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- Publisher Website: 10.1016/0026-2862(78)90055-9
- Scopus: eid_2-s2.0-0018251796
- PMID: 368521
- WOS: WOS:A1978FY68800003
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Article: Local control of venous function
Title | Local control of venous function |
---|---|
Authors | |
Issue Date | 1978 |
Publisher | Academic 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? |
Abstract | The 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 Identifier | http://hdl.handle.net/10722/170567 |
ISSN | 2023 Impact Factor: 2.9 2023 SCImago Journal Rankings: 0.731 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Vanhoutte, PM | en_US |
dc.contributor.author | Janssens, WJ | en_US |
dc.date.accessioned | 2012-10-30T06:09:59Z | - |
dc.date.available | 2012-10-30T06:09:59Z | - |
dc.date.issued | 1978 | en_US |
dc.identifier.citation | Microvascular Research, 1978, v. 16 n. 2, p. 196-214 | en_US |
dc.identifier.issn | 0026-2862 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/170567 | - |
dc.description.abstract | The 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.language | eng | en_US |
dc.publisher | Academic Press. The Journal's web site is located at http://www.elsevier.com/locate/ymvre | en_US |
dc.relation.ispartof | Microvascular Research | en_US |
dc.subject.mesh | Acidosis - Physiopathology | en_US |
dc.subject.mesh | Anoxia | en_US |
dc.subject.mesh | Autonomic Agents - Pharmacology | en_US |
dc.subject.mesh | Cations | en_US |
dc.subject.mesh | Chlorides - Pharmacology | en_US |
dc.subject.mesh | Extracellular Space | en_US |
dc.subject.mesh | Glucose - Metabolism | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Muscle, Smooth - Physiology | en_US |
dc.subject.mesh | Osmolar Concentration | en_US |
dc.subject.mesh | Temperature | en_US |
dc.subject.mesh | Vasomotor System - Physiology | en_US |
dc.subject.mesh | Veins - Drug Effects - Innervation - Physiology | en_US |
dc.subject.mesh | Venous Pressure | en_US |
dc.title | Local control of venous function | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1016/0026-2862(78)90055-9 | - |
dc.identifier.pmid | 368521 | - |
dc.identifier.scopus | eid_2-s2.0-0018251796 | en_US |
dc.identifier.volume | 16 | en_US |
dc.identifier.issue | 2 | en_US |
dc.identifier.spage | 196 | en_US |
dc.identifier.epage | 214 | en_US |
dc.identifier.isi | WOS:A1978FY68800003 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.scopusauthorid | Janssens, WJ=7006876881 | en_US |
dc.identifier.issnl | 0026-2862 | - |