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At least 865 records · Page 48Linked to original sources
PubMed1992

Ultrafast CT and the cardiovascular system.

Ultrafast computed tomography (CT) is a new imaging technique that relies on electron beam technology. Its rapid image acquisition speeds make it ideal for evaluating the cardiovascular system. The high-resolution, flow, and cine-modes are unique and provide complimentary information about cardiovascular anatomy, function, and flow dynamics. Ultrafast CT can provide quantitative measurements of cardiac output, ejection fraction, ventricular volumes, and ventricular mass as well as evaluation of segmental cardiac function. This technique can be used to assess coronary artery bypass graft patency as well as to screen for coronary artery calcium. Intracardiac thrombus or tumor, valvular disease, and disorders of the pericardium can be evaluated and characterized using ultrafast CT. The diagnosis of congenital lesions of the heart and great vessels is facilitated by this imaging modality, which can help determine complex anatomic abnormalities and quantitate shunt lesions. Acquired lesions of the great vessels, such as aortic dissection and aneurysm, can be diagnosed by ultrafast CT, which can also be used for serial examination and conservative management.

Heart↗
PubMed1992

The effects of exercise on blood flow with reference to the human cardiovascular system: a finite element study.

This paper reports on a theoretical investigation into the effects of vasomotion on blood through the human cardiovascular system. The finite element method has been used to analyse the model. Vasoconstriction and vasodilation may be effected either through the action of the central nervous system or autoregulation. One of the conditions responsible for vasomotion is exercise. The proposed model has been solved and quantitative results of flows and pressures due to changing the conductances of specific networks of arterioles, capillaries and venules comprising the arms, legs, stomach and their combinations have been obtained.

Blood Circulation↗
PubMed1999

The effects of diadenosine polyphosphates on the cardiovascular system.

Diadenosine polyphosphates are members of a group of dinucleoside polyphosphates that are ubiquitous, naturally occurring molecules. They form a recently identified class of compounds derived from ATP and consist of two adenosine molecules bridged by up to six phosphate groups. These compounds are stored in high concentrations in platelet dense granules and are released when platelets become activated. Some of the compounds promote platelet aggregation, while others are inhibitory. Possible roles as neurotransmitters, extracellular signalling molecules or 'alarmones' secreted by cells in response to physiologically stressful stimuli have been postulated. Recent studies suggest a role for these compounds in atrial and synaptic neurotransmission. Studies using isolated mesenteric arteries indicate an important role of phosphate chain length in determining whether diadenosine polyphosphates produce vasodilation or vasoconstriction, but in the coronary circulation, diadenosine polyphosphates generally produce vasodilation via mechanisms thought to involve release of NO or prostacyclin (PGI2). They produce cardiac electrophysiological effects by altering ventricular refractoriness at submicromolar concentrations and reduce heart rate. Mechanisms involving KATP channels have been proposed in addition to the involvement of P1- and P2-purinergic receptors and the specific diadenosine polyphosphate receptor identified on isolated cardiac myocytes. Clinical evidence suggests a role for diadenosine polyphosphates in hypertensive patients and those with the Chédiak-Higashi syndrome. This review outlines the effects of these compounds on the cardiovascular system and considers their potential involvement in mediating the pathophysiological effects associated with platelet activation during myocardial ischaemia.

Action Potentials↗
PubMed1988

New approaches to the study of the cellular biology of the cardiovascular system.

Recent findings suggest that the local renin-angiotensin systems, locally generated catecholamines, and possibly other locally generated peptides interact in a complex fashion to regulate the cellular biology of the myocardium, the vascular wall, and other tissues. New evidence indicates that the components of the renin-angiotensin system are synthesized in cardiovascular tissues, that the synthesis of these components can be modulated by pharmacologic agents, and that angiotensin II, the effector protein of the renin system, appears to be capable of producing hypertrophy or hyperplasia in specific tissues. In addition, recent studies suggest the participation of enhanced proto-oncogene transcriptional activity in the development of hyperplasia and hypertrophy in cardiovascular tissue. Taken together, these data raise the possibility that angiotensin and perhaps other components of the renin system can be viewed as locally active growth factors capable of acting in a fashion similar to that associated with cytokines in other systems.

