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Article: Local control of venous function

TitleLocal control of venous function
Authors
Issue Date1978
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ymvre
Citation
Microvascular Research, 1978, v. 16 n. 2, p. 196-214 How to Cite?
AbstractThe main physiological role of the veins is to adjust the capacity of the vascular system, ensuring an appropriate return of blood to the heart. The veins are also a determinant of capillary pressure. The veins can behave as a passive reservoir, due to the connective structure of their wall and the presence of valves in the limbs. The amount of blood which is passively mobilized from this reservoir towards the heart is determined by the venous distending pressure, which is dependent on the hydrostatic pressure load and the degree of arteriolar constriction. The veins contain adrenergically innervated smooth muscle. The splanchnic capacitance vessels can act as an active blood mobilization system, under sympathetic control; the cutaneous veins are linked more specifically to the thermoregulatory centers. Given a constant sympathetic drive, local factors can modulate venous reactivity. Among these, the local effects of temperature variations are of particular importance for the cutaneous veins, where they reinforce the central thermoregulatory control and greatly facilitate heat preservation or dissipation. Metabolic regulation factors, such as anoxia and acidosis have little effect on venous function, in marked contrast to their importance at the precapillary level: this may explain the vascular behavior in situations such as cardiovascular shock. Many neurohumoral substances (e.g. acetylcholine, histamine, and adenine nucleotides) alter the function of both adrenergic nerves and smooth musle cell in the venous wall; for certain of them (e.g., angiotensin II) modulation of adrenegic neurotransmission probably represents the physiological mechanism by which they control venous function. Different commonly used therapeutic agents also interfere with the adrenergic neuroeffector interaction in the venous wall; this can be beneficial to the patient (e.g., nitrites and cardiac glycosides) or cause unwanted cardiovascular dysfunction (e.g., halothane).
Persistent Identifierhttp://hdl.handle.net/10722/170567
ISSN
2015 Impact Factor: 2.3
2015 SCImago Journal Rankings: 1.030
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorJanssens, WJen_US
dc.date.accessioned2012-10-30T06:09:59Z-
dc.date.available2012-10-30T06:09:59Z-
dc.date.issued1978en_US
dc.identifier.citationMicrovascular Research, 1978, v. 16 n. 2, p. 196-214en_US
dc.identifier.issn0026-2862en_US
dc.identifier.urihttp://hdl.handle.net/10722/170567-
dc.description.abstractThe main physiological role of the veins is to adjust the capacity of the vascular system, ensuring an appropriate return of blood to the heart. The veins are also a determinant of capillary pressure. The veins can behave as a passive reservoir, due to the connective structure of their wall and the presence of valves in the limbs. The amount of blood which is passively mobilized from this reservoir towards the heart is determined by the venous distending pressure, which is dependent on the hydrostatic pressure load and the degree of arteriolar constriction. The veins contain adrenergically innervated smooth muscle. The splanchnic capacitance vessels can act as an active blood mobilization system, under sympathetic control; the cutaneous veins are linked more specifically to the thermoregulatory centers. Given a constant sympathetic drive, local factors can modulate venous reactivity. Among these, the local effects of temperature variations are of particular importance for the cutaneous veins, where they reinforce the central thermoregulatory control and greatly facilitate heat preservation or dissipation. Metabolic regulation factors, such as anoxia and acidosis have little effect on venous function, in marked contrast to their importance at the precapillary level: this may explain the vascular behavior in situations such as cardiovascular shock. Many neurohumoral substances (e.g. acetylcholine, histamine, and adenine nucleotides) alter the function of both adrenergic nerves and smooth musle cell in the venous wall; for certain of them (e.g., angiotensin II) modulation of adrenegic neurotransmission probably represents the physiological mechanism by which they control venous function. Different commonly used therapeutic agents also interfere with the adrenergic neuroeffector interaction in the venous wall; this can be beneficial to the patient (e.g., nitrites and cardiac glycosides) or cause unwanted cardiovascular dysfunction (e.g., halothane).en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ymvreen_US
dc.relation.ispartofMicrovascular Researchen_US
dc.subject.meshAcidosis - Physiopathologyen_US
dc.subject.meshAnoxiaen_US
dc.subject.meshAutonomic Agents - Pharmacologyen_US
dc.subject.meshCationsen_US
dc.subject.meshChlorides - Pharmacologyen_US
dc.subject.meshExtracellular Spaceen_US
dc.subject.meshGlucose - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshMuscle, Smooth - Physiologyen_US
dc.subject.meshOsmolar Concentrationen_US
dc.subject.meshTemperatureen_US
dc.subject.meshVasomotor System - Physiologyen_US
dc.subject.meshVeins - Drug Effects - Innervation - Physiologyen_US
dc.subject.meshVenous Pressureen_US
dc.titleLocal control of venous functionen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/0026-2862(78)90055-9-
dc.identifier.pmid368521-
dc.identifier.scopuseid_2-s2.0-0018251796en_US
dc.identifier.volume16en_US
dc.identifier.issue2en_US
dc.identifier.spage196en_US
dc.identifier.epage214en_US
dc.identifier.isiWOS:A1978FY68800003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridJanssens, WJ=7006876881en_US

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