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At least 379 records · Page 21Linked to original sources
PubMed1993

Distribution and activity of dogfish NPY and peptide YY in the cardiovascular system of the common dogfish.

Neuropeptide Y is present in sympathetic nerves in the mammalian cardiovascular system. This study has investigated the distribution of neuropeptide Y in the cardiovascular and gastrointestinal systems and the effect of dogfish neuropeptide Y and related peptides on cardiovascular tissue of an elasmobranch fish, the common dogfish (Scyliorhinus canicula). Neuropeptide Y-like immunoreactivity is present in varicose nerve fibers innervating dogfish gut and cardiovascular tissue and in endocrine cells of the dogfish spiral intestine. Dogfish neuropeptide Y, dogfish peptide YY, and porcine neuropeptide Y contract the dogfish afferent branchial artery in a concentration-dependent manner. The effect is not inhibited by the presence of tetrodotoxin or by removal of the endothelium. The mammalian Y1 receptor selective agonist [Leu31Pro34]NPY but not the mammalian Y2 receptor selective agonist neuropeptide Y-(13-36) peptide has vasoconstrictor properties in this system, suggesting that the receptor mediating the vasoconstriction resembles the mammalian Y1 receptor more than the Y2 receptor.

Absorption↗
PubMed1986

Role of ventrolateral medulla in regulation of respiratory and cardiovascular systems.

It is now widely accepted that the ventrolateral aspect of the medulla oblongata (VLM) plays an important role in regulation of the respiratory and cardiovascular systems. The VLM has been implicated as being involved in a number of different physiological functions, including central chemoreception, integration of afferent inputs from certain sense organs to the respiratory and cardiovascular controllers, the source of excitatory input to preganglionic sympathetic neurons in the spinal cord, and location of synaptic relay between the higher brain defense areas and spinal cord sympathetic elements. In recent years there have been a number of important findings concerning both the anatomical substrate and neurophysiological characteristics of VLM neurons involved in regulation of the respiratory and cardiovascular systems. New anatomical findings show that neuronal networks located in the VLM send projections to and receive projections from brain stem nuclei that have traditionally been associated with respiratory and cardiovascular regulation. Nevertheless, there are still many important questions concerning the role of the VLM in control of these vital systems that have yet to be answered. For instance, are the same VLM neurons involved in control of both systems? Is the VLM the only site for central respiratory chemoreception? This review will endeavor to examine new findings and to reexamine some older findings concerning the VLM.

Animals↗
PubMed2001

[Human biological age, cardiovascular system, and its aging rate].

Mathematical model of biological age of the cardiovascular system was determined by multiple linear regression analysis in 100 normal subjects aged 30-74 years on the basis of central hemodynamic, microcirculation, and vascular reactivity parameters. The rate of cardiovascular aging is decreased in elderly subjects. Before 60 years of age the rate of aging is higher in men than in women.

Adult↗
PubMed1994

Repeated administration of a F(ab')2 fragment of an anti-tumor necrosis factor alpha monoclonal antibody in patients with severe sepsis: effects on the cardiovascular system and cytokine levels.

In an uncontrolled clinical trial the effects of repeated administration of the F(ab')2 fragment of a murine monoclonal anti-tumor necrosis factor alpha (TNF alpha)-antibody (MAK 195F) on cytokine levels and the cardiovascular system were studied in 20 patients with severe sepsis. Patients were treated with a total of 11 single dosages of the anti-TNF alpha-antibody intravenously over 5 days using either 1 mg/kg (n = 10) or 3 mg/kg (n = 10). The anti-TNF alpha-antibody was well tolerated in all patients without signs of toxicity and without development of anti-murine antibodies. As assessed by cytokine levels (TNF alpha, Interleukin-6) and hemodynamics there was no evidence that the higher dosage of the anti-TNF alpha-antibody (3 mg/kg per dose) was more effective than the lower dosage (1 mg/kg per dose). Comparison of our data with recent data from phase I or II trials using a complete murine monoclonal anti-TNF alpha-antibody suggest that the F(ab')2 fragments of the murine monoclonal anti-TNF alpha-antibody may be of similar efficacy. Definitive conclusions, however, with respect to improvement of mortality and improvement of the cardiovascular system, await the results of larger ongoing placebo-controlled trials.

Adult↗
PubMed2004

Drug targeting of estrogen receptor signaling in the cardiovascular system: preclinical and clinical studies.

