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At least 1,153 records · Page 64Linked to original sources
PubMed2005

Carvedilol exerts more potent antiadrenergic effect than metoprolol in heart failure.

BACKGROUND: It is still uncertain whether or not there is a difference between metoprolol and carvedilol for the treatment of congestive heart failure. We attempted to determine the difference between the two beta-blockers in terms of their antiadrenergic effect during exercise in patients with heart failure and their efficacy based on the baseline plasma brain natriuretic peptide concentration. METHODS: Fifty-three patients with mild to moderate heart failure with a radionuclide left ventricular ejection fraction <40% received open label metoprolol or carvedilol in a randomized fashion. The increase in the heart rate normalized to the increase in the plasma norepinephrine concentration during exercise, was calculated as an index of adrenergic responsiveness during exercise. RESULTS: The increase in heart rate normalized by the increase in plasma norepinephrine concentration, decreased after the initiation of beta-blockers in the carvedilol group, but not in the metoprolol group. The change in cardiac function was more favorable for carvedilol than metoprolol in patients who exhibited a higher baseline brain natriuretic peptide concentration. CONCLUSIONS: Carvedilol exerts a more potent antiadrenergic effect than metoprolol during stress in patients with mild to moderate heart failure. Carvedilol appears to be more efficacious than metoprolol in patients who exhibit higher baseline brain natriuretic peptide concentrations. These differences should be kept in mind when selecting appropriate pharmacologic agents in the treatment of heart failure.

Adrenergic beta-Antagonists↗
PubMed2005

Psychological distress and exertional angina in men and women undergoing thallium scintigraphy.

UNLABELLED: The relation between psychological factors and angina has mostly been studied in male patients with confirmed CAD and few have evaluated this relation during actual provocation of ischemia. This study evaluated gender differences in the association between psychological distress and angina pain experience in 907 Caucasian patients (479 women, mean age = 60 years) undergoing exercise stress testing with thallium scintigraphy. Data were analyzed separately for patients with and without exercise related ischemia using a series of 2 (low/high distress) x 2 (gender) ANOVAs as well as binary logistic regressions. Among all patients, distress and gender were associated with greater risk and intensity of angina pain during testing (p < 0.05) and more angina following exertion (p < 0.05) or stress (p < 0.05) at home. CONCLUSION: angina pain was more severe in women and individuals with high levels of distress, regardless of their ischemic status. A generalized hypersensitivity to pain/symptoms may be indicated in these patients.

Analysis of Variance↗
PubMed1980

Angiographic demonstration of different pathogenetic mechanisms in patients with spontaneous and exertional angina associated with S-T segment depression.

Three patients complained of spontaneous and exertional chest pain, both associated with S-T segment depression in anterior electrocardiographic leads. In each, coronary spasm was demonstrated on coronary arteriography during a spontaneous attack of pain. Coronary arteriograms taken during exercise-induced angina did not show evidence of spastic obstruction; this suggests that exercise-induced chest pain and S-T segment depression were secondary to the increase in oxygen requirements rather than to a sudden decrease in coronary blood flow. Thus, two pathogenetic mechanisms coexisting in the same patient may cause chest pain associated with subendocardial ischemia.

Angina Pectoris↗
PubMed1981

Hemodynamic effects of molsidomine at rest and during submaximal and maximal exercise in patients with coronary artery disease limited by exertional angina pectoris.

To analyze the mechanisms of action of molsidomine, a new antianginal drug, 10 patients with coronary artery disease and exertional angina pectoris were studied. Hemodynamic measurements were made at rest, during submaximal exercise and during angina-limited exercise before and 1 hour after intravenous administration of 2 mg of molsidomine. When angina pectoris was prevented after the drug was given (6 of 10 patients), the exercise intensity was increased until the recurrence of angina (3 patients) or until exhaustion (3 patients), and hemodynamic data were recorded at this higher exercise capacity. At rest and during submaximal exercise, molsidomine increased heart rate and decreased cardiac output and mean systemic and pulmonary arterial pressures. The prevention of angina pectoris was attended by lower mean systemic and pulmonary arterial pressures and pressure-rate product; cardiac output and heart rate were unchanged. The greater exercise capacity (+26 percent) after molsidomine was attended by increases in maximal cardiac output (+19 percent) and in arteriovenous oxygen difference (+6 percent); the maximal pressure-rate product was unchanged and systemic vascular resistance was lower. The mechanisms of action of molsidomine are very similar to those of nitrates and imply a decrease in venous and arterial tone. Molsidomine deserves further study in patients with angina or congestive heart failure.

