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PubMed1979

Poly-plethysmographic study on the effects of ritodrine on the cardiovascular system of patients in labour.

The effects of ritodrine infusion on the cardiovascular system of six women in threatened or premature labour are reported. In contrast to other betamimetics, ritodrine caused a moderate rise in systolic blood pressure, the corresponding fall in diastolic pressure leading to a widened pulse pressure but no risk of hypotension. Ritodrine caused a rise in cardiac output, and was well tolerated by the patients. Special care should be taken in treating patients with known heart disease.

Adolescent↗
PubMed1975

Muscular reflex stimuli to the cardiovascular system during isometric contractions of muscle groups of different mass.

1. The cardiovascular responses to voluntary isometric contractions performed by human subjects are determined by the proportion of maximal tension achieved by the muscles contracting, and not by the mass of the contracting muscles, nor by the absolute tension achieved (Lind & McNicol, 1967; confirmed here). When two or more muscle groups contract simultaneously at different relative tensions, the increments in heart rate and blood pressure are the same as when the muscle group at the higher relative tension contracts alone at that tension (Lind & McNicol, 1967). It is known that there are both central and reflex stimuli to the cardiovascular system in exercise, and the present study examines whether the muscular reflex stimuli are related to the proportion of maximal tension achieved or to the mass of contracting muscle. 2. Isometric hind-limb contractions were induced in anaesthetized dogs and cats by stimulation of spinal ventral roots. Pressor responses to contraction of both hind limbs were greater than responses to contractions of either hind limb alone. No differences were observed between heart rate responses to single or combined hind-limb contractions. 3. When human subjects perform isometric contractions, a pressor response can be maintained beyond the conclusion of the exercise by occluding muscle blood flow. This response is generally attributed to a reflex set up in the muscle by the action of chemical factors on afferent nerves. When comparable pressor responses were evoked by comparable proportional efforts with either the whole hand or the little finger, it was found here that the pressor responses remaining during the period of post-exercise occlusion were greater when the greater mass of muscle had been exercised. 4. It is concluded that the muscular reflex drive in isometric exercise is related to the bulk of contracting muscle.

Adult↗
PubMed1992

The integrated response of the cardiovascular system to food.

To obtain information about the integrated response of the cardiovascular system to food, cardiac output and regional blood flow (superior mesenteric artery, renal artery and calf blood flow) were measured in 14 normal young healthy subjects after an overnight fast and following a standard 800-kcal meal. Results were compared with 8 subjects who remained fasted throughout the study. Cardiac output increased from a mean (SEM) fasting value of 4.8 (0.3) l/min to a peak after 30 min of 6.1 (0.5) l/min (p < 0.001). Superior mesenteric blood flow increased from a fasting value of 463 (45) to a peak of 854 (110) ml/min also after 30 min (p < 0.001). These changes were accompanied by a significant fall in both systemic vascular resistance and superior mesenteric vascular resistance (p < 0.001). Only at the 15-min postprandial measurements was there a significant relationship between the increase in cardiac output and superior mesenteric artery blood flow (r = 0.62, p = 0.02). Calf blood flow increased and vascular resistance fell postprandially (p < 0.05), but there was little change in right renal artery blood flow. There was an insignificant fall in renal vascular resistance. Heart rate increased from a resting value of 65 (3) to a peak of 77 (4) beats/min after 15 and 30 min (p < 0.001), diastolic blood pressure fell postprandially with little change in systolic blood pressure. These results suggest that in healthy young subjects the increase in gut blood flow is met by an increase in cardiac output, with little evidence of redirection from other vascular beds. The early postprandial increase in superior mesenteric blood flow may account for the increase in cardiac output, although the magnitude of the change is much greater for cardiac output than superior mesenteric artery blood flow.

Adult↗
PubMed1986

Pharmacological studies of imidazoline derivatives. III. Actions on cardiovascular system and acute toxicity.