Atherosclerosis and associated coronary heart disease events have lower prevalence in women than in men, especially during young adult years. Although multiple lines of evidence suggest that estrogens contribute to this difference, the efficacy of hormone replacement therapy for the prevention of cardiovascular disease in postmenopausal women is controversial. The protective action of estrogen in the cardiovascular system appears to be mediated indirectly by an effect on serum lipoprotein and triglyceride profiles and on the expression of coagulant and fibrinolytic proteins, and by a direct effect on the vessel wall itself. Estrogen has both rapid effects involving alteration of membrane ionic permeability and activation of membrane-bound enzymes and increases in endothelial cell nitric oxide synthase activity, as well as longer-term effects on gene expression that are mediated, at least in part, by the ligand-activated transcription factors, estrogen receptor alpha and beta. Compounds with pure antiestrogenic activity and selective estrogen receptor modulators that regulate estrogen receptor function in a tissue-specific manner have been developed in an attempt to achieve the cardioprotective effects of estrogens while minimizing the undesirable risks associated with hormone replacement therapy (e.g., endometrial and breast cancer). In this review, we will discuss recent developments on the mechanisms of estrogen action in the cardiovascular system. The results of clinical trials testing the long-term efficacy of hormone replacement therapy for the treatment of cardiovascular disease will also be discussed.

Animals↗
PubMed1991

[Status of the cardiovascular system of the fetus and newborn infant in different degree of severity of maternal hypertensive syndrome].

Examinations of 260 pregnant women with hypertensive syndromes and their 60 full-term newborns, carried out with the use of echography of the umbilical artery, umbilical vein, aorta, and internal carotid artery of the fetus have demonstrated a high informative value of these methods for the assessment of the type of fetal condition and prediction of the newborn's adaptive mechanisms of the cardiovascular system. Significant changes of the cardiovascular system were revealed in small-for-date fetuses and in chronic fetal hypoxia, as well as functional changes in the newborns of the mothers with the hypertensive syndrome, with born signs of intrauterine suffering. These changes should be borne in mind when predicting the development of infants born of mothers with the hypertensive syndrome.

Echocardiography, Doppler↗
PubMed2001

Evidence that ranolazine behaves as a weak beta1- and beta2-adrenoceptor antagonist in the rat [correction of cat] cardiovascular system.

The clinical anti-anginal effectiveness of ranolazine is currently being evaluated. However, the mechanism of its anti-ischaemic action is still unclear. The aim of this work was to establish whether ranolazine exerts functional beta-adrenoceptor antagonist activity in the rat cardiovascular system. Radioligand binding studies were performed in rat hearts and guinea-pig lungs for beta1- and beta2-adrenoceptor affinity, respectively. Ranolazine had micromolar affinity for both beta,- and beta2-adrenoceptors (pKi5.8 and 6.3, respectively). Developed tension was measured in isolated rat left atria (electrically driven at 4 Hz) and cumulative concentration/response curves to (+/-)isoprenaline (0.01-1,000 nM) constructed. Ranolazine (0.32-10 microM) surmountably but weakly antagonised isoprenaline-induced positive inotropic responses, with an apparent pA2 of 5.85 (5.69-6.00) and a slope of -0.74 (-0.70 to -0.77). In bivagotomised, atropinised pithed rats, ranolazine per se evoked marked bradycardia at doses above 10 mg/kg i.v. (maximum variation at 80 mg/kg -125+/-15 bpm, n=6, P<0.001) by a mechanism apparently unrelated to blockade of beta1- or beta2-adrenoceptors. Cumulative incremental doses of (+/-)isoprenaline (0.63 ng/kg to 0.16 mg/kg i.v.) administered to pithed rats induced concomitant depressor and chronotropic responses. Animals received either vehicle (saline 0.9% i.v., n=12), atenolol (0.04-2.5 mg/kg i.v., n=6 per dose), ICI 118551 (0.01-0.63 mg/kg i.v., n=6 or 7 per dose), (+/-)propranolol (0.01-0.63 mg/kg i.v., n=6 per dose) or ranolazine (2.5-80 mg/kg i.v., n=6 or 7 per dose) 10 min prior to isoprenaline. Ranolazine dose-dependently and competitively antagonised isoprenaline-induced decreases in diastolic arterial pressure (DAP, dose ratio 12.2 with 80 mg/kg ranolazine) and increases in heart rate (HR, dose ratio 20.3 with 80 mg/kg ranolazine). Collectively, these results demonstrate that ranolazine behaves as a weak beta1- and beta2-adrenoceptor antagonist in the rat cardiovascular system.