Animals↗
PubMed1995

Systemic cardiovascular response in hemodialysis without and with ultrafiltration with membranes of high and low biocompatibility.

In order to test whether dialyzer membrane biocompatibility influences systemic cardiovascular function, we treated 8 hemodialysis patients (4 men and 4 women, aged 24-73 years) with a low-biocompatible (cuprophane) and a high-biocompatible (polyacrylonitrile) membrane in a randomized double-blind crossover protocol using bicarbonate hemodialysis without ultrafiltration for the first 60 min and with ultrafiltration for the remaining treatment time. Left ventricular function and systemic hemodynamics were assessed noninvasively at baseline and during treatment by Doppler echocardiography combined with external subclavian artery pulse trace calibrated with oscillometrically measured brachial artery blood pressures. There was no significant difference in the cardiovascular response to the 2 membranes, neither during isolated hemodialysis nor when ultrafiltration was added. Mean arterial pressure increased 10% (p < 0.001) during isolated hemodialysis and returned to baseline levels with ultrafiltration. The cardiac index decreased 22% (p < 0.001) during ultrafiltration, due to the greater decrease in left ventricular stroke index (30%, p < 0.001) than increase in heart rate (9%, p < 0.05). Total peripheral resistance increased 10% (p < 0.05) during isolated hemodialysis and a further 19% (p < 0.01) when ultrafiltration was added. Hence, profound cardiovascular alterations were observed during hemodialysis treatment; however, these changes were not related to the biocompatibility of the membranes.

Acrylic Resins↗
PubMed2002

Some aspects of arsenic toxicity and carcinogenicity in living organism with special regard to its influence on cardiovascular system, blood and bone marrow.

This paper gathers data on the most current aspects of arsenic action, especially its influence on the cardiovascular system, blood and bone marrow. A potential carcinogenic mechanism of arsenic is also discussed. Arsenic is a potent toxicant that may exist in several valencies and in a number of inorganic and organic forms. Most cases of arsenic-induced toxicity in humans are due to exposure to inorganic arsenic, and there is an extensive database on the human health effects of common arsenic oxides and oxyacids. Exposure of humans living near hazardous waste sites may involve inhalation of arsenic dusts in the air, ingestion of arsenic in water, food or soil, or dermal contact with contaminated soil or water. The exposure to arsenic via the inhalation route is responsible for the increased risk of lung cancer, although respiratory irritation, nausea and skin effects may also occur. The oral route of exposure to arsenic predominates in the general population. The most common effects of arsenic ingestion are gastrointestinal irritation, peripheral neuropathy, vascular lesions, anemia, skin diseases, including skin cancer and other cancers of the internal organs like bladder, kidney, liver or lung. Relatively little information is available on the effects of direct dermal contact with inorganic arsenicals, but several studies indicate local irritation and dermatitis as the major ones.

Anemia↗
PubMed2000

Evaluation for roles of nitric oxide generated in the anteroventral third ventricular region in controlling vasopressin secretion and cardiovascular system of conscious rats.

OBJECTIVE: To examine local actions of nitric oxide (NO) on the neural mechanisms controlling the release of vasopressin (AVP) and the cardiovascular system in the anteroventral third ventricular region (AV3V), a pivotal area for autonomic functions, and to pursue the problem of whether it may have any role in the AVP and cardiovascular responses evoked by plasma hypertonicity or by increased prostaglandin E(2) (PGE(2)) in the AV3V - one possible factor implicated in osmotic responses. METHODS: We infused NO-related agents into the AV3V, its adjacent area, the nucleus of the vertical limb of the diagonal band (VDB), or into the lateral cerebral ventricle of conscious rats, monitoring effects on plasma AVP, osmolality, sodium, potassium and chloride, arterial pressure and heart rate in the presence or absence of an osmotic or PGE(2) stimulus. The infusion sites were determined histologically. RESULTS: Infusion of L-arginine, the substrate of NO synthase (NOS), into the AV3V structures such as the median preoptic nucleus and periventricular nucleus produced dose-related increases in plasma AVP, arterial pressure and heart rate 5 or 15 min later, whereas infusion of D-arginine (which is not a substrate for NO synthesis) was without significant effect on these variables. Plasma osmolality or electrolytes were not changed by these treatments. The AV3V infusion of sodium nitroprusside (SNP), a spontaneous releaser of NO, also induced dose-dependent augmentations of plasma AVP, without evoking remarkable alteration in the cardiovascular parameters. The infusion of L- or D-arginine into the VDB affected none of the variables significantly. When applied intracerebroventricularly, L-arginine caused only increases in plasma AVP, whereas SNP caused only reductions in arterial pressure, leaving other variables at stable values. The effects of AV3V L-arginine on plasma AVP and the cardiovascular variables were abolished by N(G)-nitro-L-arginine methyl ester (L-NAME), a potent inhibitor of NOS, applied 15 min before. In contrast, infusion of L-NAME to the AV3V did not exert a significant effect on the responses of plasma AVP or cardiovascular variables to AV3V application of PGE(2) or i.v. infusion of hypertonic NaCl. The infusion of L-NAME alone did not affect plasma variables including AVP, although it tended to increase basal arterial pressure and heart rate. CONCLUSION: These results suggest that NO generated in or near the AV3V may act to enhance AVP release, arterial pressure and heart rate, but it may not play an essential role in eliciting the responses of these variables to osmotic or PGE(2) stimuli.

