Cyclo-oxygenase-2 mediated prostaglandin release regulates blood flow in connective tissue during mechanical loading in humans
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Cyclo-oxygenase-2 mediated prostaglandin release regulates blood flow in connective tissue during mechanical loading in humans. / Langberg, H; Boushel, Robert Christopher; Skovgaard, D; Risum, N; Kjaer, M.
In: Journal of Physiology, Vol. 551, No. Pt 2, 01.09.2003, p. 683-9.Research output: Contribution to journal › Journal article › Research › peer-review
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T1 - Cyclo-oxygenase-2 mediated prostaglandin release regulates blood flow in connective tissue during mechanical loading in humans
AU - Langberg, H
AU - Boushel, Robert Christopher
AU - Skovgaard, D
AU - Risum, N
AU - Kjaer, M
PY - 2003/9/1
Y1 - 2003/9/1
N2 - Mechanical loading is known to increase connective tissue blood flow of human tendons and to cause local release of vasodilatory substances. The present study investigated the importance of prostaglandins (PG) formed by cyclo-oxygenase isoforms (COX-1 and 2) for the exercise-related increase in blood flow in connective tissue. Healthy individuals (n = 24, age: 23-31 years) underwent 30 min of intermittent, isometric, plantarflexion with both calf muscles either without (n = 6, Control, C) or with blockade of PG formation, either COX-2 specific (n = 10, Celecoxib 2 x 100 mg day-1 for 3 days prior to the experiment) or COX unspecific (n = 8, indomethacin 100 mg (12 and 1 h pre-experiment) and acetyl salicylic acid 500 mg day-1 for 3 days pre-experiment). Prostaglandin E2 (PGE2) concentration was determined by microdialysis and blood flow by 133Xe washout. In C, interstitial PGE2 rose from (0.8 +/- 0.2 (rest) to 1.4 +/- 0.5 ng ml-1 (exercise), P <0.05), whereas during unspecific COX inhibition, tissue PGE2 was completely inhibited at rest and during exercise. COX-2 specific blockade did not inhibit tissue PGE2 at rest, but totally abolished the exercise induced increase. Blood flow was similar in the three groups at rest (P > 0.05), whereas the increase in flow with exercise was reduced by 35 and 43 % with COX-2 specific blockade (3.2 +/- 0.7 to 6.1 +/- 1.5 ml (100 g tissue)-1 min-1 or COX unspecific blockade (3.0 +/- 0.8 to 7.6 +/- 1.6), respectively, compared to C (2.7 +/- 0.8 to 10.2 +/- 2.0)(P <0.05). The findings indicate that COX-2 specific mechanisms are responsible for the exercise-induced increase in prostaglandin synthesis, and that increase in tissue prostaglandin plays an important role for blood flow in peritendinous connective tissue during physical loading in vivo.
AB - Mechanical loading is known to increase connective tissue blood flow of human tendons and to cause local release of vasodilatory substances. The present study investigated the importance of prostaglandins (PG) formed by cyclo-oxygenase isoforms (COX-1 and 2) for the exercise-related increase in blood flow in connective tissue. Healthy individuals (n = 24, age: 23-31 years) underwent 30 min of intermittent, isometric, plantarflexion with both calf muscles either without (n = 6, Control, C) or with blockade of PG formation, either COX-2 specific (n = 10, Celecoxib 2 x 100 mg day-1 for 3 days prior to the experiment) or COX unspecific (n = 8, indomethacin 100 mg (12 and 1 h pre-experiment) and acetyl salicylic acid 500 mg day-1 for 3 days pre-experiment). Prostaglandin E2 (PGE2) concentration was determined by microdialysis and blood flow by 133Xe washout. In C, interstitial PGE2 rose from (0.8 +/- 0.2 (rest) to 1.4 +/- 0.5 ng ml-1 (exercise), P <0.05), whereas during unspecific COX inhibition, tissue PGE2 was completely inhibited at rest and during exercise. COX-2 specific blockade did not inhibit tissue PGE2 at rest, but totally abolished the exercise induced increase. Blood flow was similar in the three groups at rest (P > 0.05), whereas the increase in flow with exercise was reduced by 35 and 43 % with COX-2 specific blockade (3.2 +/- 0.7 to 6.1 +/- 1.5 ml (100 g tissue)-1 min-1 or COX unspecific blockade (3.0 +/- 0.8 to 7.6 +/- 1.6), respectively, compared to C (2.7 +/- 0.8 to 10.2 +/- 2.0)(P <0.05). The findings indicate that COX-2 specific mechanisms are responsible for the exercise-induced increase in prostaglandin synthesis, and that increase in tissue prostaglandin plays an important role for blood flow in peritendinous connective tissue during physical loading in vivo.
KW - Achilles Tendon
KW - Adult
KW - Calibration
KW - Connective Tissue
KW - Cyclooxygenase 2
KW - Cyclooxygenase 2 Inhibitors
KW - Cyclooxygenase Inhibitors
KW - Dinoprostone
KW - Exercise
KW - Humans
KW - Immunohistochemistry
KW - Isoenzymes
KW - Leg
KW - Membrane Proteins
KW - Microdialysis
KW - Prostaglandin-Endoperoxide Synthases
KW - Prostaglandins
KW - Regional Blood Flow
KW - Rest
KW - Xenon
U2 - 10.1113/jphysiol.2003.046094
DO - 10.1113/jphysiol.2003.046094
M3 - Journal article
C2 - 12813143
VL - 551
SP - 683
EP - 689
JO - The Journal of Physiology
JF - The Journal of Physiology
SN - 0022-3751
IS - Pt 2
ER -
ID: 33816798