THE VENULAR NETWORK OF SKELETAL MUSCLE AND MICROCIRCULATORY HOMEOSTASIS.

Persistent Link:
http://hdl.handle.net/10150/186735
Title:
THE VENULAR NETWORK OF SKELETAL MUSCLE AND MICROCIRCULATORY HOMEOSTASIS.
Author:
HOUSE, STEVEN DONALD.
Issue Date:
1983
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
It has been deduced from indirect evidence that significant adjustments of vascular resistance take place in the venous network when blood flow changes in a organ. In the following experiments, we attempted to test the hypotheses that changes in postcapillary resistance in skeletal muscle may be due to changes in venous diameter, changes in the number of venules with blood flow, and/or changes in the apparent viscosity of blood in venules. The hypotheses were tested by observing the response of cat sartorius muscle venules (7-200 μm diameter) during arterial pressure reduction and muscle contraction. There was no observable change in venular diameter during any of the above perturbations. There was a significant decrease in the already low normalized velocity of blood in venules from a mean of 13 sec⁻¹ under control conditions to 5 sec⁻¹ during arterial pressure reduction to 20 mm Hg. At very low pressures, the number of venules with blood flow decreased. Combining our findings with Lipowsky's (1975) in vivo viscometry data, it was predicted that resistance in venules would increase 100% as a result of increases in blood viscosity when blood flow was reduced 60%. During post-contraction hyperemia the normalized velocity of blood in venules increased from 16 sec⁻¹ to 38 sec⁻¹ and the number of venules with blood flow increased a modest amount. Combining our observations with Lipowsky's data, we predict that venular resistance would fall 54% when blood flow increased 250% If shear rate changes cause substantial changes in blood viscosity in venules as suggested by the findings cited above, hydrostatic pressure in the small venules should tend to remain relatively constant as flow is altered. To determine whether this is the case, pressures of venules were measured using the servo-null technique during arterial pressure reduction. Pressures in the larger venules were a linear function of blood pressure and blood flow with an intercept not significantly different from the systemic venous pressure. Pressures in the smallest venules studied (24 μm), however, were somewhat insensitive to alterations in blood pressure (intercept of 10.4 mm Hg) and blood flow (intercept of 13.2 mm Hg). The stability of pressure in 40 venules supports the hypothesis that variable blood viscosity maintains the pressure drop in the venous network and the capillary hydrostatic pressure somewhat constant during changes in blood flow.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Musculoskeletal system -- Blood-vessels.; Blood -- Circulation.; Microcirculation.; Veins.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Physiology; Graduate College
Degree Grantor:
University of Arizona
Advisor:
Johnson, Paul C.

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleTHE VENULAR NETWORK OF SKELETAL MUSCLE AND MICROCIRCULATORY HOMEOSTASIS.en_US
dc.creatorHOUSE, STEVEN DONALD.en_US
dc.contributor.authorHOUSE, STEVEN DONALD.en_US
dc.date.issued1983en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractIt has been deduced from indirect evidence that significant adjustments of vascular resistance take place in the venous network when blood flow changes in a organ. In the following experiments, we attempted to test the hypotheses that changes in postcapillary resistance in skeletal muscle may be due to changes in venous diameter, changes in the number of venules with blood flow, and/or changes in the apparent viscosity of blood in venules. The hypotheses were tested by observing the response of cat sartorius muscle venules (7-200 μm diameter) during arterial pressure reduction and muscle contraction. There was no observable change in venular diameter during any of the above perturbations. There was a significant decrease in the already low normalized velocity of blood in venules from a mean of 13 sec⁻¹ under control conditions to 5 sec⁻¹ during arterial pressure reduction to 20 mm Hg. At very low pressures, the number of venules with blood flow decreased. Combining our findings with Lipowsky's (1975) in vivo viscometry data, it was predicted that resistance in venules would increase 100% as a result of increases in blood viscosity when blood flow was reduced 60%. During post-contraction hyperemia the normalized velocity of blood in venules increased from 16 sec⁻¹ to 38 sec⁻¹ and the number of venules with blood flow increased a modest amount. Combining our observations with Lipowsky's data, we predict that venular resistance would fall 54% when blood flow increased 250% If shear rate changes cause substantial changes in blood viscosity in venules as suggested by the findings cited above, hydrostatic pressure in the small venules should tend to remain relatively constant as flow is altered. To determine whether this is the case, pressures of venules were measured using the servo-null technique during arterial pressure reduction. Pressures in the larger venules were a linear function of blood pressure and blood flow with an intercept not significantly different from the systemic venous pressure. Pressures in the smallest venules studied (24 μm), however, were somewhat insensitive to alterations in blood pressure (intercept of 10.4 mm Hg) and blood flow (intercept of 13.2 mm Hg). The stability of pressure in 40 venules supports the hypothesis that variable blood viscosity maintains the pressure drop in the venous network and the capillary hydrostatic pressure somewhat constant during changes in blood flow.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectMusculoskeletal system -- Blood-vessels.en_US
dc.subjectBlood -- Circulation.en_US
dc.subjectMicrocirculation.en_US
dc.subjectVeins.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplinePhysiologyen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorJohnson, Paul C.en_US
dc.identifier.proquest8322643en_US
dc.identifier.oclc690020656en_US
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