Physical and psychosocial stress and the cardiovascular system.
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Cardiovascular Diseases↗
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Synergistic hypotensive effect of vasoactive intestinal polypeptide and alpha-blockade with phentolamine. Evidence for vasoactive intestinal peptide alpha-adrenoceptor coupling in the cardiovascular system of newborn dogs.
Vasoactive intestinal polypeptide (VIP) is a neuropeptide with potent circulatory effects in the adult animal and human. Little is known about its effects or mechanism of action in the immature animal. These series of experiments evaluated the effects and possible mechanism of action of VIP on the developing canine cardiovascular system. In all three series, measurements of mean heart rate and blood pressure were taken in the control state, after parasympathetic denervation with bilateral cervical vagotomies, and after autonomic blockade with propranolol (1 mg/kg) and phentolamine (0.5 mg i.v.). In series 1, we characterized the role of alpha-adrenergic receptors in early newborn puppies by investigating the hemodynamic effects of phentolamine alone in five early newborn puppies. In series 2, the hemodynamic effects of intravenous VIP infusion (0.2 microgram/kg/min) were recorded and compared in six early newborn puppies and in 10 late newborn puppies. In series 3, the hemodynamic effects of phentolamine in the presence of VIP receptor binding inhibitor were studied. In early newborn puppies, VIP had essentially no effect on heart rate or blood pressure until phentolamine was given; then, blood pressure decreased by 17% (p less than 0.005). In late newborn puppies, VIP resulted in an increase in heart rate in the control state but not after parasympathetic or sympathetic denervation. In early newborn puppies, phentolamine alone resulted in a 24% decrease (p less than 0.005) in blood pressure, compared with a 54% decrease (p less than 0.005) in early newborn puppies preexposed to VIP infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
[The cardiovascular system function of the cosmonauts of the 6th prime expedition on the Mir station].
Medical results of inflight cardiovascular measurements made in the 6th prime crew at rest and during provocative graded bicycle exercises and LBNP tests are presented. The methods of electrocardiography, tetrapolar rheography, kinetocardiography, arteriovenous pulsography and tacho-oscillography have been used to examine the cosmonauts. Together with regular cardiovascular changes typical of microgravity effect the individual peculiarities of developing the control mechanisms are noted. Thus in one of the cosmonauts a number of symptoms responsible for a decreased venous return. As a whole the functional state of the cardiovascular system on all flight stages was characterized by a sufficiently high physiological level.
Cardiovascular Physiological Phenomena↗
Long-term administration of D-NAME induces hemodynamic and structural changes in the cardiovascular system.
N(G)-nitro-D-arginine-methyl ester (D-NAME) is considered to be an inactive enantiomer of L-NAME and is generally used as the negative control for NO synthase inhibition with L-NAME. With the aim to compare the effects of 4-week L-NAME and D-NAME treatments on hemodynamic and cardiovascular structural parameters, four groups of male Wistar rats were investigated: the controls and groups administered 40 and 20 mg/kg/day of L-NAME and 40 mg/kg/day of D-NAME. At the end of the experiment, myocardial NO synthase activity decreased by 42, 24 and 25%; aortic NO synthase activity decreased by 35, 15 and 13% vs. controls in the L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. The DNA concentrations in the myocardium and the aorta increased significantly after L-NAME and D-NAME treatments. The inhibition of NO synthase was accompanied by a significant elevation in systolic blood pressure in all three groups. The LVW/BW ratio increased by 27, 14 and 13% vs. controls in the L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. The aortic wall mass, measured as the cross-sectional area, increased by 45, 17 and 25% vs. controls in the L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. Myocardial fibrosis represented 0.94% in the controls, but 7.96, 4.70 and 5.25% in L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. It is concluded that D-NAME, although less affective than L-NAME, inhibits NO synthase activity resulting in hemodynamic and structural changes in the cardiovascular system similar to the changes induced by half the dose of L-NAME. Thus, the consideration of D-NAME as an inactive enantiomer and its use as the negative control needs to be reevaluated.
Animals↗
Peroxisome proliferator-activated receptors and the cardiovascular system.