Animals↗
PubMed1999

[Sexual activity and the cardiovascular system in health and disease. Use of sildenafil in heart patients].

Sexual intercourse involves mild to medium severe physical exertion of the cardiovascular system. The risk of sudden death associated with sexual activity is very low, and so is the risk of developing infarction. In patients with pre-existing ischaemic heart disease sexual activity is safe in case of controlled angina with tolerance of a medium-grade load on examination on a treadmill. After acute myocardial infarction with a non-complicated course sexual activity can be resumed in a familiar environment with a familiar partner after about 10 days. In stabilized anginous patients sildenafil administration is safe assuming that the patient does not take long-acting nitrates and does not need frequent administration of short-term acting nitrates. It is important to avoid nitrates also in the treatment of acute ischaemic conditions in these patients. At present we do not possess adequate information on the clinical importance of influencing sildenafil elimination by competition with other substances excreted by the same route.

Erectile Dysfunction↗
PubMed2003

The role of ionotropic receptors of glutaminic acid in cardiovascular system. A. The influence of ionotropic receptor NMDA agonist - 1R,3R-ACPD and antagonist - DL-AP7 on the systemic pressure in rats.

The aim of our study was to estimate the involvement of the peripheral N-methyl-D-aspartate receptors in regulation of cardiovascular function. For this purpose we examined the effects of intravenous injection of the agonists - NMDA (0.025; 0.05 and 1.0 mg/kg iv) and 1R-3R-ACPD (0.025; 0.05 and 1.0 mg/kg iv) - and antagonist of NMDA receptors DL-AP7 (0.02; 0.07 and 0.2 mg/kg iv). To determine if the effects of NMDA come from central or peripheral action we observed the effect during blockade of autonomic ganglion by using the nicotinic receptor antagonist - chlorisondamine (1.25 mg/kg iv). Administration of NMDA in three doses evoked slight hypotension after injection of the medium dose, 0.05 mg/kg. In the condition of pretreatment with 1.25 mg/kg chlorisondamine the hypotensive effect of NMDA was markedly reduced, what might suggest that NMDA-induced hypotension raised from the action within the brain. The competetive NMDA receptor antagonist DL-AP7 slightly increased the blood pressure. None of the injected drug had an influence on the heart rate in our in vivo study. It is concluded that the peripherally localized NMDA receptors may take a part in regulation of cardiovascular system, since their stimulation or blockade evoked the changes of systemic pressure.

2-Amino-5-phosphonovalerate↗
PubMed2001

The cardiovascular system as coupled oscillators?

Based on physiological knowledge, and on an analysis of signals related to its dynamics, we propose a model of the cardiovascular system. It consists of coupled oscillators. Each of them describes one of the subsystems involved in the regulation of one passage of blood through the circulatory system. The flow of blood through the system of closed tubes-the blood vessels-is described by wave equations.

Blood Pressure↗
PubMedDate not supplied

Interaction of cholecystokinin (CCK-33) and its C-terminal fragments: CCK-8 and CCK-4 with alpha- and beta-adrenoceptor agonists and antagonists in the cardiovascular system of diabetic rats. Part B.

