Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cardiovascular System”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources
PubMed2004

Leptin and the cardiovascular system.

Obesity is associated with increased cardiovascular morbidity and mortality, in part through development of hypertension. Recent observations suggest that the cardiovascular actions of leptin may help explain the link between excess fat mass and cardiovascular diseases. Leptin is an adipocyte-derived hormone that acts in the central nervous system to promote weight loss by decreasing food intake and increasing metabolic rate. Leptin causes a significant increase in overall sympathetic nervous activity, which appears to be due to direct hypothalamic effects and is mediated by neuropeptide systems such as the melanocortin system and corticotropin-releasing hormone. Renal sympathoactivation to leptin is preserved in the presence of obesity, despite resistance to the metabolic effects of leptin. Such selective leptin resistance, in the context of circulating hyperleptinemia, could predispose to obesity-related hypertension. Some in vitro studies have suggested that leptin may have peripheral actions such as endothelium-mediated vasodilation that might oppose sympathetically induced vasoconstriction. However, we and others have shown that leptin does not have direct vasodilator effects in vivo. The fact that chronic leptin administration or overexpression of leptin produces hypertension supports the concept that the hemodynamic actions of leptin are due predominantly to sympathetic activation. Exploration of the sites and mechanisms of leptin resistance should provide novel therapeutic strategies for obesity, insulin resistance, and hypertension.

Animals↗
PubMedDate not supplied

A behavioral link between the oculomotor and cardiovascular systems.

Although the eyes and the heart serve very different purposes, each receives autonomic innervation. Capitalizing on recent theoretical and technological innovations in the understanding and assessment of oculomotor and cardiovascular behavior, three experiments measured behavioral covariation between the oculomotor and cardiovascular systems. Measures of dark focus and dark vergence indexed oculomotor tone, and the spectral decomposition of variations in heart rate indexed cardiovascular control mechanisms. In Experiment 1, individual differences in cardiovascular parameters could predict individuals' dark vergence (R2 = .806) but not their dark focus (R2 = .404). In Experiment 2, the same parameters were measured from subjects who experience either panic attacks (n = 11) or blood phobia (n = 9). Heart rate was positively correlated with dark vergence and the two subject groups were separable based on both oculomotor and cardiovascular variables. Using a within-subjects approach, Experiment 3 found that both dark vergence and dark focus tended to be nearer during sympathetic dominance of the heart than during parasympathetic dominance, within-subjects variations in cardiovascular parameters could predict dark focus, and between-subjects variations in interbeat intervals could predict dark vergence. Shared patterns of autonomic activation may be responsible for this eye-heart link.

Accommodation, Ocular↗
PubMedDate not supplied

[Oxidative stress and antioxidants in the diet in pathological processes at the level of the cardiovascular system].

After a short review of the data on the free radicals occurring in the human body (hydroxyl radical, superoxide, nitric acid, peroxynitrite), the possible effects of these radical upon the cardiovascular system are presented. The preservation of the oxidants-antioxidants balance is highly important for preventing the cardiovascular diseases. Endogenous antioxidants are not 100 per cent effective, reason why for the individuals with atherosclerosis and ischemic heart disease antioxidant supplements (tocopherols, carotenes, vitamin C, selenium) are essential especially during the seasons when diets are deficient in fruits and vegetables.

Animals↗
PubMed2006

New biotechnological methods to reduce oxidative stress in the cardiovascular system: focusing on the Bach1/heme oxygenase-1 pathway.

Oxidative stress is involved in the mechanism of atherosclerotic lesion formation and in the mechanisms underlying the development of other pathogenic conditions of the cardiovascular system, including endothelial dysfunction, hypertension, and heart failure. Reducing oxidative stress may be a reasonable therapeutic approach to treat cardiovascular diseases. HO-1 is a cytoprotective enzyme that is induced in response to oxidative stress and degrades heme into carbon monoxide (CO) and bilirubin, both of which have cytoprotective effects. A substantial body of evidence suggests that introduction of HO-1, either pharmacologically or by a gene delivery technique, confers cytoprotection in ischemic heart disease and atherosclerosis in animals. Recent studies have revealed that CO has anti-inflammatory properties and that administration of CO provides protection against atherosclerosis and ischemic heart disease. Discovery of Bach1, a transcriptional repressor of HO-1, has greatly contributed to the understanding of the regulation of HO-11 expression, providing a clue to a development of alternative method to enhance HO activity. Bach1 normally represses HO-1 expression. However, upon exposure to oxidative stress, Bach1 loses its repressive activity and is exported out of the nucleus, which in turn results in the upregulation of HO-1. Bach1 knockout mice, expressing an increased amount of HO-1, are resistant to pro-atherosclerotic and ischemic stresses. These findings indicate that inhibition of Bach1 may be a novel approach to enhance protection against stress. In summary, the Bach1-HO-1 system is an important defense mechanism against oxidative stress. Development of a safe and effective method to enhance this pathway, such as Bach1 inhibitor, may be of great clinical relevance.

Animals↗
PubMed1980

[Functional change in the cardiovascular system in respiration through an additional dead space (its importance for preventive cardiology)].