The effects of 8 imidazoline derivatives on the cardiovascular system and their acute toxicity were investigated. In anesthetized rats, K-6341 and K-6343 produced relatively long-lasting elevation of blood pressure. This hypertensive response was prevented by prazosin. In contrast, K-4011, K-3827 and K-4300 exerted long-lasting hypotensive actions. Norepinephrine-induced increase in blood pressure was competitively antagonized by these three derivatives. Therefore, the hypertensive and hypotensive actions of imidazoline derivatives are conceivably exerted by activating and blocking alpha 1-adrenoceptors. In the isolated guinea-pig atrial preparations, K-4011, K-3827, K-6341 and K-6343 produced positive inotropic responses which were independent of beta-adrenoceptor activation. The positive inotropic effect of K-6341, which was the most potent, was specifically attenuated or abolished by diltiazem, suggesting that a change in Ca2+ movement across the cell membrane is contributing to K-6341-induced increase in atrial contractions. The main symptoms of mice manifested when injected with imidazoline derivatives were a decrease in spontaneous movement, exophthalmos, an increase in palpebral opening, paralysis of four limbs and respiratory depression. Acute LD50 values of imidazoline derivatives in mice (i.v., i.p.) were between these of tolazoline and naphazoline.

Animals↗
PubMed2000

Growth hormone-releasing peptides and the cardiovascular system.

Growth Hormone (GH)-releasing peptides (GHRPs) and their non peptidyl analogues are synthetic molecules which exhibit strong, dosedependent and reproducible GH-releasing activity but also significant PRL- and ACTH/cortisol-releasing effects. An influence of these compounds on food intake and sleep pattern has been also shown. The neuroendocrine activities of GHRPs are mediated by specific receptors subtypes that have been identified in the pituitary gland, hypothalamus and various extra-hypothalamic brain regions with (125)I-Tyr-Ala-hexarelin, an octapeptide of the GHRP family. In addition, GHRP receptors were also present in different peripheral tissues such as heart, adrenal, ovary, testis, lung and skeletal muscle, with a density significantly higher than that found in the hypothalamo-pituitary -system. A remarkable specific (125)I-Tyr-Ala-hexarelin binding was observed in the human cardiovascular system where the highest binding levels were detected in ventricles, followed by atria, aorta, coronaries, carotid, endocardium and vena cava. The binding of the radioligand to cardiac membranes was inhibited by unlabeled Tyr Ala hexare lin and hexarelin as well as by GHRP-6, GHRP-1 and GHRP-2 but not by MK-677, a non peptidyl GHRP analog. In other experiments on H9c2 myocytes, a fetal cardiomyocytes-derived cell line, specific GHRP binding was found and hexarelin showed an anti-apoptotic activity. On the other hand, in vivo studies in animals and in humans showed that GHRPs possess direct cardiotropic actions. In fact, hexarelin protects from ischemia-induced myocardial damage in aged and GH deficient rats while hexarelin shows a positive inotropic effect in normal subjects as well as in patients with GH deficiency. In conclusion, GHRPs possess extra--neuroendocrine biological activity and, particularly, show direct GH-independent cardiotropic effects.

Animals↗
PubMed2006

Landmarks in understanding the central nervous control of the cardiovascular system.

In this Paton Lecture I have tried to trace the key experiments that have developed ideas on how the brain regulates the cardiovascular system. It is a personal view and inevitably, owing to constraints on space and time, I have not been able to cover areas such as the nucleus tractus solitarius and cardiac vagal neurones, although I acknowledge that some may consider the story is incomplete without them. Starting with the crucial discovery of vasomotor nerves and 'vasomotor tone', the patterns of activity in sympathetic nerves which led to the important idea of central oscillating networks of neurones are described. I discuss how this knowledge has informed current controversies on the origin of vasomotor activity in presympathetic neurones in the ventral medulla, which identify intrinsic pacemaker activity or synaptic input from multiple oscillators as prime mechanisms. I present an emerging view that the role of other regions of the brain, in particular supramedullary sites, has been underplayed. These regions are pivotal for the non-uniform distribution of cardiac output that is unique to each reflex and behavioural state. I discuss the most recent evidence for 'central command' neurones that offers a plausible explanation for how these patterns of sympathetic activity are achieved. Finally, I stress the importance of these current ideas to the understanding of pathological changes in sympathetic activity in cardiovascular diseases such as hypertension or congestive heart failure.

