[ON THE PRACTICAL VALUE OF FUNCTIONAL TESTS IN OXYHEMOMETRY IN PATIENTS WITH DISEASES OF THE CARDIOVASCULAR SYSTEM].
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Cardiovascular Diseases↗
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Effects of low-dose hormone therapy on menopausal symptoms, bone mineral density, endometrium, and the cardiovascular system: a review of randomized clinical trials.
OBJECTIVES: First, to determine the extent of the effects of low-dose hormone therapy (HT) on menopausal symptoms, bone mineral density, endometrium, and the cardiovascular system, and, second, to determine the adverse effects of low-dose HT. METHODS: A literature review of electronic databases was conducted to identify all prospective, randomized trials comparing the effects of low-dose HT with placebo or standard-dose therapy, using key words such as: hormone replacement therapy (HRT), low-dose HRT/conjugated equine estrogens (CEE)/estradiol, lower-dose HRT/CEE/estradiol, ultra-low-dose HRT/CEE/estradiol, menopause, cardiovascular risk, bone metabolism. RESULTS: Low-dose HT has been shown to improve menopausal and vulvovaginal atrophic symptoms, compared to placebo, and is less likely to give rise to unacceptable side-effects, including irregular bleeding and/or breast tenderness. When compared to standard-dose HT, the low-dose HT has comparable effects on a range of menopausal symptoms and on bone density and has similar beneficial effects on surrogate end-points of coronary heart disease. CONCLUSIONS: A change to low-dose HT has been advocated following adverse findings in recent trials of standard-dose HT. Although a literature review has shown low-dose HT to alleviate menopausal symptoms and maintain or improve bone density with fewer side-effects than standard-dose therapy, further research is required to determine what effect the lower-dose therapy will have on fracture, cardiovascular and breast disease.
Bone Density↗
Federal old-age, survivors and disability insurance (1950- ); determining disability and blindness; extension of expiration date for cardiovascular system listing--Social Security Administration. Final rule.
We are extending the expiration date of the cardiovascular system listing found in appendix 1 of part 404, subpart P, from June 6, 1991, to June 6, 1992. We have made no revisions in the medical criteria in the cardiovascular listings; they remain the same as they now appear in the Code of Federal Regulations. We are presently considering revisions to update the medical criteria contained in part A and part B of the listing, and any revised criteria will be published as a proposed rule when we have completed our review. Insofar as Medicare eligibility is based on entitlement to disability insurance benefits under title II of the Act, this proposed regulation affects the Medicare program. To the extent that Medicaid eligibility is based on title XVI eligibility, this proposed regulation affects the Medicaid program.
Aged↗
Age Associated Alterations in Structure and Function of the Cardiovascular System.
The process of aging leads to significant changes in the structure and function of the cardiovascular system. Some of these changes result directly in pathological effects, while others serve to exacerbate the effects of cardiovascular diseases. The changes in the walls of the peripheral arteries lead to increased systolic and pulse pressures. In the myocardium, there is an age associated loss of myocytes. The remaining cells have reduced inotropic capacity. The aging heart also shows increased stiffness in both animal and human studies. Cardiac function is shown to be normal at rest in the aging population, however, during exercise, the aging heart shows a significantly smaller reserve. The increased mortality rates in setting of myocardial infarction and/or congestive heart failure in the elderly may be related to reduced muscle mass and loss of cardiac myocytes. Conversely, the aging population may receive greater benefit from the protective effects of beta-adrenergic antagonists and angiotensin converting enzyme inhibitors.
Journal Article↗
[Several features and mechanisms of lesions of the cardiovascular system in a severe course of hemorrhagic fever with renal syndrome].
Peculiarities of lesions of the cardiovascular system were studied in 332 patients with a grave course of hemorrhagic fever with the renal syndrome. Deep cardiovascular disorders manifesting themselves in low or high arterial pressure, ECG changes, hemodynamic disorders in the greater and lesser circulation, disorder of the morphological structure of the myocardium and small vessel walls were revealed.
