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PubMed1983

[General pharmacological actions of traxanox sodium. II. Effects on the cardiovascular system].

The effects of traxanox, an anti-allergic drug, on the cardiovascular system were studied in both anesthetized dogs and cats and in isolated heart preparations from guinea-pigs. In anesthetized dogs, a very small dose of traxanox (0.01 mg/kg, i.v.) had no effect, but 0.1--30 mg/kg caused an increase in respiratory rate, hypotension, bradycardia, a transient decrease followed by an increase in renal blood flow, and a decrease in femoral blood flow. These effects were abolished by vagal block, indicating they are mediated via vagal afferents. In contrast, oral administration of traxanox (100 mg/kg) had no effect on the blood pressure or heart rate of anesthetized dogs. In anesthetized cats, traxanox (3 and 30 mg/kg, i.v.) caused a slight increase in blood pressure, but showed no effect on respiratory rate and heart rate. Both traxanox and theophylline (10(-4)M) caused increases in the beat rate of the atria and the contractile force of the papillary muscle in isolated preparations from guinea-pigs, and they potentiated the positive chronotropic and inotropic responses induced by isoproterenol. On the other hand, in anesthetized and vagotomized dogs, traxanox (3 and 10 mg/kg, i.v.) affected neither the left ventricular contractile force nor the hypotension and positive inotropic and chronotropic responses produced by isoproterenol. Administration of theophylline alone (3 and 10 mg/kg, i.v.) caused hypotension and increases in contractile force and heart rate, but it did not enhance the responses produced by isoproterenol. At doses of 1 and 10 mg/kg (i.v.), traxanox had little effect on either pressor or chronotropic responses to norepinephrine, epinephrine, DMPP and stellate cardiac nerve stimulation. The same doses of traxanox slightly reduced the depressor and chronotropic responses to isoproterenol, acetylcholine and vagus nerve stimulation. These findings suggest that traxanox had no effect on the cardiovascular systems of the animals studied in the dose range (1--5 mg/kg, p.o.) showing anti-allergic activity.

Anesthesia↗
PubMed1994

Nonvalvular infections of the cardiovascular system.

PURPOSE: To review the risk factors, clinical presentation, diagnosis, and treatment of nonvalvular infections of the cardiovascular system. DATA SOURCES: A MEDLINE search of English-language articles from 1966 to 1993 relating to myocardial abscesses, mural endocarditis, infective endarteritis and mycotic aneurysms, infection of pacemakers and implantable defibrillators, prosthetic vascular graft infections, and infected atrial myxomas; manual review of article bibliographies. STUDY SELECTION AND DATA EXTRACTION: Case series and single reports, prospective and retrospective clinical studies, autopsy studies, and reviews were selected if they contained sufficient information about the prevalence, clinical manifestations, microbiologic features, management, and outcome of nonvalvular cardiovascular infections. RESULTS: Nonvalvular infections of the cardiovascular system most commonly occur on previously damaged endocardium or vascular intima and are usually associated with intravascular devices such as graft material or pacemakers. Rarely, they can involve primary cardiac tumors such as myxomas. Most patients affected are beyond the fifth decade of life. Risk factors include cardiovascular disease, diabetes mellitus, and malignancy. The sexes are affected equally. The clinical presentations of nonvalvular endovascular infections are subtle and diagnoses are difficult to make, often requiring not only a high index of suspicion but also the use of sophisticated radiologic techniques. Hence, for many of these infections, the diagnosis is made late in the course of the infection, and survival rates are poor. Complications include peripheral embolization, cardiac rupture, vascular aneurysm rupture, and pericarditis. Therapy frequently involves surgical intervention in addition to the use of antibiotics. CONCLUSIONS: Although uncommon, nonvalvular infections of the cardiovascular system will increase in frequency as the use of implantable devices and prosthetic materials increases in the elderly. Studies are needed to determine the most appropriate diagnostic methods, treatment regimens, and methods for prevention of these infections.

Cardiovascular Diseases↗
PubMed1986

[Changes in the cardiovascular system in adenovirus infection in adults].

The effect of adenovirus infection on the cardiovascular system of 37 adult patients with CHD and without signs of CHD was studied. It was shown that adenovirus infection caused lesion of the cardiovascular system with few clinical signs but with distinct ECG changes. They occurred in the 1st and 2nd weeks and were rather unstable. The most stable and noticeable ECG changes were recorded in CHD patients with a previous history of myocardial infarction and when adenovirus infection was complicated by pneumonia.