This study investigated the interaction of cholecystokinin (CCK-33) and its fragments: C-terminal octapeptide (CCK-8) and C-terminal tetrapeptide (CCK-4) with alpha- and beta-adrenoceptor agonists and antagonists. The effects of this interaction on arterial blood pressure and function of isolated heart were studied in rats with 1-month diabetes mellitus (DM) induced by 1-month administration of streptozocin (STZ). We used CCK-33, CCK-8 and CCK-4 in an equimolar dose of 425.0 pmoles/kg i.v. in in vivo, and 42.5 pmoles/0.1 ml in in vitro experiments. We found that 1) DM diminished the hypertensive effect of noradrenaline (NA) and the hypotensive effects of isoprenaline (ISO), phentolamine (PHENT) and propranolol (PROP). CCK-4 and CCK-8 enhanced but CCK-33 did not change a weaker hypertensive effect of NA while all peptides showed the hypotensive effect of PHENT and did not change the hypotensive effect of ISO and PROP. 2) The influence of NA and PROP on isolated heart of diabetic rats remained unchanged after administration of the peptides but that of ISO and PHENT was diminished. CCK-4 enhanced the effects of NA and PHENT, and diminished the influence of ISO and PROP on isolated heart of diabetic rats. CCK-33 enhanced the cardiac effects of NA, ISO and PROP and did not alter PHENT action. CCK-8 did not change the influence of the studied adrenoceptor agonists and antagonists on isolated heart of diabetic rats. The results of the present study demonstrated that the smallest fragment of CCK-33 (CCK-4) modified the influence of alpha- and beta-adrenoceptor agonists and antagonists on cardiovascular system and altered the direction of disturbances caused by DM. The other peptides (CCK-33, CCK-8) interacted with these receptors to a lesser degree in diabetic subjects.

Adrenergic Agents↗
PubMed1979

Reduction of coronary flow in the native circulation after bypass. Observations in a hydraulic model of the cardiovascular system.

The effects of aorta-coronary bypass upon flow in the native coronary artery were investigated in a hydraulic model of the cardiovascular system. An aorta-coronary bypass with a diameter identical to the coronary artery was used, since a graft diameter-to-coronary diameter ratio of one has been described as optimal. Stenoses of increasing severity were created in the simulated coronary artery. Aorta-coronary bypass eliminated the pressure gradients across the stenotic coronary segments. This caused a 50% reduction of flow in the normal or mildly stenotic native coronary artery. A higher percentage reduction of flow occurred in the bypassed artery when it was severely stenotic. Such a reduction of flow in patients may accelerate the atherosclerotic-thrombotic process and contribute to the high prevalence of occlusion of natural vessels following bypass. This disadvantageous hydraulic circumstance should be considered, particularly when bypass of mildly stenotic vessels is contemplated.

Blood Pressure↗
PubMed1977

Responses of the cardiovascular system of the rat to alpha-and beta-adrenoceptor agonists.

1 The effects of intravenously infused phenylephrine and isoprenaline upon the cardiovascular system of the rat anaesthetized with pentobarbitone, have been investigated.2 Phenylephrine produces a dose-dependent rise in mean arterial blood pressure (MABP) that is due mainly to an increase in total peripheral vascular resistance (TPR), though at all doses tested cardiac output was invariably raised.3 The increase in cardiac output was due in each instance to an increase in stroke volume, heart rate being unchanged. This increase in cardiac output is probably brought about by effects of phenylephrine on the capacitance vessels rather than by an effect on the heart.4 Evidence is presented to show that the effects of phenylephrine are mediated largely by alpha-adrenoceptors, but that beta-adrenoceptors which affect TPR are also stimulated by the amine.5 Isoprenaline produces a dose-dependent fall in MABP that is due entirely to a fall in TPR since the cardiac output increases.6 Unlike phenylephrine, the increase in cardiac output obtained with isoprenaline was achieved by an increase in heart rate while stroke volume remained close to control values. It is contended that the augmented venous return required for the elevated cardiac output results in this case mainly from the isoprenaline-induced fall in TPR which enhances transfer of blood from arteries to the veins.7 Evidence is presented to show that the effects of isoprenaline are mediated mainly by beta-adrenoceptors.8 Under the present experimental conditions the adrenoceptor-mediated cardiovascular changes are little modified reflexly by the arterial baroreceptors.