Adult↗
PubMed1985

Clinical and hemodynamic evaluation of propranolol in combination with verapamil, nifedipine and diltiazem in exertional angina pectoris: a placebo-controlled, double-blind, randomized, crossover study.

The clinical and hemodynamic effects of propranolol, propranolol-verapamil (P-V), propranolol-nifedipine (P-N) and propranolol-diltiazem (P-D) were studied in 19 patients with chronic exertional angina pectoris. A placebo-controlled, double-blind, randomized, crossover study design was used in which patients took each treatment for a 4-week period. The 3 combinations equally reduced the incidence of angina attacks and decreased ST-segment depression. Left ventricular hypokinesia during exercise was lessened and end-systolic volume during exercise decreased with all combinations. Because of a corresponding reduction of normokinetic segmental function, global ejection fraction during exercise remained unchanged. Heart size increased (p less than 0.05) and the PR interval lengthened (p less than 0.001) with P-V and P-D compared to P-N. The largest number of adverse clinical reactions occurred with P-V, whereas the fewest occurred with P-D. Almost all patients preferred combined therapy over propranolol and many favored 1 combination over the others. In summary, when therapy with combined beta- and calcium channel-blocking drugs is planned, P-D should be considered the combination of first choice because of its low incidence of adverse clinical effects. In the presence of possible or definite abnormalities of atrioventricular nodal conduction or decreased left ventricular function, P-N should be considered. Although P-V is associated with frequent adverse reactions, a trial may be warranted if the other combinations are unsuccessful.

Adult↗
PubMed1986

Effect of body posture and common hand tools on peak torque exertion capabilities.

An experimental investigation was conducted to investigate the effects of body posture and of different types of common non-powered hand tools on maximum volitional torque exertion capabilities of males and females. Thirty-six males and 14 females applied peak torque in 21 different body postures while using nine different hand tools. The data analysis indicated that, for both males and females, the magnitude of volitional torque is strongly influenced by the type of tool used and the posture assumed. Between the two, however, the effect of hand tool is more profound. The correlation between the tool type and volitional torque was of the order of 0.71. No other variable was as strongly correlated with volitional torque. Maximum volitional torque profiles, as a function of posture and tool type, are provided for males and females.

Journal Article↗
PubMed1994

Development of methods for registration of the force exerted by hand-fingers in industrial work.

In a manufacturing industry producing ground hard metal inserts, a small strain-gauge pressure transducer was built into the work prefix to measure the force exerted by the fingers. The procedure did not interfere with the work. The variation of force and of the time sequences between each force measurement were measured. The coefficient of variation (CV) was used as a measure of precision of the work.

Journal Article↗
PubMed1996

Evaluation of perceived and self-reported manual forces exerted in occupational materials handling.

The main objective of the study was to evaluate the ability of workers to reproduce simulated manual work forces correctly and to quantify these forces in Newtons (N) by means of self-reports. Fourteen male and 14 female workers participated in the study. Three experiments were carried out. In the first experiment, the ability to reproduce the magnitudes of simulated manual forces occurring in daily work and to estimate these forces in Newtons was tested. A specially designed force-measuring device was used for this purpose. In the second experiment, the subjects estimated the weights of five boxes ranging from 1 to 30 kg. In the third experiment, the subjects were asked to produce five predetermined push and pull forces ranging in magnitude from 10 to 300 N on to the handle of the force-measuring device. The ability to reproduce the magnitudes of manual forces when simulating four familiar work tasks was good (the intraclass correlation coefficients ranged from 0.75 to 0.95). The ability to quantify these forces in Newtons was not as good (the product moment correlation coefficients ranged from 0.21 to 0.69). When the subjects estimated the weights of boxes they underestimated the weights. When they produced predetermined push and pull forces they exerted higher forces than expected when low force levels were requested and lower forces when high force levels were requested. However, the forces were correctly ranked. In summary, simulation of the manual push/pull forces used in familiar work tasks seemed to offer sufficient reproducibility to be worth testing for validity. Self-reports, used without previous training or without known 'reference forces', seemed to be very rough when the aim was to estimate in kg or Newtons. However, the fact that individuals could rank the forces correctly opens a potential for refinement of self-reports as a method for quantifying manual forces in objective terms, e.g. kg or Newtons.