Adult↗
Pharmacological properties of 5-[(6,7,8-trimethoxy-4-quinazolinyl) amino]-1-pentanyl nitrate maleate in cardiovascular system.
Effects of 5-[6,7,8-trimethoxy-4-quinazolinyl)amino]-1-pentanyl nitrate maleate (KT-1, CAS 47487-05-8), whose chemical structure has both a prazosin and a nitrate moiety, on cardiovascular system were investigated in in vivo and in vitro experiments. KT-1 i.v. decreased aortic pressure, renal blood flow, left ventricular enddiastolic pressure and resistances of total peripheral, vertebral, coronary and renal vasculatures and increased aortic blood flow, vertebral blood flow, coronary blood flow, peak positive left ventricular dP/dt and heart rate in anesthetized open-chest dogs. These cardiovascular effects of KT-1 were similar to those of glyceryl trinitrate (nitroglycerin, GTN). Nitrate-deleted KT-1 from its chemical structure (denitro KT-1) equimolar to KT-1 produced no marked changes in these cardiovascular parameters, but 3 or 10 times large doses of denitro KT-1 showed relatively long persisting vasodilator effects. In isolated dog coronary artery preparations contracted with KCl, the order of relaxant potency was GTN greater than KT-1 greater than denitro KT-1. In isolated dog mesenteric artery preparations, phenylephrine produced concentration-dependent contractions which were significantly inhibited by prazosin and KT-1 but not by denitro KT-1. In anesthetized open-chest dogs, phenylephrine produced pressor responses which were significantly inhibited by KT-1 but not by GTN or denitro KT-1. In isolated rat thoracic aorta strips, in contrast to GTN, KT-1 hardly developed a tachyphylaxis. Thus, KT-1 showed cardiovascular effects similar to those of both nitrates and a1-adrenoceptor blocking agents with no development of a tachyphylaxis.
Animals↗
Interaction of the novel inotropic agent, ASL-7022, with alpha and beta adrenoceptors in the cardiovascular system of the pithed rat: comparison with dobutamine and dopamine.
Three selective inotropic agents, ASL-7022, dobutamine and dopamine, were evaluated for their effects at alpha and beta adrenoceptors in the cardiovascular system of the pithed rat. ASL-7022, dobutamine and dopamine were equipotent as pressor agents in propranolol- and reserpine-pretreated pithed rats; however, the mechanisms involved in their alpha adrenoceptor-mediated pressor effects were markedly different. The pressor response of ASL-7022 was mediated entirely by postsynaptic vascular alpha-2 adrenoceptors, whereas the pressor response of dobutamine was mediated exclusively by postsynaptic vascular alpha-1 adrenoceptors. The pressor response of dopamine was mediated by both postsynaptic vascular alpha-1 and alpha-2 adrenoceptors. All three compounds elicited beta-2 adrenoceptor-mediated vasodepressor responses in pithed rats when vascular tone was elevated by a constant infusion of angiotensin II. In contrast to the equal vasopressor potencies of these compounds, the vasodepressor activities varied by more than two orders of magnitude with ASL-7022 being the most potent and dopamine the least potent. Based on ratios of relative potencies for alpha adrenoceptor-mediated vasopressor effects and beta-2 adrenoceptor-mediated vasodepressor effects, it appears that dobutamine possesses an equal balance between its vasopressor and vasodepressor potencies, such that the net effect in the vasculature is a physiological antagonism with little or no change in blood pressure, consistent with clinical observations and experiments in animals. In contrast, the vasopressor potency of dopamine exceeds its potency as a depressor agent, such that the net effect is vasoconstriction, consistent with clinical and animal studies.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
[Changes in hemodynamics during increase of functional loading of the cardiovascular system].
It has been executed 26 experiments on dogs in order to investigate the changes of haemodynamics during narrowing of ascending aorta and brain ischaemia. It has been setted during investigation, that cardiovascular system possesses high compensatory abilities. This system fully restored the disorders in blood circulation during 3 minutes of occlusion of brachiocephalic trunk or during 5 minutes of narrowing. The restoration of normal blood circulation after 5 minutes leads to normalization of indicators of haemodynamics also in 5 minutes and does not lead to decompensation of cardiac function. The heart decreases the rate of contractions in order to support the high level of its force in such a conditions.