Animals↗
PubMed2006

Beta-adrenergic receptors and nitric oxide generation in the cardiovascular system.

Nitric oxide plays a crucial role in cardiovascular homeostasis, with important vasodilatory, anti-thrombotic and anti-atherogenic properties. Beta-adrenergic receptors (betaARs), present on a wide variety of cardiovascular cells, including vascular endothelial cells, platelets, cardiac myocytes and leukocytes, have long been established as key players in maintaining cardiovascular homeostatic control. During the last few years a wealth of evidence has emerged which directly links stimulation of these cardiovascular betaARs to nitric oxide (NO) generation, suggesting a new and important mechanism of adrenergic control of cardiovascular function. This review explores the cardiovascular cell systems in which this coupling of betaARs and NO occurs, the intracellular signalling and regulatory mechanisms involved and the abnormalities in betaAR-NO oxide coupling found in cardiovascular disease states.

Aging↗
PubMedDate not supplied

[Blood catecholamine levels in rabbits with varying resistance of the cardiovascular system to emotional stress].

The content of catecholamines and some products of their metabolism in the blood of rabbits with different resistance of the cardiovascular system to acute emotional stress was determined by high performance liquid chromatography with electrochemical detection. It was shown that in rabbits with mild arterial pressure (AP) changes in noradrenaline (NA) concentration increased by 145% by the end of the 3rd hour of the experiment. In rabbits with progressively reducing AP the blood NA concentration increased (by 272%) 10 minutes after the beginning of stimulation of the ventromedial nuclei of the hypothalamus and remained increased (to 500%) to the end of the experiment. The concentration of adrenaline and 3-4 dioxyphenylacetic acid was also increased in these animals.

Animals↗
PubMed1999

Age and the cardiovascular system.

Congestive heart failure is a common cause of morbidity and mortality in the elderly population. Important changes occur in the structure and function of the cardiovascular system with advancing age. An understanding of these changes is vital for optimum management of these patients.

Age Factors↗
PubMed2006

Hydrogen sulfide as a new endogenous gaseous transmitter in the cardiovascular system.

Hydrogen sulfide (H(2)S) is a well-known toxic gas with the smell of rotten eggs. Recent studies have shown that H(2)S is generated in vivo in human and animal organisms and that it participates in many pathophysiological processes. H(2)S is produced endogenously in mammalian tissues from L-cysteine metabolism mainly by 3 enzymes: cystathionine beta-synthetase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptosulfurtransferase (MST). H(2)S may not only function as a neuromodulator in the central nervous system but it also relaxes gastrointestinal smooth muscles. More importantly, present evidence shows that H(2)S exerts regulatory effects on the pathogenesis of various cardiovascular diseases such as hypertension, pulmonary hypertension, shock and myocardial injury. The genomic basis of cystathioninuria in humans is 2 nonsense and 2 sense mutations in CSE. This review reveals that H(2)S is a new endogenous gaseous transmitter in the cardiovascular system.

Animals↗
PubMed2005

[Peculiarities of NO-syntase expression in experimental hypertension caused by inhibition during low frequency laser irradiation of cardiovascular system and kidneys].

