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VENOUS ADENOSINE CONTENT AND VASCULAR RESPONSES IN DOG HIND‐LIMB SKELETAL MUSCLES DURING TWITCH CONTRACTION
Author(s) -
Ballard H. J.,
Cotterrell D.,
Karim F.
Publication year - 1987
Publication title -
quarterly journal of experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0144-8757
DOI - 10.1113/expphysiol.1987.sp003088
Subject(s) - contraction (grammar) , hindlimb , adenosine , skeletal muscle , femoral artery , perfusion , medicine , chemistry , muscle contraction , chloralose , vasodilation , vascular resistance , stimulation , anatomy , denervation , blood flow , anesthesia , endocrinology , hemodynamics
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 . 100 g −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 〈 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 µM, 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 µM adenosine caused a decrease in resistance of 36·1±7·1% ( n = 10) and 51·7±7·4 µM 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.