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Cardiovascular Homeostasis (cardiovascular + homeostasi)
Selected AbstractsCardiovascular Regulation through Hypothalamic GABAA Receptors in a Genetic Absence Epilepsy Model in RatEPILEPSIA, Issue 2 2002Rezzan Gülhan Aker Summary: ,Purpose: ,-Aminobutyric acid (GABA) plays a vital role in both central cardiovascular homeostasis and pathogenesis of epilepsy. Epilepsy affects autonomic nervous system functions. In this study, we aimed to clarify the role of GABAA receptors in hypothalamic cardiovascular regulation in a genetically determined animal model of absence epilepsy. Methods: Nonepileptic Wistar rats and genetic absence epilepsy rats from Strasbourg (GAERS) were instrumented with a guide cannula for drug injection and extradural electrodes for EEG recording. After a recovery period, iliac arterial catheters were inserted for direct measurement of mean arterial pressure and heart rate. Bicuculline, a GABAA -receptor antagonist, was injected into the dorsomedial (DMH) or posterior (PH) hypothalamic nuclei of nonepileptic control rats or GAERS. Blood pressure, heart rate, and EEG recordings were performed in conscious unrestrained animals. Results: Bicuculline injections into the hypothalamus produced increases in blood pressure and heart rate of both control rats and GAERS. The DMH group of GAERS showed a twofold increase in the blood pressure and the heart rate compared with those of control rats. Pressor responses to bicuculline, when microinjected into the PH, were similar in the nonepileptic animals and GAERS. Conversely, the amplitude of tachycardic responses to the administration of bicuculline into the PH was significantly higher in GAERS compared with those of control rats. Conclusions: The bicuculline-induced increases in blood pressure and heart rate were more prominent when given in the DMH of GAERS. These results indicate an increased GABAA receptor,mediated cardiovascular response through the DMH in conscious rats with absence epilepsy. [source] Contribution of endothelium-derived hyperpolarizing factors to the regulation of vascular tone in humansFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 4 2008Jeremy Bellien Abstract Endothelium plays a crucial role in the regulation of cardiovascular homeostasis through the release of vasoactive factors. Besides nitric oxide (NO) and prostacyclin, increasing evidences show that endothelium-derived hyperpolarizing factors (EDHF) participate in the control of vasomotor tone through the activation of calcium-activated potassium channels. In humans, the role of EDHF has been demonstrated in various vascular beds including coronary, peripheral, skin and venous vessels. The mechanisms of EDHF-type relaxations identified in humans involved the release by the endothelium of hydrogen peroxide, epoxyeicosatrienoic acids (EETs), potassium ions and electronical communication through the gap junctions. The role of EETs could be particularly important because, in addition contributing to the maintenance of the basal tone and endothelium-dependent dilation of conduit arteries, these factors share many vascular protective properties of NO. The alteration of which might be involved in the physiopathology of cardiovascular diseases. The evolution of EDHF availability in human pathology is currently under investigation with some results demonstrating an increase in EDHF release to compensate the loss of NO synthesis and to maintain the endothelial vasomotor function whereas others reported a parallel decrease in NO and EDHF-mediated relaxations. Thus, the modulation of EDHF activity emerges as a new pharmacological target and some existing therapies in particular those affecting the renin,angiotensin system have already been shown to improve endothelial function through hyperpolarizing mechanisms. In this context, the development of new specific pharmacological agents especially those increasing EETs availability may help to prevent endothelial dysfunction and therefore enhance cardiovascular protection in patients. [source] Insulin resistance, a new target for nitric oxide-delivery drugsFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 6 2002Stéphane Cook Abstract In the Western hemisphere, the incidence of insulin resistance and its complications has been growing rapidly and is reaching epidemic proportions. Over the past decade, evidence has accumulated, indicating that nitric oxide (NO) plays a key role in the regulation of metabolic and cardiovascular homeostasis. Defective endothelial nitric oxide synthase (eNOS) driven NO synthesis causes insulin resistance, arterial hypertension and dyslipidemia in mice, and characterizes insulin-resistant humans. On the other hand, stimulation of inducible nitric oxide synthase (iNOS) and NO overproduction in mice, may also cause metabolic insulin resistance, suggesting a Yin,Yang effect of NO in the regulation of glucose homeostasis. Here, we will review the evidence for this novel concept, and thereby provide the conceptual framework for the use of NO-delivery drugs and pharmacological agents that modulate the bioavailability of endogenously produced NO for the treatment of insulin resistance. [source] Withdrawal of Fall-Risk-Increasing Drugs in Older Persons: Effect on