Journal Article↗
PubMed1992

Oxidized low density lipoproteins exert arrhythmogenic effects in rabbit Purkinje fibers.

The electrophysiological effects of oxidized low density lipoproteins (ox-LDLs) have been studied in rabbit Purkinje fibers using standard microelectrode techniques, in comparison with native LDLs (n-LDLs) and lysophosphatidylcholine (LPC). At the concentration of 100 micrograms protein/ml, ox-LDL but never n-LDL induced the abrupt occurrence of abnormal electrical activities during the basic stimulation of 1 Hz (6/13 fibers) and the development of either early afterdepolarizations (6/13 fibers) or abnormal automaticity (4/13 fibers) at low frequencies (0.1 and 0.03 Hz). Short trains of rapid stimulation (2, 3, 4 and 5 Hz) did not trigger delayed afterdepolarizations. However, early afterhyperpolarizations were commonly seen after each action potential. 30 microM LPC caused quite similar electrophysiological derangements. The results suggest that ox-LDLs may exert arrhythmogenic effects partly explained by their LPC content.

Action Potentials↗
PubMed1983

A theoretical kinetic analysis of the protective action exerted by eserine and other carbamate anticholinesterases against poisoning by organophosphorus compounds.

The protection exerted by carbamate anticholinesterases against the lethal effects of organophosphate anticholinesterases is interpreted kinetically. The protective action is shown to depend on the provision (by carbamylation) of a pool of sequestered cholinesterase resistant to organophosphates but which furnishes (by decarbamylation) sufficient active enzyme to essential cholinergic synapses to ensure survival until all free organophosphate is cleared from the tissues. The two main factors governing the extent of protection are the minimum cholinesterase activity compatible with survival and the "enzyme conservation index" defined essentially as the ratio of the rate of enzyme decarbamylation to the rate of enzyme phosphorylation; the lower the "minimum essential cholinesterase" and the higher the "enzyme conservation index", the greater the protection. The theory is shown to be in excellent qualitative agreement with experiment.

Animals↗
PubMed1984

Inhibitory GABAergic influence on striatal serotonergic transmission exerted in the dorsal raphe as revealed by in vivo voltammetry.

In vivo differential pulse voltammetry with electrochemically treated carbon fiber microelectrodes has been used to investigate the anatomical nature of the GABAergic influence on striatal serotonergic transmission in the rat. Lesion studies and pharmacological treatments demonstrated that the electrochemical signal recorded at 300 mV in the striatum probably corresponds to the oxidation of extracellularly released 5-hydroxyindoleacetic acid. Thus, dorsal raphé lesions or systemic administration of alpha-propyldopacetamide, NSD 1015, pargyline and MK212 decreased, whereas reserpine injection increased the amplitude of the signal. Moreover, L-5-hydroxytryptophan administration caused an increase in the signal which was almost completely prevented by pargyline pretreatment. Acute administration of dipropylacetamide (150 mg/kg i.p.) reduced the amplitude of the signal from the striatum, while injection of gamma-acetylenic GABA (200 mg/kg i.p.) was without effect. Repeated (but not acute) treatment with the GABA receptor agonist, progabide (400 mg/kg i.p.b.i.d. for 14 days), led to a pronounced decrease in the amplitude of the signal from the striatum. A similar effect was observed after intradorsal raphé infusion of GABA (10 and 100 micrograms), gamma-vinyl GABA (100 micrograms) and SL 75102 (10 micrograms), a principal metabolite of progabide. In contrast, local injection of the GABA receptor antagonists, bicuculline (1 and 10 micrograms) or R5135 (0.05 microgram), failed to affect the peak amplitude in the striatum. When infused into the dorsal raphé, R5135 (0.05-0.1 microgram) antagonized the diminution of the signal induced by intradorsal raphé infusion of GABA (100 micrograms) or SL 75102 (10 micrograms). Finally, electrolytic lesion of the habenular nuclei completely blocked the diminution of the signal from striatum induced by an intradorsal raphé infusion of GABA (100 micrograms). These results indicate that the inhibitory GABAergic control of striatal serotonergic transmission is exerted at the level of the dorsal raphé cells and depends upon the integrity of the habenulo-dorsal pathway.

