.

The present study reports on a new calibration of the magnetic resonance imaging (MRI) signal intensity of a fast gradient-echo sequence used for in vivo myocardial perfusion quantification in patients. The signal from a FAST sequence preceded by a arrhythmia-insensitive magnetization preparation was calibrated in vitro using tubes filled with various gadolinium (Gd) solutions. Single short-axis views of the heart were obtained in patients (n = 10) with normal cardiac function. Myocardial and blood signal intensity were converted to concentration of Gd according to the in vitro calibration curve and fitted by a one-compartment model. K1 [first-order transfer constant from the blood to the myocardium for the gadolinium-diethylenetriamine-pentaacetic acid (Gd-DTPA)] and Vd (distribution volume of Gd-DTPA in myocardium) obtained from the fit of the MRI-derived perfusion curves were 0.72+/-0.22 (mL/min/g) and 15.3+/-5.22%. These results were in agreement with previous observations on animals and demonstrated that a reliable measurement of myocardial perfusion can be obtained by MRI in patients with an in vitro calibration procedure.

Calibration↗
PubMed1999

[Involvement of central and peripheral cholinergic structures in regulation of cerebral electric activity and cardiac function in rabbits during hypoxia].

In the normoxic conditions, prior to the "ascent" of rabbits, the i.v. injection of M-choline blocking benactyzine slowed down the ECG rhythm already within the next few minutes. Irritation of the reticular formation against this background did not initiate the reaction of activation; yet, heart rate was essentially unaltered by benactyzine. This was ascribed to low effectiveness of the benactyzine M-cholinergic mediation with respect to the cardiac function in contrast to the electric activity of the brain cortex due to, apparently, the abundance of M-choline receptors in this structure. The effect of N-cholinolytic ganglerone on the spontaneous and induced cortical activities was weak and, as compared with benactyzine, more expressed upon the heart rate. These choline blockers combined with hypoxia and the benactyzine-produced slow ECG waves on the initial phase (4000-5000 m) brought about neither spontaneous nor induced by the reticular formation irritation activation of ECG. At the maximal "altitude" (8500-9000 m) the benactyzine-synchronized ECG rhythm tended to become deeper assuming the low delta-type activity observed at the same "altitude" without i.v. benactyzine. With this ECG, irritation of Dieters' formation was impotent to trigger the reaction of activation.

Animals↗