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PubMed2001

Depression, anxiety, and the cardiovascular system: the psychiatrist's perspective.

It is becoming clear that the comorbidity of depression and cardiovascular disease does not occur by chance but rather is an inevitable consequence of the relationship between the conditions. Depression in patients with cardiovascular disease is a significant risk factor for developing symptomatic and fatal ischemic heart disease. Moreover, depressed patients have a higher than expected rate of sudden cardiovascular death. Therefore, appropriate treatment of patients with depression and cardiovascular disease cannot be restricted to considerations of either depression or cardiovascular disease in isolation. The tricyclic antidepressants (TCAs) have various effects on the cardiovascular system, including Type IA antiarrhythmic activity that has been associated with an increased risk of mortality in post-myocardial infarction patients. The selective serotonin reuptake inhibitors (SSRIs) are not associated with adverse cardiac effects. The SSRI paroxetine was compared with a therapeutic level of the TCA nortriptyline in a randomized, controlled study and demonstrated a benign cardiovascular profile, while the TCA induced a significantly higher rate of serious adverse cardiovascular events. On the basis of this favorable cardiovascular profile, the SSRIs should therefore be the preferred choice for the treatment of most patients with comorbid depression and cardiovascular disease. Investigation of putative pathophysiologic mechanisms linking depression and cardiovascular mortality, such as the role of platelet activation, will form the basis for further investigation of antidepressant treatments in order to establish if the antidepressants have a beneficial effect on the prognosis of cardiovascular diseases.

Antidepressive Agents, Tricyclic↗
PubMed2000

Heart rate and blood pressure variability in normal subjects compared with data from beat-to-beat models developed from de Boer's model of the cardiovascular system.

The objective of this study was to assess the ability of de Boer's model of the cardiovascular system to reproduce the heart rate and blood pressure variability observed in a range of normal subjects, and to make modifications to improve its performance. ECG, blood pressure and chest wall movement were recorded from 12 normal human subjects during controlled breathing. For each beat, systolic pressure, diastolic pressure, arterial time constant and RR interval were extracted. RR interval and systolic pressure spectral power in low and high frequency bands and the baroreflex sensitivity index, alpha, were then determined. For each subject, mean values were input to the model and the beat-to-beat output compared with the actual data for that subject. Finally, the effects of reducing the influence of baroreflex on peripheral vascular resistance and of providing separate sympathetic and vagal baroreflex sensitivities were assessed. Simulations resulted in data which were qualitatively similar to those of each subject's recording. With the modifications, the log ratio of simulated to real data improved from 7.2 to 1.5 (p = 0.003) for low frequency RR, from 0.27 to 0.55 (p = 0.011) for high frequency RR and from 8.5 to 0.9 (p = 0.003) for low frequency systolic pressure. We conclude that de Boer's model reproduces many of the characteristics of heart rate and blood pressure variability, and our modifications to baroreflex sensitivities and the feedback effect on peripheral resistance resulted in significant improvements.

Adult↗
PubMed1992

Effects of peptide YY on the human cardiovascular system: reversal of responses to vasoactive intestinal peptide.

