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At least 793 records · Page 44Linked to original sources
PubMed1983

[Effects of guanabenz on the cardiovascular system, in comparison with clonidine and guanethidine].

Cardiovascular actions of guanabenz, a new antihypertensive agent, were studied in comparison with those of clonidine and guanethidine. Guanabenz, administered intravenously, produced a rise of blood pressure which was followed by a prolonged fall in anesthetized dogs. Guanabenz also decreased the heart rate, inhibited the respiration, and produced an alteration in T wave and a prolongation of PQ or TP interval in the ECG of the dog. Such effects of guanabenz on blood pressure and heart rate were observed in the cat, rabbit and rat, but there was a slight species-difference in the effects. Clonidine, but not guanethidine, produced responses similar to those of guanabenz. The potency of guanabenz to produce hypotension and bradycardia was approximately 1/10 that of clonidine and 10 times higher than that of guanethidine. The depressor effect of guanabenz was not observed in the spinal cats; thus, the blood pressure rose after the administration. When guanabenz was administered intracerebroventricularly or into the nucleus tractus solitarius of rats, the initial pressor response was not produced, and the depressor and bradycardiac responses were observed. Guanabenz, administered intravenously or intra-arterially, produced an inhibition of cardiac functions, decreased the blood flow of common carotid and femoral arteries, and elevated the perfusion-pressure of the hindlimb in the dog. In the isolated rabbit and guinea-pig atria, guanabenz produced negative inotropic and chronotropic effects and attenuated the rate of rise of the action potential. The contractile responses to serotonin and histamine in the isolated rabbit thoracic aorta were noncompetitively inhibited by guanabenz. From these results, it is suggested that the hypotensive and bradycardiac actions of guanabenz are mediated via central actions, as well as those of clonidine. Furthermore, in addition to the central actions, it was found that guanabenz acts directly on cardiovascular tissues and attenuates the responsiveness.

Animals↗
PubMed2000

[Nitric oxide in the cardiovascular system: its role in adaptive protection].

Nitric oxide (NO) is involved virtually in all processes occurring in the body. In the cardiovascular system, it regulates cardiac contractility, blood coagulability, cell proliferation, vascular tone, and blood pressure (BP). NO deficiency leads to the development of severe cardiovascular diseases associated with endothelial dysfunction, abnormally increased vascular tone and BP (such as hypertension, angina pectoris, atherosclerosis, diabetic angiopathy, etc.) At the same time, NO hyperproduction makes a contribution to the development of septic, cardiogenic, thermal, and other shocks. The most effective non-drug stimulation of NO synthesis is a gradual adaptation to environmental factors. The adaptation-induced elevation of NO levels, followed by vascular wall NO deposition, on the one hand, limits the damaging action of excess NO in shocks by the feedback, and, on the other, makes up some NO reserve which may be used in NO deficiency. Further studies of NO-dependent adaptive mechanisms will allow the agent to be used in the prevention and treatment of cardiovascular diseases associated with NO metabolic disturbances.

Adaptation, Physiological↗
PubMed1986

Capsaicin induces a depletion of calcitonin gene-related peptide (CGRP)-immunoreactive nerves in the cardiovascular system of the guinea pig and rat.

We have demonstrated that calcitonin gene-related peptide (CGRP) immunoreactivity is widely distributed in cardiac and perivascular nerves of the guinea pig and rat. In the guinea pig the number and distribution of CGRP-immunoreactive nerve fibres closely paralleled that of fibres containing substance P, the two immunoreactivities being found invariably to coexist in the same perivascular networks and terminals. In the rat, CGRP-immunoreactive cardiovascular nerves had a similar distribution to those containing substance P, but in contrast to the guinea pig the former were far more numerous. Marked regional variations were observed in the density of the CGRP-immunoreactive innervation in both species. The CGRP-immunoreactive content of tissue extracts was in close agreement with the immunocytochemical findings, the highest levels of CGRP occurring in the mesenteric artery (guinea pig and rat) and inferior vena cava (guinea pig). Following capsaicin treatment of adult guinea pigs and neonatal rats, there was a significant loss of CGRP-immunoreactive nerves in the two species. In the guinea pig, substance P-and CGRP-immunostained fibres were depleted to a similar extent, throughout the cardiovascular system. However, the loss of rat CGRP-immunoreactive nerves was dose-dependent and displayed considerable variation, some perivascular nerve networks appearing less susceptible than others to the action of capsaicin. The results suggest that there may be species differences in the sensitivity of CGRP-containing nerves to capsaicin treatment, but at least the majority of CGRP-immunoreactive cardiovascular nerves may be presumed to be sensory in origin.