Adenoviridae Infections↗
PubMed1996

Kinins in the cardiovascular system.

Growing evidence points to the existence of the components of the kallikrein-kinin-system (KKS) in cardiac and vascular tissue forming systemic and local KKS pathways involving different cell types like endothelial cells, cardiomyocytes and vascular smooth muscle cells. Kinins may contribute to the regulation of the cardiovascular system in health and disease and to the pharmacological effects of cardiovascular agents via autocrine-paracrine mechanisms. Based on observations from experimental models of hypertension, hypertrophy, ischemia, remodelling and preconditioning one can assume that modulation of local KKS pathways is instrumental for endogenous cardio- and vasculoprotective mechanisms. The role of kinins as possible mediators of such protective mechanisms is not only based on the existence of their generating pathways and their release, but also on observations that kinins, when given locally or being increased by inhibition of their breakdown, exert beneficial cardiovascular effects, whereas antagonism of their receptors worsens these effects. Indispensable pharmacological tools like ACE inhibitors and kinin receptor antagonists have helped to clarify these assumptions, which are now further elucidated by molecular biology and by clinical research. Especially the wealth of experimental and clinical findings with ACE inhibitors present a continuous challenge to investigate the role of kinins in the cardiovascular system and to have a closer look at the interdependence of KKS and the Renin-Angiotensin-System (RAS). Within our decade one might not only reach a clearer molecular perception of kinins in the cardiovascular system, and their role in human health and disease, but might also come to improved innovative treatment by modulation of the KKS pathways.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

Molecular mechanisms of the inhibitory effects of bupivacaine, levobupivacaine, and ropivacaine on sarcolemmal adenosine triphosphate-sensitive potassium channels in the cardiovascular system.

BACKGROUND: Sarcolemmal adenosine triphosphate-sensitive potassium (KATP) channels in the cardiovascular system may be involved in bupivacaine-induced cardiovascular toxicity. The authors investigated the effects of local anesthetics on the activity of reconstituted KATP channels encoded by inwardly rectifying potassium channel (Kir6.0) and sulfonylurea receptor (SUR) subunits. METHODS: The authors used an inside-out patch clamp configuration to investigate the effects of bupivacaine, levobupivacaine, and ropivacaine on the activity of reconstituted KATP channels expressed in COS-7 cells and containing wild-type, mutant, or chimeric SURs. RESULTS: Bupivacaine inhibited the activities of cardiac KATP channels (IC50 = 52 microm) stereoselectively (levobupivacaine, IC50 = 168 microm; ropivacaine, IC50 = 249 microm). Local anesthetics also inhibited the activities of channels formed by the truncated isoform of Kir6.2 (Kir6.2 delta C36) stereoselectively. Mutations in the cytosolic end of the second transmembrane domain of Kir6.2 markedly decreased both the local anesthetics' affinity and stereoselectivity. The local anesthetics blocked cardiac KATP channels with approximately eightfold higher potency than vascular KATP channels; the potency depended on the SUR subtype. The 42 amino acid residues at the C-terminal tail of SUR2A, but not SUR1 or SUR2B, enhanced the inhibitory effect of bupivacaine on the Kir6.0 subunit. CONCLUSIONS: Inhibitory effects of local anesthetics on KATP channels in the cardiovascular system are (1) stereoselective: bupivacaine was more potent than levobupivacaine and ropivacaine; and (2) tissue specific: local anesthetics blocked cardiac KATP channels more potently than vascular KATP channels, via the intracellular pore mouth of the Kir6.0 subunit and the 42 amino acids at the C-terminal tail of the SUR2A subunit, respectively.

ATP-Binding Cassette Transporters↗
PubMed1996

Effect of DV-7028, a novel serotonin 5-HT2 receptor antagonist on the cardiovascular system in rats.

The response of the cardiovascular system to DV-7028 demonstrated the complex action of this substance. In anaesthetized rats DV-7028 decreased the blood pressure and heart rate. These effects did not occur in pithed rats. The hypotensive action and bradycardia was partially reduced in vagotomized animals. DV-7028 potently inhibited the vasoconstrictory effects of serotonin in isolated perfused hindlegs of rat and caused a concentration-dependent shift to the right of response curve to serotonin in the rat tail artery. The present data demonstrate that DV-7028 is a potent 5-HT2 receptor antagonist. Besides its peripheral action, DV-7028 exerts central effects which cause hypotension and bradycardia.