Peptide YY (PYY) reverses the increased intestinal secretion stimulated by vasoactive intestinal peptide (VIP) in humans. VIP also dilates blood vessels, so we investigated the effect of PYY on the cardiovascular system. Six volunteers received PYY, 0.4 and 1.2 pmol.kg-1 x min-1 i.v. for 2 h, reproducing plasma levels seen postprandially and during a diarrheal illness, respectively. Cardiac function was assessed by echocardiography. PYY infused at 0.4 pmol.kg-1 x min-1 had no effect on cardiovascular parameters. PYY infused at 1.2 pmol.kg-1 x min-1 caused a fall in both stroke volume from 128 +/- 8 to 110 +/- 8 ml/beat (mean +/- 95 confidence interval, P < 0.01) and cardiac output from 7.2 +/- 0.4 to 6.1 +/- 0.4 l/min (P < 0.01). Effects of infusion of PYY into the brachial artery at doses of 0-16 pmol/min were assessed using venous occlusion plethysmography in six subjects. PYY infusion caused a dose-dependent fall in forearm blood flow. Six subjects received VIP, 5 pmol.kg-1 x min-1 i.v., causing a rise in heart rate from 55 +/- 3 to 70 +/- 3 beats/min and increased cardiac output from 7.3 +/- 1.1 to 13.1 +/- 1.1 l/min. The addition of PYY, 0.4 pmol.kg-1 x min-1 i.v., did not affect the heart rate significantly but decreased the cardiac output to 10.4 +/- 1.1 l/min (P < 0.01). Infusions of PYY into the brachial artery at 5 pmol/min decreased local vasodilation induced by VIP infused at 2 pmol/min at the same site by 40% (P < 0.01), even though this dose of PYY had no significant effect on local blood flow when given alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2002

Central mechanisms underlying short- and long-term regulation of the cardiovascular system.

1. Sympathetic vasomotor nerves play a major role in determining the level of arterial blood pressure and the distribution of cardiac output. The present review will discuss briefly the central regulatory mechanisms that control the sympathetic outflow to the cardiovascular system in the short and long term. 2. In the short term, the sympathetic vasomotor outflow is regulated by: (i) homeostatic feedback mechanisms, such as the baroreceptor or chemoreceptor reflexes; or (ii) feed-forward mechanisms that evoke cardiovascular changes as part of more complex behavioural responses. 3. The essential central pathways that subserve the baroreceptor reflex and, to a lesser extent, other cardiovascular reflexes, have been identified by studies in both anaesthetized and conscious animals. A critical component of these pathways is a group of neurons in the rostral ventrolateral medulla that project directly to the spinal sympathetic outflow and that receive inputs from both peripheral receptors and higher centres in the brain. 4. Much less is known about the central pathways subserving feed-forward or 'central command' responses, such as the cardiovascular changes that occur during exercise or that are evoked by a threatening or alerting stimulus. However, recent evidence indicates that the dorsomedial hypothalamic nucleus is a critical component of the pathways mediating the cardiovascular response to an acute alerting stimulus. 5. Long-term sustained changes in sympathetic vasomotor activity occur under both physiological conditions (e.g. a change in salt intake) and pathophysiological conditions (e.g. heart failure). There is evidence that the paraventricular nucleus in the hypothalamus is a critical component of the pathways mediating these changes. 6. Understanding the central mechanisms involved in the long-term regulation of sympathetic activity and blood pressure is a major challenge for the future. As a working hypothesis, a model is presented of the postulated central mechanisms that result in sustained changes in sympathetic vasomotor activity that are evoked by different types of chronic stimulation.

Animals↗
PubMed1991

[Cardiovascular system function in mitral valve prolapse in fighter pilots].

Echocardiogram examination of 250 young fighter pilots has revealed that 15 aviators had mitral valve prolapse (MVP) without symptoms of pronounced regurgitation. Their functional indexes of cardiovascular system at rest or dosed physical load at veloergometer tests were normal. Only in 3 pilots were marked rare supraventricular or ventricular extrasystoles during ECG monitoring or veloergometria. Performance capability of all pilots was sufficient. 13 pilots with MVP in examination of their tolerance to +Gz hypergravity at the levels of 6 G or more for 15 s had frequent polytop or group ventricular extrasystole. There was an ordinary aggravation of extrasystole in aviators with more deep and bilateral MVP. The article makes a conclusion that on the basis of medical flight expertise a thorough selection must be made concerning possibility of every pilot with MVP to carry out flight at high manoeuvring aircraft of new generation taking into account the gravity of prolapse and tolerance to high +Gz hypergravity more than 5 G.

Adult↗
PubMed1990

Alterations of arachidonate metabolism in cardiovascular system by cigarette smoking.