Animals↗
Expression of G protein alpha subunits in the aging cardiovascular system.
Alterations in responsiveness to stimulation of G protein-coupled receptors in the cardiovascular system have been noted during aging and may be due to changes in the G proteins. The levels of G protein alpha subunits and their mRNAs were examined in the aorta and heart of adult (6-month-old) and senescent (24-month-old) Fischer 344 rats. Western blot analysis using anti-Gs alpha antiserum revealed 4 bands in the aorta (38, 42, 45, and 52 kD). The 42 kD band decreased significantly in 24-month-old rats, whereas the other bands did not change. Western blots using anti-Go alpha and anti-Gi alpha revealed single bands of 39 kD and 41 kD respectively, which decreased significantly in the aortas from 24-month-old rats. There were no significant changes in the levels of G alpha mRNAs in the aorta during aging. In the heart, anti-Gs alpha antiserum detected 3 bands (42, 45, and 52 kD) which did not change with age. Levels of Gi alpha (41 kD) and Go alpha (39 kD) also did not change with age in the heart. The mRNAs for Gi2 alpha and Gi3 alpha were significantly increased in the heart, but there was no change in Go alpha or Gs alpha mRNAs. Reduced expression of Gi alpha may provide the molecular basis for alterations in receptor responsiveness in the aging vasculature. Altered expression of G protein alpha subunits does not appear to account for age-related alterations in cardiac function.
Aging↗
[Effects of oxybutynin on the cardiovascular system in dogs].
The effects of oxybutynin, an anticholinergic and antispasmodic agent, on the cardiovascular system were studied in comparison with those of atropine in anesthetized dogs. Oxybutynin (0.1-10 mg/kg, i.v.) caused a transient hypotension, tachycardia, increases in femoral, stomach, mesenteric and common carotid arterial blood flows and a decrease in renal arterial blood flow. Atropine (0.1-10 mg/kg, i.v.) caused a stronger and more prolonged hypotension with bradycardia, accompanied by weaker blood flow changes than those by oxybutynin. In open-chest dogs, oxybutynin caused increases in cardiac output and coronary sinus outflow and decreases in heart rate and left ventricular pressure. The agent augmented dLVP/dt/P at doses up to 3 mg/kg, i.v., but reduced it at 10 mg/kg, i.v. Atropine caused stronger cardiosuppressive responses than those of oxybutynin. Coronary sinus outflow was decreased by atropine, unlike in the case of oxybutynin. The pressor responses of norepinephrine, epinephrine and tyramine were potentiated by pretreatment with oxybutynin (15 mg/kg, i.v.). However, pressor or depressor responses induced by histamine, isoproterenol, serotonin and DMPP were unaffected by oxybutynin. Intraarterial injections of oxybutynin, atropine and papaverine caused femoral and renal arterial vasodilations dose-dependently, in the following order of potency: papaverine greater than oxybutynin greater than atropine. In the isolated blood-perfused canine papillary muscle preparation, oxybutynin and atropine caused a negative inotropic action, whereas papaverine caused a positive inotropic action. From the above results, it is suggested that oxybutynin has milder cardiosuppressive and hypotensive effects than atropine in terms of potency and duration of action, and in addition, oxybutynin has a vasodilating action probably ascribable to its anticholinergic and antispasmodic actions.
Acetylcholine↗
Mutations affecting the cardiovascular system and other internal organs in zebrafish.