Adrenergic alpha-Agonists↗
PubMed1977

The interrelation between hypothalamically induced changes in sympathetic discharge to the gastrointestinal and cardiovascular systems.

In chloralose-anesthetized, adrenalectomized cats, the sympathetically conveyed effects of topical hypothalamic stimulations on gastric volume, blood pressure and heart rate were systematically explored. The vagal nerves were cut but could be kept active by graded efferent stimulation. In the absence of such vagal activity, hypothalamic stimulation had no appreciable influence on gastric volume, even though the stomach maintained considerable myogenic tone. When, however, a vagal excitatory activity was present, hypothalamic stimulation could markedly affect gastric tone, indicating that the sympathetic fibres exert their inhibitory influence on the stomach via its cholinergic intramural neurons. Hypothalamic stimulations that induced reductions in pressure or heart rate also usually caused an enhancement of gastric tone. Similarly, pressor responses were associated with decreases in gastric volume whereas stimulation-induced tachycardia was not linked to any particular type of gastric response. Thus, the hypothalamic sympathoinhibitory influences on the cardiovascular system seem closely connected to a supression of the sympathetic outflow to the stomach. There is, on the other hand, no regular association between hypothalamic sympathoexcitatory influences on the cardiovascular and gastrointestinal systems; in fact, there is in many areas even a suppression of sympathetic discharge to the stomach in association with cardiovascular stimulation.

Adrenalectomy↗
PubMed1995

Vascular 5-HT1-like receptors mediating vasoconstriction and vasodilatation: their characterization and distribution in the intact canine cardiovascular system.

1. In anaesthetized dogs, intra-left atrial administration of 5-hydroxytryptamine (5-HT) and selected tryptamine analogues (5-carboxamidotryptamine, 5-CT; 5-methyl tryptamine, 5-MT; alpha-methyl 5-hydroxytryptamine, alpha-HT; sumatriptan, Sum) in the presence of ketanserin and MDL72222 (5-HT2 and 5-HT3 receptor antagonists, respectively), produced dose-related changes in carotid, coronary and renal vascular conductance mediated by vascular 5-HT1-like receptors. 2. In the carotid vascular bed, 5-HT, 5-MT, alpha-HT and Sum were vasoconstrictors with a rank order of potency (comparing ED50 values) of 5-HT = Sum > 5-MT > alpha-HT. By contrast in this vascular bed, 5-CT was a potent vasodilator. 3. In the coronary vascular bed, 5-HT, 5-CT, 5-MT and alpha-HT were vasodilators with a rank order of potency (comparing ED50 values) of 5-CT > 5-HT > 5-MT > alpha-HT. In this vascular bed, Sum was without effect. 4. In the renal vascular bed, 5-HT, 5-CT, 5-MT, alpha-HT and Sum were vasoconstrictors with a rank order of potency (comparing ED50 values) of 5-CT > 5-HT > Sum > 5-MT > alpha-HT. 5. The coronary (and carotid) vasodilator responses to 5-CT were antagonized by the 5-HT1-like receptor antagonists, spiperone (1 mg kg-1) and methiothepin (0.1 mg kg-1), whereas the renal vasoconstrictor responses to this tryptamine analogue were antagonized only by methiothepin. 6. It is concluded from these studies that agonist finger-printing in vivo, using tryptamine analogues,identifies and confirms the functional presence of at least two pharmacologically distinct subtypes of the 5-HT1-like receptor in the intact canine cardiovascular system. These two subtypes are located on the vascular smooth muscle and mediate direct vasoconstriction and vasodilatation responses in vivo.7. In addition, these studies confirm that the distribution of these subtypes within the major vascular beds, shows a marked heterogeneity. The carotid vascular responses to the tryptamine analogue sindicate the presence of both the vasodilator and the vasoconstrictor subtypes. The coronary vascular responses to these analogues are, however, consistent with presence of the vasodilator subtype, only. By contrast, the renal vascular responses to these analogues indicates only the presence of the vasoconstrictor subtype.

Animals↗