Male rats were exposed to freshly generated cigarette smoke once daily for various lengths of time. Inhalation of smoke was verified by elevated levels of carboxyhemoglobin. Metabolism of arachidonate in the cardiovascular system to thromboxane and prostacyclin through the cyclooxygenase pathway and their further metabolism to 15-keto-derivatives, and to 12-hydroxyeicosatetraenoic acid (12-HETE) through lipoxygenase pathway was investigated. Synthesis of thromboxane and prostacyclin in platelets and aortas respectively was not changed within 8 weeks of smoke exposure. However, formation of 12-HETE in platelets was significantly increased after 4 weeks of smoke exposure. Catabolism of thromboxane and prostacyclin as determined by NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase activity was greatly decreased in lung but not in kidney and stomach following 4 weeks of smoke exposure. Increased 12-lipoxygenase activity in platelets may lead to stimulation of migration and proliferation of smooth muscle cells and to increased synthesis of leukotrienes in neutrophils. Decreased pulmonary prostaglandin catabolic activity may result in increase in circulating thromboxane/prostacyclin ratio and subsequently alteration of vascular homeostasis. The consequence of these biochemical changes may contribute to the development of atherosclerosis, thromboembolism and emphysema commonly found in smokers.

Acrolein↗
PubMed2001

[Effects of endomorphins and their analogs on cardiovascular system].

AIM: To analyze the effects of endomorphins (EMs) and their analogs ([D-Pro2]EM-1, [D-Ala2]EM-1, [D-Pro2]EM-2 and [D-Ala2]EM-2) on the cardiovascular system of anestetized rats and to study its mechanism. METHODS: Responses to EMs and their analogs were investigated in the systemic vascular bed of rats and the mesenteric microarteria of Bufo gargarizans. Responses to EMs were investigated on the hindquarters of the rat vascular bed under constant-flow conditions and on the isolated rabbit thoracic aorta strips. RESULTS: The EMs and their analogs showed dose-related (10(-9)-10(-6) mol.L-1, i.v.) and naloxone-sensitive (2 mg.kg-1, i.v.) hypotension in mean arterial pressure of rats with similar duration and vasodilatation in mesenteric microarteria of Bufa gargarizans. The sequence of potencies was EMs > [D-Pro2] EM-2 > [D-Ala2]EM-2 > [D-Ala2]EM-1 > [D-Pro2]EM-1. EMs were shown not to relax the isolated rabbit thoracic aorta strips without endothelium. EMs, however, relaxed them with endothelium significantly. This action was blocked by Nx (10(-5) mol.L-1) and L-NNA (10(-4) mol.L-1). CONCLUSION: The significant hypotensive activity of EMs and their analogs is mainly associated with their vasodilatation, which is related to the release of NO from vascular endothelium, and their potency is not completely related to their affinity for mu-opiate receptor.

Animals↗
PubMed1996

[Adrenoreceptors of cell membranes as indicators of strain of the cardiovascular system].

The study covered 226 individuals including 40 apparently healthy subjects, 30 patients with vasoneurosis accompanied by arterial hypertension, 23 patients with I stage arterial hypertension and 83 patients with II stage arterial hypertension. The aim was to evaluate some parameters of myocardium and response of cardiovascular system exposed to modified psychoemotional Kreppelin test. Basic value of beta-adrenoreactivity in cellular membranes appeared to be important in manifold evaluation of cardiovascular strain. Higher values of beta-adrenoreactivity in cellular membranes induce inadequate hemodynamic responses to physical load, resulting in progress of morphologic and functional disorders of myocardium.

Adult↗
PubMed1999

[Distribution and function of angiotensin receptor subtypes in cardiovascular system].

