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Article: Appearance of adenosine in venous blood from the contracting gracilis muscle and its role in vasodilatation in the dog

TitleAppearance of adenosine in venous blood from the contracting gracilis muscle and its role in vasodilatation in the dog
Authors
Issue Date1987
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751
Citation
Journal Of Physiology, 1987, v. Vol. 387, p. 401-413 How to Cite?
Abstract1. In dogs anaesthetized with sodium pentobarbitone and artificially ventilated, the gracilis muscles were vascularly isolated and perfused at a constant flow rate of 51.2±9.8 ml min-1 100 g-1 muscle tissue (183±17.8% of resting blood flow; mean±S.E.; n = 13). 2. Electrical stimulation of the cut peripheral end of the obturator nerve (6 V, 4 Hz) resulted in muscle contraction (658±118 g 100 g-1 force after 5 min), and an immediate decrease in arterial perfusion pressure from 179±15.7 mmHg to 87±10.0 mmHg (51.4±4.5% decrease in vascular resistance after 2 min of contraction). Venous oxygen tension decreased from 69.2±5.1 mmHg to 18.5±1.4 mmHg (n = 6). These values did not significantly alter during the remaining period of stimulation (10-20 min). 3. The concentration of adenosine in arterial plasma did not change significantly during muscle contraction (137±23 nM; n = 10). However, the adenosine concentrations in venous plasma showed a significant (P < 0.01) increase from a control value of 164±55 nM to 455±77 nM (n = 9) after 5 min of muscle contraction and remained high during the rest of the 20 min contraction. In six of the dogs adenosine concentrations were determined after 1 and 3 min of contraction and showed a smaller but statistically significant (P < 0.05) rise in venous concentration. 4. During infusion of adenosine into the artery to give plasma concentrations between 0.3 μM and 1 mM, 72.6±2.1% (n = 29) of the infused adenosine was taken up by the tissues before it reached the vein. Comparison of vasodilatation and venous adenosine concentrations during adenosine infusion and muscle contractions showed that the released adenosine could contribute about 15% to the total vasodilatation after 1 min and about 40% between 5 and 20 min of contractions. Released adenosine could contribute about 80% to the vasodilatation that remained 5 min after the withdrawal of stimulation. Arterial perfusion pressure took 22 min to return to control, whereas adenosine release had fallen to zero within 10 min. 5. These data suggest that the released adenosine could contribute to exercise hyperaemia, but is unlikely to be the main factor, particularly in the initial stage.
Persistent Identifierhttp://hdl.handle.net/10722/171508
ISSN
2015 Impact Factor: 4.731
2015 SCImago Journal Rankings: 2.670
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBallard, HJen_US
dc.contributor.authorCotterrell, Den_US
dc.contributor.authorKarim, Fen_US
dc.date.accessioned2012-10-30T06:15:28Z-
dc.date.available2012-10-30T06:15:28Z-
dc.date.issued1987en_US
dc.identifier.citationJournal Of Physiology, 1987, v. Vol. 387, p. 401-413en_US
dc.identifier.issn0022-3751en_US
dc.identifier.urihttp://hdl.handle.net/10722/171508-
dc.description.abstract1. In dogs anaesthetized with sodium pentobarbitone and artificially ventilated, the gracilis muscles were vascularly isolated and perfused at a constant flow rate of 51.2±9.8 ml min-1 100 g-1 muscle tissue (183±17.8% of resting blood flow; mean±S.E.; n = 13). 2. Electrical stimulation of the cut peripheral end of the obturator nerve (6 V, 4 Hz) resulted in muscle contraction (658±118 g 100 g-1 force after 5 min), and an immediate decrease in arterial perfusion pressure from 179±15.7 mmHg to 87±10.0 mmHg (51.4±4.5% decrease in vascular resistance after 2 min of contraction). Venous oxygen tension decreased from 69.2±5.1 mmHg to 18.5±1.4 mmHg (n = 6). These values did not significantly alter during the remaining period of stimulation (10-20 min). 3. The concentration of adenosine in arterial plasma did not change significantly during muscle contraction (137±23 nM; n = 10). However, the adenosine concentrations in venous plasma showed a significant (P < 0.01) increase from a control value of 164±55 nM to 455±77 nM (n = 9) after 5 min of muscle contraction and remained high during the rest of the 20 min contraction. In six of the dogs adenosine concentrations were determined after 1 and 3 min of contraction and showed a smaller but statistically significant (P < 0.05) rise in venous concentration. 4. During infusion of adenosine into the artery to give plasma concentrations between 0.3 μM and 1 mM, 72.6±2.1% (n = 29) of the infused adenosine was taken up by the tissues before it reached the vein. Comparison of vasodilatation and venous adenosine concentrations during adenosine infusion and muscle contractions showed that the released adenosine could contribute about 15% to the total vasodilatation after 1 min and about 40% between 5 and 20 min of contractions. Released adenosine could contribute about 80% to the vasodilatation that remained 5 min after the withdrawal of stimulation. Arterial perfusion pressure took 22 min to return to control, whereas adenosine release had fallen to zero within 10 min. 5. These data suggest that the released adenosine could contribute to exercise hyperaemia, but is unlikely to be the main factor, particularly in the initial stage.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751en_US
dc.relation.ispartofJournal of Physiologyen_US
dc.subject.meshAdenosine - Blood - Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDogsen_US
dc.subject.meshHindlimben_US
dc.subject.meshHydrogen-Ion Concentrationen_US
dc.subject.meshMuscle Contractionen_US
dc.subject.meshVasodilationen_US
dc.subject.meshVeins - Physiologyen_US
dc.titleAppearance of adenosine in venous blood from the contracting gracilis muscle and its role in vasodilatation in the dogen_US
dc.typeArticleen_US
dc.identifier.emailBallard, HJ:ballard@hkucc.hku.hken_US
dc.identifier.authorityBallard, HJ=rp00367en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid3656179-
dc.identifier.scopuseid_2-s2.0-0023162311en_US
dc.identifier.volumeVol. 387en_US
dc.identifier.spage401en_US
dc.identifier.epage413en_US
dc.identifier.isiWOS:A1987H570000023-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridBallard, HJ=7005286310en_US
dc.identifier.scopusauthoridCotterrell, D=6602879005en_US
dc.identifier.scopusauthoridKarim, F=7005896790en_US

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