Animals↗
PubMedDate not supplied

Three-dimensional optical coherence tomography of the embryonic murine cardiovascular system.

Optical coherence tomography (OCT) is an emerging high-resolution real-time biomedical imaging technology that has potential as a novel investigational tool in developmental biology and functional genomics. In this study, murine embryos and embryonic hearts are visualized with an OCT system capable of 2-microm axial and 15-microm lateral resolution and with real-time acquisition rates. We present, to our knowledge, the first sets of high-resolution 2- and 3-D OCT images that reveal the internal structures of the mammalian (murine) embryo (E10.5) and embryonic (E14.5 and E17.5) cardiovascular system. Strong correlations are observed between OCT images and corresponding hematoxylin- and eosin-stained histological sections. Real-time in vivo embryonic (E10.5) heart activity is captured by spectral-domain optical coherence tomography, processed, and displayed at a continuous rate of five frames per second. With the ability to obtain not only high-resolution anatomical data but also functional information during cardiovascular development, the OCT technology has the potential to visualize and quantify changes in murine development and in congenital and induced heart disease, as well as enable a wide range of basic in vitro and in vivo research studies in functional genomics.

Animals↗
PubMed1996

Estrogen receptors in the cardiovascular system.

Various direct effects of estradiol on arterial tissue suggest the presence of estrogen receptors (ER) in the vascular wall. The study of ER detection has made an important progress over the last 10 years with the advent and widespread use of monoclonal antibodies against the receptor protein. Using immunocytochemical methods and monoclonal antibodies, we have detected estrogen receptors in the tunica media of arteries from the reproductive tract; their concentration depends on the hormonal status. These receptors are apparently absent from saphenous veins (taken from patients undergoing surgical removal of varicose veins). We also document here results on the cardiovascular system we discuss their implications in blood vessel relaxation and cell proliferation.

Adult↗
PubMed1991

[The effect of the acetanilide herbicide Acetochlor on the cardiovascular system of white rats].

A study is performed on the long-term effect of the chloracetanilide herbicide "Acetochlor" in doses 21.0; 10.6: 5.5 and 2.6 mg/kg-1 in conditions of 6-month oral application and 2-month rehabilitation period on the metabolite processes and the balance of the connective-tissue components in the myocardium and aorta of male white rats. A complex of biochemical and histological methods are performed (activity of succinate dehidrogenase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase, adenosin triphosphatase, cytochrome oxidase, fructoso-1,6-diphosphatase, level of the thiol groups, soluble globular, elastine, collagen fractions, insoluble collagen and elastine, general and sulphated glucosamino glycanes). The dose 21.0 mg/kg-1 leads to blocking of the thyol groups, inactivation of succinate dehydrogenase, cytochrome oxidase, adenosin triphosphatase, fructose-1,6-diphosphatase, glucose-6-phosphate dehydrogenase, activation of lactate dehydrogenase, decrease of the soluble globular, elastine, and collagen fractions and increase of the glucoseaminoglycanes in the heart muscle and aorta. The changes established in the heart muscle at 10,6 mg/kg-1 certify for stronger sensitivity of the organ of the aorta wall. The presence of single changes in the examined indices, their complete dying out after the rehabilitation period and absence of structural changes in the myocardium and aorta permit the dose of 5.5 mg/kg-1 to be accepted as not effective in the conditions of chronic experiment concerning the cardiovascular system.

Administration, Oral↗
PubMed1978

[Ergospirometry study of the functional state of the cardiovascular system in chronic ischemic heart disease].

