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Functional Hyperemia (functional + hyperemia)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Hydrogen Peroxide-Dependent Arteriolar Dilation in Contracting Muscle of Rats Fed Normal and High Salt Diets

MICROCIRCULATION, Issue 8 2007
Paul J. Marvar
ABSTRACT Objective: High dietary salt intake decreases the arteriolar dilation associated with skeletal muscle contraction. Because hydrogen peroxide (H2O2) can be released from contracting muscle fibers, this study was designed to assess the possible contribution of H2O2 to skeletal muscle functional hyperemia and its sensitivity to dietary salt. Methods: The authors investigated the effect of catalase treatment on arteriolar dilation and hyperemia in contracting spinotrapezius muscle of rats fed a normal salt (0.45%, NS) or high salt (4%, HS) diet for 4 weeks. Catalase-sensitive 2,,7,-dichlorofluorescein (DCF) fluorescence was measured as an index of H2O2 formation, and the mechanism of arteriolar dilation to H2O2 was probed in each group using pharmacological inhibitors. Results: DCF fluorescence increased with muscle contraction, but not if catalase was present. Catalase also reduced arteriolar dilation and hyperemia during contraction in both dietary groups. Exogenous H2O2 dilated arterioles in both groups, with greater responses in HS rats. Guanylate cyclase inhibition did not affect arteriolar responses to H2O2 in either group, but KCa or KATP channel inhibition equally reduced these responses, and KATP channel inhibition equally reduced functional hyperemia in both groups. Conclusions: These results indicate that locally produced H2O2 contributes to arteriolar dilation and hyperemia in contracting skeletal muscle, and that the effect of H2O2 on arteriolar tone in this vascular bed is mediated largely through K+ channel activation. High dietary salt intake does not reduce the contribution of H2O2 to active hyperemia, or alter the mechanism through which H2O2 relaxes arteriolar smooth muscle. [source]

Regulation of Muscle Blood Flow in Obesity

MICROCIRCULATION, Issue 4-5 2007
Benjamin L. Hodnett
ABSTRACT Obesity has been shown to impair muscle blood flow in humans. Vasodilatory control mechanisms such as metabolic control, myogenic mechanisms, conducted vasodilation, and release of endothelium-derived factors may be impaired in obesity due to insulin resistance, hyperglycemia, dyslipidemia, inflammation, oxidative stress, and endothelial dysfunction. The physiological importance of these blood flow control mechanisms has predominately been determined during the increase in blood flow (functional hyperemia) that occurs in response to the increased metabolism associated with exercise. This review examines the mechanisms by which functional hyperemia may be impaired in obesity and indicates areas where further studies are needed. The most extensively studied area of obesity-induced changes in muscle blood flow has been the role of endothelium-derived mediators during resting blood flow and exercise-induced hyperemia. Elevations in oxidative stress alter endothelium-derived factors, resulting in impaired vasodilatory responses. Alterations in metabolic and conducted vasodilatory regulation of blood flow have not been extensively studied in obesity, providing a potential area of research. [source]

Regulation of Blood Flow in the Microcirculation

MICROCIRCULATION, Issue 1 2005
STEVEN S. SEGAL
ABSTRACT The regulation of blood flow has rich history of investigation and is exemplified in exercising skeletal muscle by a concerted interaction between striated muscle fibers and their microvascular supply. This review considers blood flow control in light of the regulation of capillary perfusion by and among terminal arterioles, the distribution of blood flow in arteriolar networks according to metabolic and hemodynamic feedback from active muscle fibers, and the balance between peak muscle blood flow and arterial blood pressure by sympathetic nerve activity. As metabolic demand increases, the locus of regulating oxygen delivery to muscle fibers "ascends" from terminal arterioles, through intermediate distributing arterioles, and into the proximal arterioles and feed arteries, which govern total flow into a muscle. At multiple levels, venules are positioned to provide feedback to nearby arterioles regarding the metabolic state of the tissue through the convection and production of vasodilator stimuli. Electrical signals initiated on smooth muscle and endothelial cells can travel rapidly for millimeters through cell-to-cell conduction via gap junction channels, rapidly coordinating vasodilator responses that govern the distribution and magnitude of blood flow to active muscle fibers. Sympathetic constriction of proximal arterioles and feed arteries can restrict functional hyperemia while dilation prevails in distal arterioles to promote oxygen extraction. With vasomotor tone reflecting myogenic contraction of smooth muscle cells modulated by flow-induced vasodilator production by endothelium, the initiation of functional vasodilation and its modulation by shear stress and sympathetic innervation dictate how and where blood flow is distributed in microvascular networks. A remarkable ensemble of signaling pathways underlie the integration of smooth muscle and endothelial cell function in microvascular networks. These pathways are being defined with new insight as novel approaches are applied to understanding the cellular and molecular mechanisms of blood flow control. [source]

3251: From elementary concept in animal models to new frontiers in humans: neurovascular coupling in the ocular circulation

ACTA OPHTHALMOLOGICA, Issue 2010
C RIVA
Purpose The retina and optic nerve, both optically accessible components of the central nervous system, are ideally suited for the investigation of the intrinsic physiological process by which blood ,ow, metabolism and neural activity are tightly coupled (Roy and Sherrington. 1890). Methods Using various techniques in the cat and human eye, the changes in blood flow in the retina and optic nerve in response to increased neural activity by flicker stimulation have been determined. The effect of varying the stimulus parameters, such as flicker modulation depth, frequency, luminance and red-green color ratio, on the blood flow response was investigated. Putative mediators of the activity-induced flow changes and the relationship between activity, blood flow and metabolic changes were assessed. Results Visual stimulation with flicker increases rapidly and markedly both retinal and optic nerve blood ,ows (functional hyperemia). Moreover, the data reveal unequivocally the presence, under specific conditions of flicker, of a neurovascular/neurometabolic coupling in these tissues, partly mediated by local potassium ions and nitric oxide production. Furthermore, the activity-induced hyperemia is altered during a number of physiological and pharmacological interventions and in some pathologic conditions. Conclusion Flicker stimulation of the retina offers a new and powerful means to modulate blood flow and investigate the neurovascular coupling in the neural eye tissues. Exploration of this activity-induced hyperemia and the mechanism(s) underlying the neurovascular coupling will lead to an increased understanding of the pathophysiology of various ocular diseases. [source]