Animals↗
PubMed1989

Dopamine D2 receptors exert tonic regulation over discrete neurotensin systems of the rat brain.

Blockade of dopamine D2 receptors with either the selective antagonist, sulpiride, or the non-selective antagonist, haloperidol, induces 2- to 3-fold increases in the content of neurotensin-like immunoreactivity in the striatum and the nucleus accumbens of the rat brain. Quantitatively similar increases were also observed (a) in the striatum following selective degeneration of more than 85% of the nigrostriatal dopamine pathway with 6-hydroxydopamine and (b) in both the striatum and the nucleus accumbens after non-selective depletion of brain dopamine using reserpine plus alpha-methyl-p-tyrosine. Interestingly, treatment of animals with sulpiride or haloperidol, following the depletion of dopamine by either 6-hydroxydopamine or reserpine plus alpha-methyl-p-tyrosine, did not add to the elevation in neurotensin content of either structure caused by the dopamine depletion alone. These data suggest that an intact dopamine system is required for the neuroleptics to exert their effects on individual neurotensin systems. In addition, the same mechanism appears to underlie the responses of the neurotensin pathways to treatments with the neuroleptics or dopamine-depleting drugs. A likely explanation for the effects of neuroleptics and dopamine-depleting drugs is that they eliminate tonic activity on D2 receptors by basally released dopamine in the striatum and the nucleus accumbens. Supportive evidence for this hypothesis is that concurrent administration of the D2 receptor agonist, LY 171555, with reserpine, completely blocked the effects of reserpine-induced dopamine depletion on neurotensin systems of the striatum and the nucleus accumbens.

Animals↗
PubMed1992

Dopamine-, NMDA- and sigma-receptor antagonists exert differential effects on basal and amphetamine-induced changes in neostriatal ascorbate and DOPAC in awake, behaving rats.

Amphetamine and other dopamine agonists elevate the extracellular level of neostriatal ascorbate, which has been shown to modulate neuronal function. To assess the receptor mechanisms underlying neostriatal ascorbate release, drug-induced changes in both basal and amphetamine-induced ascorbate release were monitored voltammetrically in the neostriatum of freely moving rats. A variety of dopamine receptor antagonists decreased basal ascorbate and reversed the increase induced by 2.5 mg/kg D-amphetamine. Thus, compared to vehicle treatment, administration of classical (haloperidol) and atypical (clozapine) neuroleptics or selective D1 (SCH-23390) and D2 (sulpiride) antagonists completely reversed the amphetamine-induced rise in ascorbate and also lowered basal levels by 20-40%. These same effects occurred following injection of dizocilpine (MK-801), a non-competitive NMDA antagonist, whereas BMY-14802, a sigma ligand, reversed the amphetamine-induced rise without altering basal levels. Simultaneous measurements of extracellular DOPAC, a major dopamine metabolite, revealed that haloperidol, clozapine, sulpiride and BMY-14802 elevated basal levels and reversed the amphetamine-induced decline. Dizocilpine also increased basal DOPAC but failed to alter the DOPAC response to amphetamine, whereas both basal and amphetamine-induced changes in DOPAC were unaffected by SCH-23390. A combination of subthreshold doses of SCH-23390 and sulpiride, however, reversed both the amphetamine-induced release of ascorbate and the corresponding decline in DOPAC. Collectively, these results suggest that whereas dopamine, sigma, and NMDA receptors modulate neostriatal ascorbate release, they exert an opposing influence on extracellular DOPAC. All drugs attenuated at least some components of the amphetamine behavioral response, suggesting a role for multiple mechanisms in the behavioral effects of this drug.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Lithium exerts a time-dependent and tissue-selective attenuation of the dexamethasone-induced polyamine response in rat brain and liver.