Sixty three patients were examined. The diagnosis of all was made on the base of clinical picture, electrocardiographic examinations and the results from the selective coronarography. The following indices of the oxygen consumption and gas metabolism were analysed in the paper: oxygen consumption per kilogram body weight, oxygen consumption per kilogramometer work performed, labour effectivity and restoration coefficient. The results obtained reveal that the adaptation ability of the respiratory and cardiovascular system in conditions of physical loading was disturbed in patients with chronic ischemic heart disease. At the same time, the physical capacity for work and the restoration coefficient were also disturbed. The decrease of oxygen consumption per kilogram body weight, deteriorated labour effectivity, restoration coefficient and the increased oxygen consumption per kilogramometer work performed occur in parallel with the extension of the lesions of the coronary arteries and the diminution of coronary reserve. The results from those examinations, together with the results from a series of non-invasive methods for the examination of cardio-vascular system could aid the thorough diagnostic-prognostic character of ischemic heart disease and give a tentative idea for the stage of the coronary arteries lesions prior to coronarography.

Adult↗
PubMed1990

Magnetic resonance imaging of the cardiovascular system: application in function and tissue characterization.

Magnetic resonance imaging (MRI) is a new noninvasive technique for visualization of the cardiovascular system, and is used to evaluate tissue characteristics, cardiac function and blood flow abnormalities, as well as to obtain morphological information. In this paper we presented results of clinical and laboratory research obtained using conventional spin echo MRI with regard to cardiovascular anatomy, tissue characterization and physiology. Furthermore, experience with two new techniques, cine-MRI and volume-selected MR spectroscopy, and their potential clinical usefulness in detecting cardiovascular diseases are documented.

Cardiovascular Diseases↗
PubMed1993

Effects of NG-nitro-L-arginine methyl ester on the cardiovascular system of the anaesthetized rabbit and on the cardiovascular response to thyrotropin-releasing hormone.

1. The effects of 300 mg kg-1 of the nitric oxide (NO) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on the regional blood flow, on the flow response to 1 mg kg-1 of thyrotropin-releasing hormone (TRH) and on cerebral blood flow autoregulation were studied in urethane anesthetized rabbits subjected to unilateral sectioning of the cervical sympathetic claim. The blood flow measurements were performed by the tracer microspheres method. 2. The cerebral arteriovenous difference in oxygen saturation (CAVOD) was measured before and after the administration of L-NAME and TRH in order to ascertain whether the effects on cerebral blood flow that were observed were secondary to changes in cerebral metabolism. 3. L-NAME caused a significant decrease in blood flow in several cerebral regions; CBFtot decreased to 72 +/- 4% of control (P < 0.001). An increase in blood pressure and a concurrent decrease in heart rate and cardiac output were noted. 4. In the eye, L-NAME caused a reduction in uveal blood flow which was more pronounced on the sympathetically intact side; in the retina the blood flow decreased to 50% of control on both sides. 5. The administration of TRH in animals pretreated with L-NAME caused a significant increase in blood pressure and cerebral blood flow. 6. In L-NAME-treated animals the CBF was not affected when the mean arterial blood pressure was increased by ligation of the abdominal aorta. 7. The CAVOD increased from 56.0 +/- 5.2 to 73.6 +/- 3.5%, 20 min after the administration of L-NAME. In animals given 1 mg kg-1 TRH after L-NAME the CAVOD decreased to 54.6 +/- 4.6%, 5 min after the injection of TRH.8. The results of the present study indicate that endogenous NO is involved in the regulation of regional blood flow and blood pressure in the anaesthetized rabbit. The reduction in cerebral blood flow that was caused by L-NAME was not due to a reduction in cerebral metabolism. An interaction between the NO synthesis/release/effect and the sympathetic nervous system was found in the uvea. There was no evidence for a major involvement of NO in the cardiovascular responses to TRH and autoregulation of cerebral blood flow was not abolished by L-NAME.

Anesthesia↗
PubMed1997

The roles of adenosine in regulating the respiratory and cardiovascular systems in chronically hypoxic, adult rats.

