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- Publisher Website: 10.1113/expphysiol.1987.sp003088
- Scopus: eid_2-s2.0-0023430083
- PMID: 3423195
- WOS: WOS:A1987L577400005
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Article: Venous adenosine content and vascular responses in dog hind-limb skeletal muscles during twitch contraction.
Title | Venous adenosine content and vascular responses in dog hind-limb skeletal muscles during twitch contraction. |
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Authors | |
Issue Date | 1987 |
Citation | Quarterly Journal Of Experimental Physiology, 1987, v. 72 n. 4, p. 461-471 How to Cite? |
Abstract | In 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 Identifier | http://hdl.handle.net/10722/171512 |
ISSN | |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ballard, HJ | en_US |
dc.contributor.author | Cotterrell, D | en_US |
dc.contributor.author | Karim, F | en_US |
dc.date.accessioned | 2012-10-30T06:15:29Z | - |
dc.date.available | 2012-10-30T06:15:29Z | - |
dc.date.issued | 1987 | en_US |
dc.identifier.citation | Quarterly Journal Of Experimental Physiology, 1987, v. 72 n. 4, p. 461-471 | en_US |
dc.identifier.issn | 0144-8757 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171512 | - |
dc.description.abstract | In 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.language | eng | en_US |
dc.relation.ispartof | Quarterly Journal of Experimental Physiology | en_US |
dc.subject.mesh | Adenosine - Blood | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Chromatography, High Pressure Liquid | en_US |
dc.subject.mesh | Dogs | en_US |
dc.subject.mesh | Electric Stimulation | en_US |
dc.subject.mesh | Femoral Nerve | en_US |
dc.subject.mesh | Hindlimb - Physiology | en_US |
dc.subject.mesh | Muscle Contraction | en_US |
dc.subject.mesh | Muscles - Blood Supply - Innervation | en_US |
dc.subject.mesh | Sciatic Nerve | en_US |
dc.subject.mesh | Veins | en_US |
dc.title | Venous adenosine content and vascular responses in dog hind-limb skeletal muscles during twitch contraction. | en_US |
dc.type | Article | en_US |
dc.identifier.email | Ballard, HJ:ballard@hkucc.hku.hk | en_US |
dc.identifier.authority | Ballard, HJ=rp00367 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1113/expphysiol.1987.sp003088 | - |
dc.identifier.pmid | 3423195 | - |
dc.identifier.scopus | eid_2-s2.0-0023430083 | en_US |
dc.identifier.volume | 72 | en_US |
dc.identifier.issue | 4 | en_US |
dc.identifier.spage | 461 | en_US |
dc.identifier.epage | 471 | en_US |
dc.identifier.isi | WOS:A1987L577400005 | - |
dc.identifier.scopusauthorid | Ballard, HJ=7005286310 | en_US |
dc.identifier.scopusauthorid | Cotterrell, D=6602879005 | en_US |
dc.identifier.scopusauthorid | Karim, F=7005896790 | en_US |
dc.identifier.issnl | 0144-8757 | - |