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Article: Venous adenosine content and vascular responses in dog hind-limb skeletal muscles during twitch contraction.

TitleVenous adenosine content and vascular responses in dog hind-limb skeletal muscles during twitch contraction.
Authors
Issue Date1987
Citation
Quarterly Journal Of Experimental Physiology, 1987, v. 72 n. 4, p. 461-471 How to Cite?
AbstractIn dogs anaesthetized with pentobarbitone sodium and chloralose and artificially ventilated, the skeletal muscles of a hind limb were vascularly and neurally isolated and perfused at a constant flow of 150% of the resting blood flow (5.8 +/- 0.3 ml.min-1.100g-1 muscle tissue, mean +/- S.E.M., n = 6) obtained after denervation of the limb. Electrical stimulation of the cut peripheral ends of the femoral and sciatic nerves for 20 min resulted in muscle contraction and a decrease in arterial perfusion pressure to a new steady level (59.7 +/- 8.6% decrease in vascular resistance) within 2 min; the pressure remained constant throughout the remaining 20 min. Similarly venous oxygen tension decreased from 38.2 +/- 1.3 (control) to 16.4 +/- 1.7 mmHg (n = 5) during contractions. The concentration of adenosine in arterial plasma did not change significantly during muscle contraction (122.5 +/- 28 nM, n = 8). However, the adenosine concentrations in venous plasma increased significantly (P less than 0.05) from a control value of 94.8 +/- 33 nM (n = 8) to 256 +/- 82 nM (n = 8) after 10 min and 235 +/- 31 nM (n = 8) after 20 min of muscle contraction. During infusion of adenosine into the femoral artery to give a range of arterial plasma concentrations between 0.17 and 90 microM, 89.2 +/- 2.8% (n = 20) of the infused adenosine was removed (taken up by tissues) from the blood before it reached the vein. Infusion of adenosine caused dose-dependent decreases in vascular resistance ranging between 7 and 79%; 5.58 +/- 1.50 microM adenosine caused a decrease in resistance of 36.1 +/- 7.1% (n = 10) and 51.7 +/- 7.4 microM adenosine caused a decrease of 51.2 +/- 4.1% (n = 9). Comparison of venous plasma adenosine concentrations during adenosine infusions with those seen during contractions suggests that the released adenosine can contribute about 60% of the total vasodilatation seen during contractions of the muscle. These results show that adenosine appears in the venous blood during muscle contraction and is likely to contribute to exercise hyperaemia.
Persistent Identifierhttp://hdl.handle.net/10722/171512
ISSN
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBallard, HJen_US
dc.contributor.authorCotterrell, Den_US
dc.contributor.authorKarim, Fen_US
dc.date.accessioned2012-10-30T06:15:29Z-
dc.date.available2012-10-30T06:15:29Z-
dc.date.issued1987en_US
dc.identifier.citationQuarterly Journal Of Experimental Physiology, 1987, v. 72 n. 4, p. 461-471en_US
dc.identifier.issn0144-8757en_US
dc.identifier.urihttp://hdl.handle.net/10722/171512-
dc.description.abstractIn dogs anaesthetized with pentobarbitone sodium and chloralose and artificially ventilated, the skeletal muscles of a hind limb were vascularly and neurally isolated and perfused at a constant flow of 150% of the resting blood flow (5.8 +/- 0.3 ml.min-1.100g-1 muscle tissue, mean +/- S.E.M., n = 6) obtained after denervation of the limb. Electrical stimulation of the cut peripheral ends of the femoral and sciatic nerves for 20 min resulted in muscle contraction and a decrease in arterial perfusion pressure to a new steady level (59.7 +/- 8.6% decrease in vascular resistance) within 2 min; the pressure remained constant throughout the remaining 20 min. Similarly venous oxygen tension decreased from 38.2 +/- 1.3 (control) to 16.4 +/- 1.7 mmHg (n = 5) during contractions. The concentration of adenosine in arterial plasma did not change significantly during muscle contraction (122.5 +/- 28 nM, n = 8). However, the adenosine concentrations in venous plasma increased significantly (P less than 0.05) from a control value of 94.8 +/- 33 nM (n = 8) to 256 +/- 82 nM (n = 8) after 10 min and 235 +/- 31 nM (n = 8) after 20 min of muscle contraction. During infusion of adenosine into the femoral artery to give a range of arterial plasma concentrations between 0.17 and 90 microM, 89.2 +/- 2.8% (n = 20) of the infused adenosine was removed (taken up by tissues) from the blood before it reached the vein. Infusion of adenosine caused dose-dependent decreases in vascular resistance ranging between 7 and 79%; 5.58 +/- 1.50 microM adenosine caused a decrease in resistance of 36.1 +/- 7.1% (n = 10) and 51.7 +/- 7.4 microM adenosine caused a decrease of 51.2 +/- 4.1% (n = 9). Comparison of venous plasma adenosine concentrations during adenosine infusions with those seen during contractions suggests that the released adenosine can contribute about 60% of the total vasodilatation seen during contractions of the muscle. These results show that adenosine appears in the venous blood during muscle contraction and is likely to contribute to exercise hyperaemia.en_US
dc.languageengen_US
dc.relation.ispartofQuarterly Journal of Experimental Physiologyen_US
dc.subject.meshAdenosine - Blooden_US
dc.subject.meshAnimalsen_US
dc.subject.meshChromatography, High Pressure Liquiden_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshFemoral Nerveen_US
dc.subject.meshHindlimb - Physiologyen_US
dc.subject.meshMuscle Contractionen_US
dc.subject.meshMuscles - Blood Supply - Innervationen_US
dc.subject.meshSciatic Nerveen_US
dc.subject.meshVeinsen_US
dc.titleVenous adenosine content and vascular responses in dog hind-limb skeletal muscles during twitch contraction.en_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.pmid3423195-
dc.identifier.scopuseid_2-s2.0-0023430083en_US
dc.identifier.volume72en_US
dc.identifier.issue4en_US
dc.identifier.spage461en_US
dc.identifier.epage471en_US
dc.identifier.isiWOS:A1987L577400005-
dc.identifier.scopusauthoridBallard, HJ=7005286310en_US
dc.identifier.scopusauthoridCotterrell, D=6602879005en_US
dc.identifier.scopusauthoridKarim, F=7005896790en_US

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