Acetanilides↗
PubMed1998

The interleukin-1 and interleukin-1 converting enzyme families in the cardiovascular system.

The multifunctional cytokine interleukin-1 (IL-1) is a key mediator in the cytokine network. The IL-1 family consists of two zymogen isoforms of IL-1 (IL-1alpha and IL-1beta), the IL-1 receptor antagonists, two receptors and receptor-associated proteins. Identification of the enzyme responsible for cleavage and activation of the IL-1beta precursor, the IL-1beta converting enzyme (ICE; caspase 1), unexpectedly linked the IL-1 family to the apoptosis machinery, since ICE is the founding molecule of the caspase family, which is important for regulation of apoptosis. Although it has been suggested that cytokines are involved in pathogenesis of cardiovascular diseases only few informations exist regarding the endogenous production and function of IL-1 and the associated enzyme(s) of the caspase family in the cardiovascular system. Here, we summarize informations regarding the IL-1 and the caspase family in the cardiovascular system.

Animals↗
PubMedDate not supplied

[Capacity and resistance parameters of the athlete's cardiovascular system and their dynamics in regular training].

Viscosity and elasticity of the cardiovascular system are assessed by a new method based on evaluation of correlations between deposit properties of the left ventricular chamber, aortic wall and vascular resistance in different parts of the arterial tree. This method examines individual hemodynamic characteristics of healthy untrained persons and hemodynamic changes due to regular training.

Adolescent↗
PubMed2005

Alcohol and the cardiovascular system: research challenges and opportunities.

Excessive alcohol consumption has long been associated with cardiovascular disorders, including cardiomyopathy, hypertension, coronary artery disease, and stroke. However, recent evidence suggests that moderate alcohol intake can actually provide a measure of cardioprotection, particularly against coronary heart disease and ischemia-reperfusion injury. To explore the various dimensions of these opposing actions of alcohol, the National Institute on Alcohol Abuse and Alcoholism and the National Heart, Lung, and Blood Institute sponsored a state-of-the-art workshop on "Alcohol and the Cardiovascular System: Research Challenges and Opportunities" in Bethesda, Maryland, in May 2003. Speakers discussed the following topics: the epidemiology of alcohol and cardiovascular disease, clinical manifestations of alcohol, genetics of alcohol and cardiovascular disease, mechanisms underlying the molecular and cellular effects of alcohol, the application of new and emerging technology, and translation from discovery to therapeutic modalities of treatment. The panel concluded that future studies are needed to: 1) determine the role of genes and the environment in assessing mechanisms underlying the benefits of alcohol use and cardiovascular disease risk; 2) define the biological mechanisms underlying alcohol-induced peripheral vascular damage; 3) clarify the role of genetic variation in alcohol-metabolizing enzymes, genetic susceptibility, and pharmacogenomics in determining cardiovascular disease risk and effective treatment; 4) determine common mechanisms underlying alcohol-induced cardiovascular disease, such as oxidative stress and inflammation; 5) assess the role of insulin resistance, blood clotting, protein kinase C isoforms, and signal transduction mechanisms mediating alcohol's beneficial effects; and 6) explore the potential of stem cells in myocardial regeneration and repair in hearts damaged by alcohol.

Alcohol Drinking↗
PubMed1992

Angiotensin converting enzyme inhibitors and the cardiovascular system.

OBJECTIVE: To show that angiotensin converting enzyme (ACE) inhibitors benefit the cardiovascular system to a greater extent than other antihypertensive agents. DATA EXTRACTION: An extensive literature search has shown that ACE inhibitors can induce regression of left ventricular hypertrophy, which may improve systolic and/or diastolic function in the left ventricle; increase in arterial compliance; and improve clinical signs of congestive heart failure and reduce mortality in patients with severe heart failure. In addition, ACE inhibitors have either a neutral or a beneficial effect on blood lipids and lipoproteins. These agents also have potential anti-ischaemic and anti-arrhythmic activity but do not depress resting cardiac function. CONCLUSION: ACE inhibitors are uniquely valuable first-line antihypertensive agents, especially in patients with cardiovascular risk.

Angiotensin-Converting Enzyme Inhibitors↗