Animals↗
PubMed1997

Simulation study of the interaction between respiration and the cardiovascular system.

Many studies have been done on the respiratory and the cardiovascular system. Among them, only a few are on the interaction of these two physiologic systems. To explore the mechanism of the integration of these two physiological systems, computer simulation has been done; we report the preliminary results obtained in our laboratory. In this study, a mathematical model of the cardiovascular system integrated with the respiratory mechanical system has been established. The model is based on our previous work on cardiovascular modeling. The previous lumped lung model has been replaced by a multielement model with more detail. Interthoracic and abdominal pressures and modeled as external pressure sources on the related cardiovascular elements. Using this model, a sequence of simulation studies have been carried out. Different respiratory modes have been simulated and the different effects are observed in the simulation results. The results indicate that by following a certain respiratory pattern, the circulation status can be improved. These results agree with clinical observations.

Cardiovascular Physiological Phenomena↗
PubMed1990

Application of the root locus technique to the closed-loop SO2 pacemaker-cardiovascular system.

A previously developed nonlinear model of the pacemaker-cardiovascular system contained a term of the form 1/CO in the forward loop. CO, the cardiac output, is a linear function of heart rate and exercise level. To evaluate the dynamic behavior of the system over a range of pacemaker controller gains, a piecewise linear model was developed. The model was linearized by taking the first two terms of the Taylor's series expansion of 1/CO about the steady state heart rate. A root locus algorithm, with the unique feature of a time delay element in the forward loop, was used to calculate the linear model closed-loop poles as a function of pacemaker controller gain for exercise levels of 25, 50, and 100 W. Step response simulation of the complete nonlinear model showed dynamics close to that predicted from the pole location in the root locus plot. Thus, the root locus technique can be used to quantify systematically the dynamics of the pacemaker-cardiovascular system for different exercise levels and over a wide range of controller gain values.

Cardiac Output↗
PubMed2006

Angiotensin II and insulin crosstalk in the cardiovascular system.

Under normal physiology, insulin exerts vasodilatory and pro-survival actions via the phosphatidylinositol 3-kinase (PI3-kinase) pathway and vasoconstrictive and mitogenic actions via the mitogen-activated protein kinase (MAPK) pathway in the vasculature. In the insulin resistant states, insulin signals through the PI3-kinase pathway are blunted but its signals through the MAPK cascade remain intact. This imbalance predisposes insulin resistant patients to hypertension and atherosclerosis. The renin-angiotensin system (RAS) is expressed both systemically and locally in the cardiovascular system. Insulin resistance up-regulates the local RAS which contributes to the pathogenesis of hypertension, heart failure, and atherosclerosis. Angiotensin II impairs insulin signaling, induces inflammation via the NF-kappaB pathway, reduces nitric oxide availability and facilitates vasoconstriction, leading to insulin resistance and endothelial dysfunction. Thus the RAS, insulin resistance and inflammation perpetuate each other and coordinately contribute to endothelial dysfunction, vascular injury and atherosclerosis. RAS inhibition decreases cardiovascular and renal morbidity and mortality and the incidence of new onset Type 2 diabetes.

Angiotensin II↗
PubMed1999

Cocaine stimulates the human cardiovascular system via a central mechanism of action.

BACKGROUND: Cocaine is thought to stimulate the cardiovascular system by blocking peripheral norepinephrine reuptake. This study was designed to test the novel hypotheses that cocaine also stimulates the human cardiovascular system by (1) increasing central sympathetic outflow, or (2) decreasing parasympathetic control of heart rate. METHODS AND RESULTS: In 14 healthy cocaine-naive humans, we measured blood pressure, heart rate, and skin sympathetic nerve activity (SNA) with intraneural microelectrodes before, during, and for 90 minutes after intranasal cocaine (2 mg/kg, n=7) or lidocaine (2 mg/kg, n=7). Intranasal cocaine caused an initial but transient 3. 3-fold increase in skin SNA during the period of intranasal administration followed by a sustained 2.4-fold increase lasting for up to 90 minutes after cocaine. Unlike cocaine, intranasal lidocaine caused only a small transient increase in skin SNA due to local nasal irritation. The cocaine-induced increase in SNA was accompanied by decreased skin blood flow, increased skin vascular resistance, and increased heart rate. In 11 additional subjects, we showed that the cocaine-induced increase in heart rate was eliminated by beta-adrenergic receptor blockade (propranolol) but unaffected by muscarinic receptor blockade (atropine), indicating sympathetic mediation. CONCLUSIONS: These studies provide direct microneurographic evidence in humans that intranasal cocaine stimulates central sympathetic outflow. This central sympathetic activation appears to be targeted not only to the cutaneous circulation promoting peripheral vasoconstriction but also to the heart promoting tachycardia.