Tilt-Table Test OutcomesJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 5 2007Nathalie Van Der Velde MD OBJECTIVES: To determine whether outcomes of tilt-table tests improved after withdrawal of fall-risk-increasing drugs (FRIDs). DESIGN: Prospective cohort study. SETTING: Geriatric outpatient clinic. PARTICIPANTS: Two hundred eleven new, consecutive outpatients, recruited from April 2003 until December 2004. MEASUREMENTS: Tilt-table testing was performed on all participants at baseline. Subsequently, FRIDs were withdrawn in all fallers in whom it was safely possible. At a mean follow-up of 6.7 months, tilt-table testing was repeated in 137 participants. Tilt-table testing addressed carotid sinus hypersensitivity (CSH), orthostatic hypotension (OH), and vasovagal collapse (VVC). Odds ratios (ORs) of tilt-table-test normalization according to withdrawal (discontinuation or dose reduction) of FRIDs were calculated using multivariate logistic regression analysis. RESULTS: After adjustment for confounders, the reduction of abnormal test outcomes (ORs) according to overall FRID withdrawal was 0.34 (95% confidence interval (CI)=0.06,1.86) for CSH, 0.35 (95% CI=0.13,0.99) for OH, and 0.27 (95% CI=0.02,3.31) for VVC. For the subgroup of cardiovascular FRIDs, the adjusted OR was 0.13 (95% CI=0.03,0.59) for CSH, 0.44 (95% CI=0.18,1.0) for OH, and 0.21 (95% CI=0.03,1.51) for VVC. CONCLUSION: OH improved significantly after withdrawal of FRIDs. Subgroup analysis of cardiovascular FRID withdrawal showed a significant reduction in OH and CSH. These results imply that FRID withdrawal can cause substantial improvement in cardiovascular homeostasis. Derangement of cardiovascular homeostasis may be an important mechanism by which FRID use results in falls. [source] The chronic fatigue syndrome , an updateACTA NEUROLOGICA SCANDINAVICA, Issue 2007Vegard Bruun Wyller Background ,, In this article, current scientific knowledge on the chronic fatigue syndrome (CFS) is reviewed. The US case definition of CFS (the CDC-definition) is most widespread in research and clinical practice. Estimates of prevalence vary from 0.2% to above 2%. The female,male ratio is approximately 3:1. Clinical Features ,, Severe fatigue is the dominating complaint; it is worsened from exertions and not substantially relieved by rest. In addition, the patients might have a varying combination of accompanying symptoms. Clinical evaluation should be based upon standardized guidelines, including an assessment of functional impairments. Pathophysiology ,, The pathophysiology should be interpreted within a biopsychosocial framework. Present knowledge suggests that certain genetic polymorphisms and personality traits might be regarded as predisposing factors, some infections and severe psychosocial stress constitute precipitating factors, whereas disturbances of immunity, skeletal muscle, cognitive abilities, endocrine control and cardiovascular homeostasis are possible perpetuating factors. Treatment ,, Cognitive behavioural therapy and graded exercise therapy are of proven value in randomized controlled trials. Several pharmaceutical measures have been explored and found to have no beneficial effect. Most patients might expect long-term improvement, but full recovery is rare; however, the prognosis is better among adolescents. [source] Cardiac diastolic dysfunction in renal-transplant recipients is associated with increased circulating AdrenomedullinCLINICAL TRANSPLANTATION, Issue 3 2006Bernard Geny Abstract:, Background:, Renal transplantation is an excellent therapeutic alternative for end-stage renal diseases. Nevertheless, the cardiac function is often impaired in renal-transplant patients (RTR) and importantly determines their prognosis. Adrenomedullin (ADM), a peptide involved in cardiovascular homeostasis, is believed to protect both cardiac and renal functions , by increasing local blood flows, attenuating the progression of vascular damage and remodelling and by reducing glomerular injury , and might be involved in renal-transplantation physiopathology. This work was performed to investigate whether an increase in circulating ADM might be related to RTR cardiac function. Methods:, Twenty-nine subjects, 19 RTR and 10 healthy subjects, participated in the study. After 15 min rest in supine position, heart rate and systemic blood pressure were measured together with cyclosporine through levels, creatinine and ADM. Systolic and diastolic cardiac functions were assessed, using Doppler echocardiography. Results:, Subjects were similar concerning age, weight, heart rate and blood pressure. Creatinine and ADM (53.8±6.9 vs. 27.2±4.1 pmol/L, p = 0.02) were significantly increased in RTR (73±10 months after transplantation). Cardiac systolic function was normal, but a reduced mitral E:A ratio was observed in RTR (0.90±0.06 vs. 1.38±0.10, p<0.001), reflecting their impaired left ventricular relaxation. Such a ratio was negatively correlated with ADM (r = ,0.55, p = 0.002). Conclusions:, RTR present with an increased ADM is likely related to cardiac diastolic dysfunction. In view of its protective effect on the cardiovascular system, these data support further studies to better define the role and the therapeutic potential of ADM after renal transplantation. [source] | ||||||||||