In a screen for early developmental mutants of the zebrafish, we have identified mutations specifically affecting the internal organs. We identified 53 mutations affecting the cardiovascular system. Nine of them affect specific landmarks of heart morphogenesis. Mutations in four genes cause a failure in the fusion of the bilateral heart primordia, resulting in cardia bifida. In lonely atrium, no heart venticle is visible and the atrium is directly fused to the outflow tract. In the overlooped mutant, the relative position of the two heart chambers is distorted. The heart is enormously enlarged in the santa mutant. In two mutants, scotch tape and superglue, the cardiac jelly between the two layers of the heart is significantly reduced. We also identified a number of mutations affecting the function of the heart. The mutations affecting heart function can be subdivided into two groups, one affecting heart contraction and another affecting the rhythm of the heart beat. Among the contractility group of mutants are 5 with no heart beat at all and 15 with a reduced heart beat of one or both chambers. 6 mutations are in the rhythmicity group and specifically affect the beating pattern of the heart. Mutations in two genes, bypass and kurzschluss, cause specific defects in the circulatory system. In addition to the heart mutants, we identified 23 mutations affecting the integrity of the liver, the intestine or the kidney. In this report, we demonstrate that it is feasible to screen for genes specific for the patterning or function of certain internal organs in the zebrafish. The mutations presented here could serve as an entry point to the establishment of a genetic hierarchy underlying organogenesis.
Animals↗
Psychosomatic perspectives: the cardiovascular system.
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Cardiovascular Diseases↗
Histamine H3 receptors--general characterization and their function in the cardiovascular system.
The histamine H3 receptor was initially identified as a presynaptic autoreceptor controlling histamine release and synthesis in the brain. It belongs to the superfamily of G protein-coupled receptors. The existence of the H3 receptor which has not yet been cloned was definitely established by the design of highly potent and selective agonists (R-(-)-alpha-methylhistamine, imetit) and antagonists (thioperamide, clobenpropit). These receptors also occur as heteroreceptors both in the central nervous system and on peripheral neurons of the gastrointestinal and bronchial tract, where they regulate the release of a variety of neurotransmitters. In the cardiovascular system, histamine H3 receptors are mainly located presynaptically on the postganglionic sympathetic nerve fibers innervating the blood vessels and the heart. Their activation leads to the inhibition of noradrenaline release and consequently to the reduction of the neurogenic vasopressor and cardiostimulatory responses. The presence of such receptors has been shown both in vitro (human, pig, guinea-pig, rabbit, rat isolated tissues) and in vivo (rat, guinea-pig). The vascular and cardiac presynaptic H3 receptors may be activated by endogenous histamine. The vascular H3 receptors appear to be operative in hypertension and interact with presynaptic alpha 2-adrenoceptors. Postsynaptic vasodilatatory H3 receptors have been detected in several vascular beds as well. H3 receptor ligands affect basal cardiovascular parameters in conscious and anesthetized guinea-pigs but not rats. Presynaptic H3 receptors may play a role in the pathophysiology of headache and cardiac ischemia.
Animals↗
[The characteristics of the alpha-adrenergic regulation of the cardiovascular system in middle-aged and elderly subjects].
97 practically healthy young adult, elderly and old people were examined to study the age-associated changes in alpha-adrenergic regulation of the cardiovascular system. The values of central and renal hemodynamics, systolic and diastolic cardiac functions, skin and bulbar microcirculation and arterial blood pressure were determined in dynamics after injection of the alpha-stimulator phenylephrine (0.15 mg/kg of body mass intramuscularly) or alpha-blocker prazosin (0.015 mg/kg of body mass orally). In old age alpha-adrenergic effects on the heart were found to decrease. In elderly and old people the changes of peripheric blood circulation prevail in the structure of hemodynamic shifts arising in stimulation and alpha-adrenergic receptors blockage.
Adult↗
[Morphologic and functional abnormalities of the cardiovascular system in patients with hepatic cirrhosis].
During liver cirrhosis many important changes occur in the cardiovascular system and these abnormalities appear more evident as portal hypertension and liver dysfunction progress. The cirrhotic heart develops a series of structural and functional abnormalities consisting in diastolic dysfunction and reduced myocardial reactivity during exercise, likely due to a diminished myocardial beta-adrenergic receptor function. Nevertheless, the peculiarity of the cardiovascular involvement during liver cirrhosis is represented by a progressive development of a hyperdynamic circulation that seems to be due to portal hypertension rather than to liver insufficiency. In fact, it has been hypothesized that this syndrome raise from the venous portal bed and is primarily determined by an increase in blood volume that leads to an enhanced cardiac output. Later, as liver cirrhosis progresses, new important pathogenetic elements occur and lead to a reduction in peripheral vascular resistances and to the full clinical expression of hyperdynamic circulation. The pathogenesis of hyperdynamic circulation is very interesting for scientific research because of the complex and still in part unknown origin. In addition, this syndrome has an important clinical meaning for its severely adverse prognostic value and it represents the pathogenetic background for a number of severe complications of advanced liver cirrhosis.