Training breathing through the additional dead space improves the function of the cardiovascular system both in experimental animals and in healthy persons, increases the resistance to the effect of high-altitude hypoxia, and improves the working capacity and tolerance to physical load. The method is economical and may be used in the training of population masses under ordinary conditions.

Adaptation, Physiological↗
PubMed1980

Effects of chronic administration of delta 9-tetrahydrocannabinol on the cardiovascular system, and pressor and behavioral responses to brain stimulation in freely moving rats.

The effects of chronic administration of delta 9-THC on the cardiovascular system, and the pressor and behavioral responses to brain stimulation were investigated in freely moving rats with chronic electrode and arterial cannula implants. delta 9-THC at a dose of 6 mg/kg was injected intraperitoneally once a day for 10 days through an abdominal cannula. On the first day, delta 9-THC induced a significant decrease in heart rate and rise in blood pressure. The animals exhibited abnormal behavior such as catalepsy, walking backward and pivoting. On the 5th day, the bradycardia induced by delta 9-THC markedly decreased and on the 10th day tachycardia was observed. The pressor effect of delta 9-THC significantly increased on the 5th and 10th days. However, delta 9-THC-induced abnormal behavior was observed without any changes following chronic administration. delta 9-THC inhibited the pressor response and behavioral changes to electrical stimulation of the posterior hypothalamus and midbrain reticular formation. No tolerance developed to these depressive effects of delta 9-THC after chronic treatment. These data suggest that tolerance develops only to bradycardic effect of delta 9-THC and that the decrease in vagal activity may play some role in the development of tolerance.

Animals↗
PubMed2006

Tachykinins and the cardiovascular system.

The tachykinin family of vasoactive peptides comprises the neuropeptides substance P, neurokinin A and neurokinin B, and the newly discovered endokinins and hemokinins. Their cardiovascular effects are predominantly mediated by the family of neurokinin receptors. This review summarises the most recent advances in understanding the effects of tachykinins on the vasculature, and summarises their therapeutic potential. Tachykinins stimulate plasma extravasation, particularly acting through neurokinin-1 receptors in an endothelium-dependent manner. They therefore play prominent roles in tissue oedema and inflammation (called neurogenic inflammation). Pro-inflammatory effects of tachykinins are enhanced by their capacity to stimulate inflammatory cell recruitment, and to initiate angiogenesis. Tachykinins also regulate vascular tone and blood flow, although differences between species and between different vascular beds make this a highly complex area of research. They may relax vessels in some scenarios whilst inducing vasoconstriction in other situations, the state of the endothelium appearing to be of key importance. Tachykinins also modulate blood pressure and heart rate, acting both peripherally, and on the central nervous system. Cardiovascular effects of tachykinins and neurokinin receptors may be important therapeutic targets in diverse disorders such as pulmonary oedema, hypertension, pre-eclampsia, complex regional pain syndrome type 2, stroke and chronic inflammatory diseases such as arthritis. Sophisticated modelling of human disease is required to enable neurokinin receptor antagonists to achieve this therapeutic potential.

Animals↗
PubMed2000

[Study of modeling and simulation of the multi-branch cardiovascular system].

By the Power Band Graph(PBG) method, this paper presents a computer simulation model of the multi-branch cardiovascular circulation system, which describes the blood fluid dynamic law in the cardiovacular system by the state equation. The model gives a minute description on physiological characters of cardiovascular circulation system (CVS). An integrate computer model on CVS has been established. The model can simulate physiological characters of cardiovascular circulation system and get the simulation data and the curves of CVS hemodynamics variables. The model can be used widely in the field of physiological system simulation study, medical study, and computer-aided instruction.

Computer Simulation↗
PubMed2006

Glutamatergic systems in the bed nucleus of the stria terminalis, effects on cardiovascular system.

The bed nucleus of the stria terminalis (BST) is a part of the limbic system. Two studies have shown that microinjection of L: -glutamate in the BST elicited cardiovascular depressive and bradycardic responses, but in one study, both pressor and depressor responses were observed in the chemical stimulation of BST by glutamate in the urethane-anesthetized rats. Also, the roles of glutamate receptor subtypes have not been investigated yet. The aim of this study was to find the effects of glutamate and its receptors on the blood pressure and heart rate in the BST of urethane-anesthetized rats. The drugs (50 nl) were microinjected into the BST of anaesthetized rats. The blood pressure and heart rate were recorded throughout each experiment. The average changes in the mean arterial pressure and heart rate at different intervals were compared both within each case group and between the case and the control groups, using repeated measures ANOVA. Microinjection of L: -glutamate (0.25 M) into the BST resulted in the decrease of the mean arterial pressure (-18.85 +/- 3.84 mmHg) and heart rate (-18 +/- 4 beats/min). Injection of AP5, antagonist of glutamate NMDA receptor (2.5 , 5 mM) and CNQX, antagonist of glutamate AMPA receptor (0.5, 1 mM) had no significant effect on the mean arterial pressure and heart rate. Either Ap5 or CNQX, when co-injected with glutamate, abolished the depressor and bradycardic effects of glutamate, suggesting that simultaneous activation of both glutamate receptors is necessary for the effect of glutamate system to emerge.

Animals↗