It has previously been shown that chronic, but not acute, lithium treatment indirectly prevents the dexamethasone-induced increase in brain polyamine-metabolizing enzymes. In the present study we determined the effects of lithium treatment on changes in cellular polyamines, 6 h after dexamethasone challenge (3 mg/kg intraperitoneally). The findings demonstrate that chronic lithium (daily intraperitoneal 2.5 mmol/kg injections for 2 weeks) treatment completely prevents the accumulation of putrescine, in parallel to its prevention of the dexamethasone-induced increase in ornithine decarboxylase activity. A partial attenuation of this polyamine response was also observed in the liver. Only minor and inconsistent changes were observed in the concentrations of the polyamines, spermidine and spermine. Acute lithium treatment (a single injection at times ranging from 1 to 24 h prior to dexamethasone challenge) did not attenuate the dexamethasone-induced increases in brain putrescine concentration nor in ornithine decarboxylase activity. It is suggested that prevention of the stress-induced polyamine response in the brain may be an important mechanism through which prophylactic lithium may exert its beneficial effect in manic-depressive illness.

Animals↗
PubMed1984

Human cytotoxic T lymphocytes (CTL) against Epstein-Barr virus (EBV) infected cells: EBV specificity and involvement of major histocompatibility complex determinants in the lysis exerted by anti-EBV CTL toward HLA-compatible and allogeneic target cells.

Human peripheral blood lymphocytes (PBL), from anti-Epstein-Barr virus (EBV)-seropositive donors, were stimulated by EBV and were shown to be cytotoxic toward autologous, HLA-compatible, and fully allogeneic EBV-transformed target cells. The lysis was not due to natural killer (NK) cells since the target cells used were resistant to lysis by fresh PBL and by virus-stimulated PBL-depleted of AET-SRBC-rosetting T cells (the latter being still fully cytotoxic on K562 NK-susceptible target cells). Conversely only E-rosette-purified (T) lymphocytes killed EBV-transformed HLA-compatible and allogeneic target cells. Moreover, anti-MHC antibodies inhibited the cytotoxicity exerted by EBV-induced cytotoxic T lymphocytes (CTL) on both autologous and allogeneic target cells. Finally the lysis was EBV specific since PHA blasts were not killed and since only EBV-transformed cells could compete for lysis with the EBV-positive target cells. Efficient competition was achieved by EBV-transformed cells autologous or allogeneic to the targets, even when effector and target cells were fully allogeneic. All together, the data suggest that human anti-EBV CTL may recognize nonpolymorphic HLA determinants on the target cells in association with the virus-induced antigens.

Antibodies, Monoclonal↗
PubMed1985

Cyclophosphamide inhibits antibody-dependent cellular cytotoxicity (ADCC) suppression exerted by lymph node cells.

The effect of cyclophosphamide (Cy) on suppression of antibody-dependent cellular cytotoxicity (ADCC) by lymph node cells (LNC) was evaluated. The results show that the suppression of ADCC exerted by LNC was abrogated when mice had been treated with Cy. Moreover, it was shown that ADCC inhibition induced by LNC was mediated by soluble factor(s) and that treatment with a single dose of 200 mg/kg ip of Cy, significantly decreased its release. In addition, suppressor activity of normal LNC was enriched by depletion of adherent cells and was not affected by treatment with monoclonal anti-Thy 1.2 plus complement. These observations indicate that modulatory cells are nonadherent and lack characteristic T-cell markers. Thus, we conclude that this suppressor system, which normally controls ADCC activity, can be inhibited by treatment of mice with Cy and that this effect may explain the enhancement of ADCC observed in splenocytes of Cy-treated animals.

Animals↗
PubMed1988

Regulation of B-cell expression as revealed in the congenic barrier: exerted by B cells, augmented by T cells, and directed toward memory as well as naive donor B lymphocytes.

Donor's memory cell expression is reduced in nonirradiated recipients as compared to irradiated ones. This "barrier" was studied in Igh-congenic BALB/c mice as transfer partners, making use of their allotypic markers, under two aspects: (I) Does the barrier apply to naive B-cells also, not only to memory cells? (II) Does a barrier exist in nude recipient mice also? (I) Naive donor B cells were subject to a barrier in nonirradiated recipients as well as memory cells. (II) Nude recipients showed a barrier toward naive donor cells like euthymic hosts, but toward memory cells this was less stringent. The allotypically marked donor B cells survived and were active in the nonirradiated host. In some situations they even dominated the host's response. The results favor a concept of the barrier as an "intrinsic" interlymphocytic control, exerted by B cells, augmented by T cells, best explained by Jerne's theory of idiotypic interactions.

Animals↗