The aim of our study was the investigation of expression of NO-syntase endothelial (eNOS) and inducted (iNOS) forms in cardiovascular system and kidneys at experimental hypertension caused by laser irradiation. For investigation of experimental model of hypertension the rats of Vister species together with the drinking water were administered by L-NAME, NO inhibitor. Rats were divided into the following groups: in group I, irradiation with laser was started immediately after L-NAME administration, in group II - on the third day, in group III - on the 12th day, but in group IV - on the 28th day, respectively. The animals have been killed on the 10th day after irradiation. The morphological and immunohistochemical studies of heart and blood vessels (coronary arteries, aorta and kidney artery) and kidneys have been performed, with determination of eNOS and iNOS expression. The obtained results show that at irradiation by laser irradiation of low-frequency immediately after administration of L-NAME, eNOS expression is kept as in heart and blood vessels as in kidneys then iNOS expression is started firstly in myocardium and kidney (II group) and then in all studied blood vessels (III group). The mentioned facts prove that the irradiation by a laser of low - frequency inhibits eNOS inhibition after L-NAME action that must represent the background of antihypertensic effect after laser irradiation. Due to the results of study, an irradiation by a laser of low - frequency might be used for prevention of hypertension in preclinical stage to avoid the further complications, but its using with the aim to relieve the clinical evidences is not recommended.

Animals↗
PubMed1987

Influence of long-term aldose reductase inhibitor therapy on autonomic dysfunction of urinary bladder, stomach and cardiovascular systems in diabetic patients.

The effects of the aldose reductase inhibitor (ARI) sorbinil (250 mg/day) were tested in an open-label pilot study over 1 year, in eight diabetics with peripheral neuropathy, seven of whom had symptomic autonomic neuropathy (AN). Autonomic function studies of the urinary bladder, stomach and cardiovascular system were performed at baseline, 6 and 12 months. Six patients reported improvement in symptoms of AN by 6 months which was maintained or further improved by 12 months. Bladder sensation, as measured by cystometrographic parameters, improved at 6 months (P less than 0.02- less than 0.04), but by 12 months had reverted to baseline. Residual urine volume decreased at 6 months (P less than 0.06) and 12 months (P less than 0.06). Vagally mediated gastric acid secretion improved at 6 months (P less than 0.06); the subgroup of patients with subnormal secretion showed improvement to the normal range at 6 months (P less than 0.03). Gastric emptying of solid food was normal in six of eight subjects and showed no significant change at 6 months. Both patients with delayed emptying normalized. No change in beat-to-beat variability in heart rate with respiration was noted. Resting minimum heart rate decreased at 12 months (P less than 0.05). Glycohemoglobin levels showed no statistically significant changes. No toxic reactions were observed. These data suggest a beneficial effect of ARI treatment on symptomatic and asymptomatic manifestations of diabetic autonomic neuropathy and indicate a need for large controlled trials.

Adult↗
PubMed1998

[Epithalamin effects on carbohydrate metabolism and cardiovascular system in patients with non-insulin dependent diabetes mellitus].

Epithelamine made in Russia (Samson, St. Petersburg) was tried for effects on carbohydrate metabolism and cardiovascular system in 33 patients with non-insulin-dependent diabetes mellitus (NIDDM). Adjuvant use of epithelamine in combined treatment of NIDDM promoted a stable compensation of carbohydrate metabolism, lowering of glycosylated hemoglobin, immunoreactive insulin. There was also a moderate hypotensive effect and improvement of left ventricular diastolic function.

Antineoplastic Agents↗
PubMed2002

[Effect of hormone replacement therapy on the cardiovascular system].