Insulin resistance syndrome (also called syndrome X) includes obesity, diabetes, hypertension, and dyslipidemia and is a complex phenotype of metabolic abnormalities. The disorder poses a major public health problem by predisposing individuals to coronary heart disease and stroke, the leading causes of mortality in Western countries. Given that hypertension, diabetes, dyslipidemia, and obesity exhibit a substantial heritable component, it is postulated that certain genes may predispose some individuals to this cluster of cardiovascular risk factors. Emerging data suggest that peroxisome proliferator-activated receptors (PPARs), including alpha, gamma, and delta, are important determinants that may provide a functional link between obesity, hypertension, and diabetes. It has been well documented that hypolipidemic fibrates and antidiabetic thiazolidinediones are synthetic ligands for PPAR alpha and PPAR gamma, respectively. In addition, PPAR natural ligands, such as leukotriene B4 for PPAR alpha, 15-deoxy-delta 12,14-prostaglandin J2 for PPAR gamma, and prostacyclin for PPAR delta, are known to be eicosanoids and fatty acids. Studies have documented that PPARs are present in all critical vascular cells: endothelial cells, vascular smooth muscle cells, and monocyte-macrophages. These observations suggest that PPARs not only control lipid metabolism but also regulate vascular diseases such as atherosclerosis and hypertension. In this review, we present structure and tissue distribution of PPAR nuclear receptors, discuss the mechanisms of action and regulation, and summarize the rapid progress made in this area of study and its impact on the cardiovascular system.
Animals↗
Pharmacology of thromboxane A2, prostacyclin and other eicosanoids in the cardiovascular system.
The eicosanoids, a group of endogenous metabolites of the cell membrane phospholipid-derived fatty acid arachidonic acid (AA), are formed from AA via three main enzymatic pathways (cyclooxygenase, lipoxygenase, cytochrome P450) and include the classical prostaglandins (PGF2 alpha, E2, D2), TxA2, PGI2, the leukotrienes and HETEs/HPETEs, the lipoxins and various epoxy metabolites. In the cardiovascular system the current interest is focussed on TxA2 and PGI2. TxA2 is released from activated platelets, shows potent platelet aggregating and vasoconstricting properties and is therefore considered to be important in thrombotic and ischaemic diseases. Therapeutic strategies directed at interfering with endogenous TxA2 include inhibition of synthesis (aspirin, selective TxA2 synthase inhibitors) and, more recently, specific blockade of TxA2 receptors. PGI2 is released mainly from the vascular intima, potently inhibits platelet aggregation and shows vasodilator and cytoprotective properties. PGI2 and chemically stable PGI2-derivatives have been shown to be effective in the treatment of severe peripheral ischaemic diseases and offer further interesting prospectives like prevention of vascular reocclusion in bypass surgery and balloon catheter angioplasty as well as organ preservation in transplant surgery. Other eicosanoids like PGD2 and the leukotrienes may also be important mediators in cardiovascular disease. Whether they represent targets for innovative drug therapy in cardiovascular disease remains to be investigated.
Cardiovascular System↗
Effects of Brugia pahangi infection on the cardiovascular system of stroke-prone spontaneously hypertensive rats.
To determine if filarial infection causes any effect on the cardiovascular system of the host animal, stroke-prone spontaneously hypertensive rats were infected with Brugia pahangi under the assumption that these rats would reveal pathological changes more clearly and in a shorter period than would ordinary rats. The infection resulted in loss of body weight, increase in heart weight, enlargement of left ventricle, and higher mortality rate.
Animals↗
A mathematical model for fundamental regulation processes in the cardiovascular system.
Based on the four compartment model by Grodins we develop a model for the response of the cardiovascular system to a short term submaximal workload. Basic mechanisms included in the model are Starling's law of the heart, the Bowditch effect and autoregulation in the peripheral regions. A fundamental assumption is that the action of the feedback control is represented by the baroceptor loop and minimizes a quadratic cost functional. Simulation results show that the model provides a satisfactory description of data obtained in bicycle ergometer tests.
Blood Pressure↗
The cardiovascular system in kidney disease.
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Cardiovascular System↗
[Natural and decaffeinized coffee on the cardiovascular system].
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Caffeine↗
[Cardiovascular system in peptic ulcer].
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Cardiovascular System↗
Reversal by aminoguanidine of the age-related increase in glycoxidation and lipoxidation in the cardiovascular system of Fischer 344 rats.
