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Arterial Vasoconstriction (arterial + vasoconstriction)

Distribution by Scientific Domains
Medical Sciences75%

Selected Abstracts

No effect of venoconstrictive thigh cuffs on orthostatic hypotension induced by head-down bed rest

ACTA PHYSIOLOGICA, Issue 2 2000
M.-A. Custaud
Orthostatic intolerance (OI) is the most serious symptom of cardiovascular deconditioning induced by head-down bed rest or weightlessness. Wearing venoconstrictive thigh cuffs is an empirical countermeasure used by Russian cosmonauts to limit the shift of fluid from the lower part of the body to the cardio-cephalic region. Our aim was to determine whether or not thigh cuffs help to prevent orthostatic hypotension induced by head-down bed rest. We studied the effect of thigh cuffs on eight healthy men. The cuffs were worn during the day for 7 days of head-down bed rest. We measured: orthostatic tolerance (stand tests and lower body negative pressure tests), plasma volume (Evans blue dilution), autonomic influences (plasma noradrenaline) and baroreflex sensitivity (spontaneous baroreflex slope). Thigh cuffs limited the loss of plasma volume (thigh cuffs: ,201 ± 37 mL vs. control: ,345 ± 42 mL, P < 0.05), the degree of tachycardia and reduction in the spontaneous baroreflex sensitivity induced by head-down bed rest. However, the impact of thigh cuffs was not sufficient to prevent OI (thigh cuffs: 7.0 min of standing time vs. control: 7.1 min). Decrease in absolute plasma volume and in baroreflex sensitivity are known to be important factors in the aetiology of OI induced by head-down bed rest. However, dealing with these factors, using thigh cuffs for example, is not sufficient to prevent OI. Other factors such as venous compliance, microcirculatory changes, peripheral arterial vasoconstriction and vestibular afferents must also be considered. [source]

Pressor and vascular effects of cardiac glycosides

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue S2 2001
W. Kirch
Background: For the past two decades, it has generally been accepted ('Blaustein hypothesis') that cardiac glycosides such as ouabain and digoxin increase the sodium and calcium content of smooth muscle cells, so inducing arterial vasoconstriction and a rise in blood pressure. Recent data from an experimental study we carried out led us to question this assumption. Design: A retrospective literature survey covering 20 years and including animal and human studies was performed. Representative results are presented. Results: Contradictory effects of cardiac glycosides on blood pressure and vasculature have been described. Increased, decreased or unaltered blood-pressure values have been observed following administration of the glycosides ouabain, digoxin and digitoxin. Moreover, vasoconstricting as well as vasodilating effects of cardiac glycosides have been demonstrated. Several recent studies show that cardiac glycosides such as digoxin and digitoxin can lead to a reduction of at least diastolic blood pressure. Conclusion: A slight vasodilation of resistance vessels followed by a fall in diastolic blood pressure could be a contributing factor for the beneficial effects of cardiac glycosides in patients with congestive heart failure. This vasodilation may be caused by central (neurohumoral) effects of digitalis glycosides. [source]

Left Ventricle Afterload Impedance Control by an Axial Flow Ventricular Assist Device: A Potential Tool for Ventricular Recovery

ARTIFICIAL ORGANS, Issue 9 2010
Francesco Moscato
Abstract Ventricular assist devices (VADs) are increasingly used for supporting blood circulation in heart failure patients. To protect or even to restore the myocardial function, a defined loading of the ventricle for training would be important. Therefore, a VAD control strategy was developed that provides an explicitly definable loading condition for the failing ventricle. A mathematical model of the cardiovascular system with an axial flow VAD was used to test the control strategy in the presence of a failing left ventricle, slight physical activity, and a recovering scenario. Furthermore, the proposed control strategy was compared to a conventional constant speed mode during hemodynamic changes (reduced venous return and arterial vasoconstriction). The physiological benefit of the control strategy was manifested by a large increase in the ventricular Frank,Starling reserve and by restoration of normal hemodynamics (5.1 L/min cardiac output at a left atrial pressure of 10 mm Hg vs. 4.2 L/min at 21 mm Hg in the unassisted case). The control strategy automatically reduced the pump speed in response to reduced venous return and kept the pump flow independent of the vasoconstriction condition. Most importantly, the ventricular load was kept stable within 1%, compared to a change of 75% for the constant speed. As a key feature, the proposed control strategy provides a defined and adjustable load to the failing ventricle by an automatic regulation of the VAD speed and allows a controlled training of the myocardium. This, in turn, may represent a potential additional tool to increase the number of patients showing recovery. [source]

What is the significance of vascular hydrogen sulphide (H2S)?

BRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2006
S E O'Sullivan
The important role of nitric oxide (NO) in the regulation of vascular tone has been well studied. By contrast, the vascular significance of another gaseous mediator, hydrogen sulphide (H2S), is still poorly understood. A study published in this issue of the British Journal of Pharmacology now provides evidence that in addition to the vasorelaxant effects of H2S reported in vitro, low concentrations of H2S also cause arterial vasoconstriction, reverse NO-mediated vasorelaxation and cause an NO-dependent pressor effect in vivo. This commentary discusses the implications and questions raised by these results. British Journal of Pharmacology (2006) 149, 609,610. doi:10.1038/sj.bjp.0706907 [source]