OBJECTIVE: Analysis of contemporary knowledge of influences of hormone replacement therapy on cardiovascular system. DESIGN: Literary review. SETTING: Department of Gynecology and Obstetrics, 1st Faculty of Medicine, Charles University, Prague. METHOD: Informations were collected from full-texts which were chosen in database Medline and Ovid. CONCLUSION: Hormone replacement therapy (HRT) has positive influence on some risk factors of cardiovascular disease. Changes in the lipoprotein spectrum are well known. Oral estrogens cause a decrease of low density lipoprotein cholesterol (LDL-C) and, especially an increase of high density lipoprotein cholesterol (HDL-C) levels, which both have potentially favourable effects; they also cause a triglyceride level increase, which probably has no clinical relevance except in cases with basal hypertriglyceridemia. Transdermal estradiol causes generally a minor decrease in LDL-C and minor increase HDL-C levels, with no increase or even decrease in triglyceride levels. The addition of androgenic progestins at conventionally used doses, while not interfering with LDL-C variations, causes a HDL-C decrease, which contrasts he effect of oral estrogens and completely reverses the effect of transdermal estradiol. On the contrary, the addition of a non-adrogenic progestin does not interfere with any of the estrogen induced lipid profile modifications. Transdermal estradiol does not cause change of insulinoresistance. Estrogen substitution protects gynoid distribution of body fat that is connected with lower risk of ischemic heart disease. Estrogens have possibility to dilate vessels. Decreasing of levels of cytoadhesive molecules was verify during HRT so as lowering of homocysteine level to premenopausal levels. Newly uncovered changes like the significant increase of CRP connected with oral estrogen therapy could explain increasing of cardiovascular risk on the beginning of HRT especially in group of women with history of ischemic heart disease.

Cardiovascular Diseases↗
PubMed2000

[Sulphonylurea derivatives and the cardiovascular system].

Sulphonylurea derivatives (SUD) are a mainstay of treatment of type 2 diabetes but questions have been raised about the potential adverse effects of these drugs as far as cardiovascular functions are concerned. An early prospective study which examined the effects of glycaemic control with various agents on coronary heart disease was stopped in the 70-ies due to excess cardiovascular mortality in the group receiving SUD of first generation: tolbutamide. The discovery of ATP-sensitive potassium channels in the heart, their role in ischaemic heart disease and mechanisms of endogenous cardiac cell protection--preconditioning have brought back concerns of SUD safety. Recently, a new SUD--glimepiride--claimed as the first representant of III generation of these agents--has been introduced into clinical practice. Glimepiride appears to be devoid of vascular ATP-sensitive potassium channels binding properties. Postulated and confirmed in animal experimental studies cardioprotective features of glimepiride were evaluated in a randomised, placebo-controlled study with glimepiride and glibenclamide comparing effects of these drugs on ischaemic preconditioning during angioplasty of high grade coronary artery stenoses in patients with stable angina. Myocardial ischaemia was quantified by intracoronary electrocardiography and time to occurrence of angina during vessel occlusion was measured. The results of the study confirmed glimepiride effects of maintaining myocardial preconditioning. The article summarises current knowledge of SUD influence on cardiovascular system and discusses some differences in pharmacodynamics of glimepiride which appear to provide this agent with clinical advantages over conventional SUD at least in cardiovascular aspects.

Animals↗
PubMedDate not supplied

Mechanical stress-induced apoptosis in the cardiovascular system.

All tissues in the body are subjected to physical forces originating either from tension, created by cells themselves, or from the environment. Particularly, the cardiovascular system is continuously subjected to haemodynamic forces created by blood flow and blood pressure. While biomechanical force at physiological levels is essential to develop and maintain organic structure and function, elevated mechanical stress may result in cell death leading to pathological conditions. In recent years, however, it has been widely recognized that cell death, namely apoptosis, is not just the response to an injury but a highly regulated and controlled process. Therefore, physical stimuli must be sensed by cells and transmitted through intracellular signal transduction pathways to the nucleus, resulting in cell apoptosis. Disturbances in the regulatory mechanisms of apoptosis often precede the development of a disease. Exploration of the molecular signalling mechanisms leading to mechanical stress-induced apoptosis in cardiovascular disorders revealed the crucial role of apoptosis in the pathogenesis of these diseases. For instance, heart failure, hypertension and atherosclerosis are believed to be related to sustained mechanical overloading or stress. In this review we summarize the recent data focusing on molecular mechanisms of mechanical stress-induced apoptosis and highlight the role of apoptosis in the development of cardiovascular disorders, which may lead to new therapeutic strategies for these diseases.

Animals↗