1. We have investigated the roles of adenosine in regulating the respiratory and cardiovascular systems of rats that were made chronically hypoxic for 3-4 weeks from 6 weeks of age (CH rats) in an hypoxic chamber at 12% O2. They were studied under anaesthesia while breathing 12% O2 and during acute hypoxia (breathing 8% O2 for 5 min) before and after addition of the adenosine receptor antagonist 8-phenyltheophylline (8-PT, 10 mg kg-1). The results were compared with those obtained from normoxic (N) rats in a previous study. 2. CH rats breathing 12% O2 had greater minute ventilation (VP) than N rats breathing air, but their levels of arterial blood pressure (ABP), heart rate (HR), femoral vascular conductance (FVC) and cerebral vascular conductance (CVC) were fully comparable. 8-PT increased tidal volume (VT) in CH rats indicating a greater tonic central inhibitory influence of adenosine on VT than in N rats. However, 8-PT had no effect on cardiovascular variables, indicating no tonic cardioinhibitory or vasodilator influence of adenosine in CH rats. 3. Acute hypoxia in CH rats increased VE such that at the 5th minute of 8% O2 absolute VE was comparable to that of N rats breathing 8% O2. Moreover, in CH rats 8-PT increased VT at the 5th minute of 8% O2 indicating that the central inhibitory influence of adenosine limits the ability to maintain VT in acute hypoxia as it does in N rats. 4. Eight per cent O2 also produced a full in ABP in CH rats that was comparable to that induced in N rats by the larger change from air to 8% O2. However, the changes in HR were similar in CH and N rats while the increases in FVC and CVC were smaller in CH rats. This suggests that the ability of the secondary effects of hyperventilation and of the baroreceptor reflex to maintain cardiac output and thereby ABP is reduced in CH rats. 5. Whereas 8-PT substantially reduced the hypoxia-induced increases in FVC and CVC in N rats, it had a small effect in CH rats (P = 0.054 and 0.06, respectively). Further, acute hypoxia in CH rats had no effect on the K+ concentration in the venous efflux of hindlimb K+ (KV+) before or after 8-PT treatment. We suggest that in CH rats, the dilator influence of adenosine in acute hypoxia occurs via actions on the blood vessel walls: there was no evidence that adenosine can release dilator concentrations of K+ from skeletal muscle fibres in CH rats as proposed for N rats.

Adenosine↗
PubMed1987

Chemical sympathectomy reveals pre- and postsynaptic effects of neuropeptide Y (NPY) in the cardiovascular system.

Intravenous injection of neuropeptide Y (NPY) caused short-lasting dose-dependent pressor responses in anesthetized rats. NPY was equipotent with noradrenaline in producing proportional pressor effects. Chemical sympathectomy, following the administration of 100 mg/kg 6-hydroxydopamine (6-OHDA), significantly potentiated the systemic pressor effects elicited by NPY or noradrenaline. Pretreatment with 2 nmol NPY enhanced the noradrenaline-induced pressor response in control rats. NPY did not change the basal tension of isolated rat aortic strips but significantly potentiated the contractile activity induced by 16 nM noradrenaline. This effect of NPY was not observed in aortic strips from rats pretreated with 6-OHDA. The presence of pre- and postsynaptic sites of action for NPY in the cardiovascular system of the rat is discussed.

Animals↗
PubMed2005

Growth factor signal transduction defects in the cardiovascular system.

Growth factors are important molecules mediating both the development as well as adaptive and pathological changes within the cardiovascular system. Growth factors therefore mediate both beneficial and nonbeneficial effects. The beneficial actions include the improvement of endothelial function, stimulation of vascular repair, the formation of new capillaries (angiogenesis), and the growth of collateral arteries (arteriogenesis). These actions represent the conceptual basis for the therapeutic use of growth factors, based on the idea to therapeutically induce or accelerate a given beneficial process. The beneficial effects of growth factors have to be separated from effects where growth factors act as mediators of pathological processes such as atherogenesis and plaque destabilization. This review article focuses on the physiological and beneficial effects of growth factors in the vessel wall and describes and explains the dysfunction of these effects under certain conditions now referred to as "growth factor signal transduction defects".

Cardiovascular Diseases↗