Non-enzymatic glycoxydation and lipoxidation of proteins continues to stimulate great interest in gerontology as both markers and promoters of aging. The first aim of the study was to determine the age-related changes in levels of Nepsilon-(carboxymethyl)lysine (CML) and 4-hydroxy-2-nonenal (HNE) present on proteins of the cardiovascular system of Fischer 344 rats and identify the particular polypeptides being modified. The second objective was to evaluate whether pharmacological administration of aminoguanidine (1g/L in the drinking water) could reverse protein glycoxidation and lipoxidation. CML content in serum, aorta, and heart proteins from 28-month-old rats was double of that found in 4-month-old animals. AG administration to old rats for 3 months from the age of 25 months lowered CML content by 15 (P=.2275), 44 (P<.0001), and 28% (P=.0072) in serum, aorta, and heart, respectively. Serum albumin, transferrin and immunoglobulins were most prominently adducted by both CML and HNE. While the extent of albumin and transferrin modification was comparable between age groups, CML and HNE bound to immunoglobulins increased in the sera of old rats as a result of the accumulation of immunoglobulin heavy and light chains. AG treatment prevented immunoglobulin accumulation in serum, suggesting a beneficial action on renal filtration. Lipoxidation of heart mitochondrial proteins was prevalent over glycoxidation, either as CML or pentosidine. Although AG prevented HNE-induced inactivation of the alpha-ketoglutarate dehydrogenase complex in vitro, it had no effect in rat hearts, suggesting AG could not reach the mitochondrial matrix.
Aging↗
Effects of endurance training on the cardiovascular system and water compartments in elderly subjects.
The effects of endurance training on the water compartments and the cardiovascular system were determined in 10 elderly subjects [age 62 +/- 2 yr, pretraining maximal oxygen consumption (VO2 max)/kg = 25 +/- 2 ml . min-1 . kg-1 body wt]. They trained on a cycloergometer 3 times/wk for 16 wk (50-80% VO2 max, then 80-85% VO2 max). They were checked at 8 wk, 16 wk, and 4 mo after detraining. Training improved VO2 max (+16%) and induced plasma volume expansion (+11%). No change in total body water, extracellular fluid, interstitial and intracellular fluid volumes, fat-free mass, and body weight was detected in this small sample with training. Body fat mass decreased (-2.1 +/- 2.2 kg). Echocardiography at rest showed increased fractional shortening and ejection fraction and decreased left ventricular end-systolic dimension (P < 0.05). Blood volume expansion correlates with cardiac contractility and has an impact on cardiac function. These improvements are precarious, however, and are completely lost after 4 mo of detraining, when elderly subjects lose the constraints and the social stimulation of the imposed protocol.
Aged↗
The effect of a prostaglandin DP-receptor partial agonist (192C86) on platelet aggregation and the cardiovascular system in healthy volunteers.
1. PGD2 (DP)-receptors mediate inhibition of platelet aggregation and vasodilatation. If receptor reserve were greater on platelets it might be possible to separate these effects. To determine whether such a difference in receptor reserve exists, we have examined the effects of a highly selective DP-receptor partial agonist 192C86 on platelet aggregation and the cardiovascular system in healthy volunteers. 2. Using an open, dose-escalating study design, four male volunteers received constant rate intravenous infusions of 192C86 for up to 60 min. Ex vivo platelet aggregation to ADP and collagen in platelet-rich plasma (PRP) and whole blood (WB) was studied at baseline, after 15, 30 and 60 min of each infusion and at 180 min post-infusion. Heart rate (HR), systolic and diastolic (DBP) blood pressure were measured at frequent intervals. Adverse experiences were monitored by checklist. Facial flushing was assessed by the volunteer using a visual analogue scale, by an observer using a numerical scale and by full-face colour photographs. Blood was taken for assay of plasma 192C86 concentrations by radio-immunoassay (r.i.a.). 3. 192C86 (0.007-0.058 micrograms kg-1 min-1) inhibited platelet aggregation to ADP and collagen both in PRP and WB in a dose-dependent manner. However, this was always accompanied by a decrease in DBP, increase in HR and facial flushing. Plasma concentrations of 192C86 were at or below the limits of sensitivity of the r.i.a. (0.5 ng ml-1). 4. The highest infusion rate was stopped after 20 min due to symptomatic hypotension on standing.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Actions of 4-aminopyridine on the cardiovascular systems of anaesthetized cats and dogs.