Angiotensin II (AII) participates in regulation of arterial blood pressure through its binding to AII receptors distributing among its target organs. In addition, locally produced AII appears to play a major role in the pathogenesis of cardiovascular hypertrophy via mechanism not related to blood pressure. Two subtypes of AII receptors, AT1 and AT2, are recognized as distinct in both molecular and pharmacological basis. In adult, AT1 is a dominant subtype in cardiovascular system, and mediates virtually all the previously known actions of AII, including vasoconstriction, production of growth factors, hypertrophy of smooth muscle and cardiomyocyte, proliferation of smooth muscle and fibroblast, production of extracellular matrix and so on. Recently, upregulation of AT2 expression is revealed under certain pathological conditions, such as vascular injury, myocardial infarction, and heart failure. Biological significance of AT2 are still under investigation, however, countering actions against AT1 are often suggested.

Animals↗
PubMed1999

Venous return in the fetal-placental cardiovascular system.

For a quantitative understanding of the venous Doppler sonograms, a model of the fetal cardiovascular system is proposed which stresses the significance of flow. The model comprises three major components: the heart which provides constant power and dynamic capacitance, the peripheral fetal and placental vascular beds with flow limiting conductances (1/resistance), and the resistance of the hepato-ductal system. As long as cardiac power is maintained, the conductances control the flow rate and, depending upon hepato-ductal and ventricular filling resistance, the umbilical venous as well as the central venous pressure. According to the model, the mean flow velocity of venous return is total organ flow rate divided by cross sectional areas in the cardiac input system, i.e. the central veins, both atria and both AV valves respectively. The velocity pattern of venous return is related to cardiac performance and hepato-ductal resistance as follows: The E wave in early diastole describes the filling (driven by the central-venous pressure) of the relaxed ventricle. The time constant equals the ratio of elasticity over resistance in the ventricular wall. The A wave mirrors the contractility of atrial myocardium which is related to central venous pressure. The ratio of the forward A wave in the tricuspid valve to the backward A wave in the caval veins depends on ventricular capacitance. The S wave is related to systolic valvular shift. The velocity pulsations in the ductus venosus are transmitted backwards from the heart. The continuous velocity component in the ductus venosus and the non-pulsatile velocity in the umbilical vein are due to hepato-ductal and placental vascular resistance.

Animals↗
PubMed2003

Velocity profile method for time varying resistance in minimal cardiovascular system models.

This paper investigates the fluid dynamics governing arterial flow used in lumped parameter cardiovascular system (CVS) models, particularly near the heart where arteries are large. Assumptions made in applying equations conventionally used in lumped parameter models are investigated, specifically that of constant resistance to flow. The Womersley number is used to show that the effects of time varying resistance must be modelled in the pulsatile flow through the large arteries near the heart. It is shown that the equation commonly used to include inertial effects in fluid flow calculations is inappropriate for including time varying resistance. A method of incorporating time varying resistance into a lumped parameter model is developed that uses the Navier-Stokes equations to track the velocity profile. Tests on a single-chamber model show a 17.5% difference in cardiac output for a single-chamber ventricle model when comparing constant resistance models with the velocity profile tracking method modelling time varying resistance. This increase in precision can be achieved using 20 nodes with only twice the computational time required. The method offers a fluid dynamically and physiologically accurate method of calculating large Womersley number pulsatile fluid flows in large arteries around the heart and valves. The proposed velocity profile tracking method can be easily incorporated into existing lumped parameter CVS models, improving their clinical application by increasing their accuracy.

Animals↗
PubMed1989

The effects of copper deficiency on the pyridinium crosslinks of mature collagen in the rat skeleton and cardiovascular system.

The 3-hydroxypyridinium crosslinks of collagen were quantified in tissues of the skeleton and cardiovascular system of normal and copper-deficient rats. The copper-deficient rats used in this study displayed retarded growth, cardiac hypertrophy, anemia, and lowered liver copper concentrations. Quantification of the crosslinks by high performance liquid chromatography indicated that there were lower concentrations of collagen crosslinks in the hearts of copper-deficient animals, a finding that was manifest in both right and left ventricles. This was in contrast to the collagen of the aorta where no alteration in crosslink concentration was observed. The femoral diaphysis of copper-deficient rats also had lower amounts of collagen crosslinks than copper-supplemented animals, whereas crosslinking in the tibial diaphysis and articular cartilage was relatively unaffected by copper deficiency. These results are discussed with reference to the cardiac and skeletal abnormalities that occur in copper-deficient animals.