Blood Circulation↗
Effects of cadmium exposure on the cardiovascular system and on calcium metabolism: results of a cross-sectional population study.
This paper summarizes the findings of the Cadmibel Study, a cross-sectional population study of the health effects of cadmium, but only with respect to the cardiovascular system and calcium metabolism. The study disproved the hypothesis that exposure to cadmium would lead to an increase in blood pressure and in the prevalence of hypertension and other cardiovascular diseases. On the other hand, there was a positive relationship between urinary cadmium (Cd-U) and both serum alkaline phosphatase activity and urinary excretion of calcium. The regression coefficients obtained after adjustment for significant co-variates indicated that, when Cd-U increased two-fold, serum alkaline phosphatase and urinary calcium rose by 4% and 0.25 mmol/24 h, respectively. These findings suggest that calcium metabolism is gradually affected as cadmium accumulates in the body. The morbidity associated with the latter phenomenon is still unknown, and requires further investigation, preferably in a longitudinal prospective population study, in which the incidence of morbid events would be monitored in relation to the cadmium body burden.
Adult↗
[A comparative analysis of the effect of low-intensity physical training on a bicycle ergometer, graded walking and drug therapy on the cardiovascular system of patients with stage-II hypertension].
In contrast to standard bicycle exercise with moderate or submaximal effort, low-effort exercises were employed by the author who studied their effect on cardiovascular system of stage II hypertension patients. They were males (n-126) aged 47.2 +/- 3.6 with the disease history of 8.4 +/- 1-9 years. Associated coronary heart disease was diagnosed in 82% of the patients. The test subjects were divided randomly into three groups: group 1 patients received drugs only, group 2 received drugs and exercised walking, group 3 received drugs and exercised on bicycle ergometer in the nonstrenuous regimen. It was found that exercise tolerance of the patients was different and depended on the hemodynamic type. Hypokinetic circulation patients showed the lowest exercise tolerance. Low-effort bicycle exercise in addition to drugs is indicated for hyper- and eukinetic circulation patients. Walking is inferior to the bicycle exercise and can be recommended as a variety of nonpharmacological treatment of hypertension stage II. The combined effect of walking and chemotherapy produced the rise in cardiac capacity in the absence of the adequate increment in coronary blood flow, whereas bicycle exercise seems to enhance cardiac coronary circulation in hypertensive subjects.
Antihypertensive Agents↗
Prejunctional modulation of noradrenaline release by alpha 2-adrenoceptors: physiological and pharmacological implications in the cardiovascular system.
The modulation of noradrenaline release from sympathetic nerves by presynaptic alpha 2-adrenoceptors has now been demonstrated in a variety of tissues. The heart is a particularly useful organ in which to study the modulation of noradrenaline release both in vivo and in vitro for two reasons: (a) the postsynaptic adrenoceptors are of the beta-subtype; and (b) the ease with which the sympathetic nerve supply can be isolated and stimulated electrically. Blood vessels however have been difficult to study directly due to the fact that they possess postsynaptic alpha-adrenoceptors and to the lack of a good in vivo model of a discrete vascular bed. Using both in vivo and in vitro preparations, it was demonstrated that the sympathetic innervation of the heart and blood vessels possesses a functional negative feedback system modulating noradrenaline release mediated via alpha 2-adrenoceptors. The effect of this system depends upon the frequency of nerve stimulation and the total number of stimuli. This article covers some of the more recent contributions to the understanding of the presynaptic modulation of noradrenaline release that have been made by the study of the peripheral cardiovascular system.
Animals↗