The effects of the anti-curare agent 4-aminopyridine on the cardiovascular systems of cats and greyhounds under barbiturate-chloralose anaesthesia have been studied. In both species, 4-amino-pyridine produced a transient atropine-sensitive decrease in arterial pressure followed by a prolonged adrenergically-mediated increase. In the cat, the cardiac responses to vagal stimulation and nictitating membrane responses to sympathetic stimulation were augmented after injection of 4-aminopyridine, and the evidence indicated that these effects were the results of increased release of neurotransmitters. In the greyhound, 4-aminopyridine produced increases in the left ventricular systolic pressure and dP/dt max, right atrial pressure, stroke volume, myocardial blood flow, myocardial oxygen consumption, external cardiac work, arterial oxygen content and blood haemoglobin. These effects were attributable to facilitation of sympathetic transmission to the blood vessels, heart and spleen. Heart rate was not much affected because facilitation of vagal transmission to the S-A node counteracted the increased sympathetic effect. In the greyhound, 4-aminopyridine also produced temporary cardiac arrhythmia which was only partly attributable to facilitated sympathetic transmission. In addition there was evidence of a central stimulant action of 4-aminopyridine and of a stimulant action on visceral activity. It is concluded that, while 4-aminopyridine may be useful in certain relatively rare conditions of neuromuscular transmission failure, its actions are too widespread for routine use as an antagonist to non-depolarizing neuromuscular blocking drugs.
4-Aminopyridine↗
[Alcohol, the heart and cardiovascular system].
Any advice about the consumption of alcohol must take into account not only the relation between alcohol and cardiovascular disease but also the well-known association of heavy consumption of alcohol with a large number of health risks. Numerous observational studies have consistently demonstrated a reduction of coronary heart disease with moderate consumption of alcohol. Consumption of 1 or 2 drinks per day is associated with a reduction in risk of dying from coronary heart disease of approx. 30-50%. A drink equivalent amounts to a 12-ounce bottle of beer, a 4-ounce glass of wine, and a 1.5-ounce shot of 80-proof spirits. It has been repeatedly demonstrated that there is a J-shaped relation between alcohol consumption and total mortality. The lowest mortality occurs in those who consume 1 or 2 drinks per day. A stepwise decline in coronary heart disease death occurs with increasing drinks per day. Because coronary heart disease accounts for 1/3 or more of total death, people with no alcohol consumption have higher total mortality than those drinking 1 to 2 drinks per day. Conversely, mortality due to a large number of other diseases increases with an increasing number of drinks consumed per day. The protective effects of alcoholic against coronary heart disease are mainly related to an increase in HDL cholesterol. A number of other mechanisms have been proposed including effects of alcohol on blood clotting and non-alcoholic components of alcoholic beverages, particularly in red wine and dark beer, which may have antioxidant properties. Harmful effects of alcohol on the cardiovascular system include congestive cardiomyopathy, systemic hypertension and cerebral vascular incidents. There is a direct correlation between the amount of alcohol consumed during lifetime and a reduction in left ventricular ejection fraction.
Alcohol Drinking↗
Cyclo-oxygenase-1 and cyclo-oxygenase-2 and cardiovascular system.
Prostaglandins play important roles in the pathophysiological mechanism of action of platelets and endothelial cells in the cardiovascular system. The two isoforms of cyclo-oxygenase, respectively cyclo-oxygenase-1 and cyclo-oxygenase-2, are differently expressed in these cells. Activated platelets show a relatively large amount of cyclo-oxygenase-1, whereas endothelial cells have the gene for cyclo-oxygenase-2, the expression of which follows cell activation. In the atherosclerosis lesion, prostaglandin synthesis is mainly mediated by the inducible cyclo-oxygenase-2 expressed in macrophages/foam cells, smooth muscle cells and endothelial cells. Aspirin, a selective platelet cyclo-oxygenase-1 inhibitor still remains the most extensively studied antiplatelet agent, even though there is growing evidence that many other compounds could be valuable either in association, or alternatives in antithrombotic therapy.
Aspirin↗
Pro-fibrogenic effects of magnesium deficiency in the cardiovascular system.
Magnesium deficiency is known to produce cardiovascular injury. A large body of experimental evidence supports the postulation that an immuno-inflammatory reaction and increased oxidative stress may damage the myocardium and vasculature in magnesium deficiency. Reparative/reactive fibrosis in response to the injury has, however, received little attention. Recent evidence from a rodent model of acute magnesium deficiency suggests that humoral factors may activate cardiac fibroblasts by a free radical-mediated mechanism and contribute to cardiac fibrogenesis. A similar mechanism may also promote cellular hyperplasia and increased matrix synthesis in the vasculature.
Cardiomyopathies↗