Administration, Intranasal↗
PubMed2003

Cyclic nucleotide phosphodiesterase activity, expression, and targeting in cells of the cardiovascular system.

Cyclic AMP (cAMP) and cGMP regulate a myriad of cellular functions, such as metabolism, contractility, motility, and transcription in virtually all cell types, including those of the cardiovascular system. Considerable effort over the last 20 years has allowed identification of the cellular components involved in the synthesis of cyclic nucleotides, as well as effectors of cyclic nucleotide-mediated signaling. More recently, a central role for cyclic nucleotide phosphodiesterase (PDE) has also been elaborated in many cell types, including those involved in regulating the activities of the cardiovascular system. In this review, we introduce the PDE families whose members are expressed in cells of the cardiovascular system including cardiomyocytes, vascular smooth muscle cells, and vascular endothelial cells. Because cell behavior is a dynamic process influenced by numerous factors, we will attempt to emphasize how changes in the activity, expression, and targeting of PDE influence cyclic nucleotide-mediated regulation of the behavior of these cells.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMedDate not supplied

[Melatonin and regulation of the cardiovascular system].

Evidence from the last 10 years suggests that melatonin may influence the cardiovascular system. Vascular melatoninergic receptors/sites have been demonstrated and are functionally linked with vasoconstrictor or vasodilatory effects of low (10(-9)-10(-7) M) and high (10(-6)-10(-3) M) melatonin concentrations respectively. Furthermore several other properties of the neurohormone (e.g. sympathetic inhibition) could contribute to cardioprotection. In vivo melatonin beneficially affects the rat cerebrovascular circulation and protects the rat heart following myocardial ischaemia. In this regard, preliminary clinical data report some alteration of the melatoninergic system in human stroke and coronary heart disease. Finally, the suprachiasmatic nucleus and possibly the melatoninergic system may modulate cardiovascular rhythmicity. Clinical cardiovascular data on melatonin treatment are very scarce; the effects of a therapy modulating the melatoninergic system on cardiovascular haemodynamics and rhythmicity under several physiopathological conditions need to be further explored together with the possible impact on cardiovascular morbidity and mortality.

Animals↗
PubMed1985

Evaluation of the equine cardiovascular system.

A thorough examination of the cardiovascular system is an integral part of a physical examination in the horse. The normal equine cardiovascular parameters are discussed, with an emphasis on auscultatory findings. The availability and application of other diagnostic techniques are discussed based upon findings of the physical examination.

Angiocardiography↗
PubMed2001

Impairment rating of the cardiovascular system: Idiopathic cardiomyopathy.

Disease of the cardiovascular system is the leading cause of morbidity and mortality among the adult population in the United States. Physicians performing impairment ratings attributable to cardiovascular disease are required to correlate the extent of the disease and its impact on a person's daily activities. A person's final impairment determination may vary based on the specific guidelines used (American Medical Association Guides to the Evaluation for Permanent Impairment, Social Security, State Worker Compensation requirements, etc.), the version of the guidelines (year, edition), and each guide's specific criteria. The examiner needs to know which rating system to use, the system's criteria, critical definitions, and potential limitations.

Adult↗
PubMed1993

Mathematical modelling of the human cardiovascular system in the presence of stenosis.

This paper reports a theoretical study on the distribution of blood flow in the human cardiovascular system when one or more blood vessels are affected by stenosis. The analysis employs a mathematical model of the entire system based on the finite element method. The arterial-venous network is represented by a large number of interconnected segments in the model. Values for the model parameters are based upon the published data on the physiological and rheological properties of blood. Computational results show how blood flow through various parts of the cardiovascular system is affected by stenosis in different blood vessels. No significant changes in the flow parameters of the cardiovascular system were found to occur when the reduction in the lumen diameter of the stenosed vessels was less than 65%.

Blood Circulation↗