Animals↗
PubMed1998

[The effect of new H1-receptor antagonists on cardiovascular system].

The authors present effects of new H1-receptor antagonists--terfenadine and astemizol on cardiovascular system in humans. The role of interactions between terfenadine and astemizol and other drugs is underlined. Effects of hepatic and heart diseases as well as astemizol and terfenadine overdose on their pharmacokinetics are also showed.

Astemizole↗
PubMed1985

Effect of vasoactive intestinal polypeptide on the canine cardiovascular system.

Our purpose was to determine the effect of vasoactive intestinal polypeptide (VIP) on the cardiovascular system with special emphasis on coronary vascular effects. In section I, VIP was infused into six healthy and six cobalt-cardiomyopathic dogs at two infusion rates (0.02 and 0.05 micrograms/kg/min). Left ventricular end diastolic pressure and mean systemic pressure fell significantly in both groups. Heart rate rose in both, and maximum systolic dP/dt increased in the myopathic group. Cardiac output and regional blood flows were determined by serial left atrial injections of radioactive 15 +/- 3 mum (mean +/- SD) microspheres. In both groups, blood flow increased significantly to the esophagus, pancreas, atria, and ventricles and to the endocardial and epicardial regions of the left ventricular free wall. Blood flow to the brain decreased. In section II, VIP was infused intravenously at 0.1 micrograms/kg/min into six anesthetized dogs with coronary sinus flow, pulmonary artery, and systemic artery catheters inserted. Cardiac index rose from baseline (3.1 +/- 0.5 to 4.8 +/- 1.3 L/min/m2, P less than 0.005), as did coronary blood flow (90 +/- 25 to 159 +/- 54 ml/min, P less than 0.005) during the VIP infusion. Myocardial oxygen consumption rose from 14.1 +/- 3.9 to 19.8 +/- 5.4 ml/min (P less than 0.001), but the aorta-to-coronary sinus O2 difference decreased from 157 +/- 19 ml/L to 132 +/- 42 ml/L (P less than 0.05), and the percent O2 extracted from coronary blood also decreased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

General pharmacological studies on N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate. 3rd communication: effect on cardiovascular system.

In this general pharmacological study of N-[2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), its effects on the cardiovascular and respiratory systems were studied. SUN 1165, at doses of up to 1.0 mg/kg i.v., had almost no effect. SUN 1165, at doses of 3.0 and 6.0 mg/kg i.v., caused dose-dependent decreases in blood pressure, common carotid, vertebral, coronary, hepatic and femoral artery and portal vein blood flows, cardiac contractility, heart rate and myocardial oxygen consumption. SUN 1165 increased urine volume and urinary excretion of electrolytes in rats at a dose of 100 mg/kg p.o. SUN 1165 decreased renal plasma flow and urinary excretion of electrolytes in anesthetized dogs at 6.0 mg/kg i.v., but at the antiarrhythmic doses (1.0-3.0 mg/kg i.v. in dogs), it had almost no effects on renal function. SUN 1165 had almost no effect on the autonomic nervous systems in anesthetized dogs. These results suggest that SUN 1165 at the antiarrhythmic doses do not have any effects on the respiratory and cardiovascular systems, renal function and autonomic nervous systems in rats and dogs, but that when administered at high doses, it has inhibitory effects on respiratory and cardiovascular system and renal function. In conclusion, SUN 1165 seems to be a novel antiarrhythmic drug relatively free of cardiovascular, respiratory, renal and autonomic effects.

Animals↗