Document Detail

Resistance responses in proximal arterial vessels, arterioles and veins during reactive hyperaemia in skeletal muscle and their underlying regulatory mechanisms.
MedLine Citation:
PMID:  2248033     Owner:  NLM     Status:  MEDLINE    
The reactive hyperaemia response cat skeletal muscle to 2-120 s arterial occlusions was analysed with regard to amplitude, duration, 'excess blood flow' and site of dilator action along the vascular bed. The last-mentioned was assessed with a new whole-organ technique permitting continuous segmental resistance recordings in arterial vessels greater than 25 microns, arterioles less than 25 microns and veins. Peak amplitude, duration and excess flow all increased with increasing occlusion length, of which excess flow was linearly related to occlusion length. The site of active dilatation was preferentially confined to arterioles less than 25 microns in which complete relaxation was observed after only 20 s occlusion, although the duration of the response continued to increase with more prolonged occlusions. A graded, but less pronounced, dilatation occurred in the arterial vessels greater than 25 microns and in the veins, the former exhibiting a 63% inhibition of tone as a maximum response at 120 s occlusion. The recovery phase was characterized by a vivid active constrictor component apparently protecting the capillaries from excessive pressure load upon arterial occlusion release, but this constriction became attenuated at long occlusions, thereby prolonging the hyperaemia response. The role of myogenic regulatory mechanisms in the responses was assessed from observed segmental resistance reactions to selectively applied transmural pressure stimuli similar to those elicited by arterial occlusion/release. It was concluded that myogenic mechanisms alone could explain the amplitude of the reactive hyperaemia response at short (up to 30 s) occlusions. Metabolic mechanisms seemed to be responsible for further relaxation of the proximal arterial vessels at longer occlusions, and also for the increased duration of the hyperaemia response at occlusions exceeding 10 s. Blockade of nitric oxide formation (endothelium-derived relaxing factor) did not seem to affect the reactive hyperaemia response.
J Björnberg; U Albert; S Mellander
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Acta physiologica Scandinavica     Volume:  139     ISSN:  0001-6772     ISO Abbreviation:  Acta Physiol. Scand.     Publication Date:  1990 Aug 
Date Detail:
Created Date:  1991-01-04     Completed Date:  1991-01-04     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0370362     Medline TA:  Acta Physiol Scand     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  535-50     Citation Subset:  IM    
Department of Physiology and Biophysics, University of Lund, Sweden.
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MeSH Terms
Arterial Occlusive Diseases / complications,  physiopathology
Dilatation, Pathologic
Hyperemia / etiology,  physiopathology*
Muscles / blood supply*
Time Factors
Vascular Resistance*

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