PubMed · 5596894
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F Wyss. 1967-12-16. [Hypothyroidism].. https://pubmed.ncbi.nlm.nih.gov/5596894/
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1. Circulation around tendons may act as a shunt for muscle during exercise. The perfusion and oxygenation of Achilles' peritendinous tissue was measured in parallel with that of calf muscle during exercise to determine (1) whether blood flow is restricted in peritendinous tissue during exercise, and (2) whether blood flow is coupled to oxidative metabolism. 2. Seven individuals performed dynamic plantar flexion from 1 to 9 W. Radial artery and popliteal venous blood were sampled for O2, peritendinous blood flow was determined by 133Xe-washout, calf blood flow by plethysmography, cardiac output by dye dilution, arterial pressure by an arterial catheter-transducer, and muscle and peritendinous O2 saturation by spatially resolved spectroscopy (SRS). 3. Calf blood flow rose 20-fold with exercise, reaching 44 +/- 7 ml (100 g)-1 min-1 (mean +/- s.e.m. ) at 9 W, while Achilles' peritendinous flow increased (7-fold) to 14 +/- 4 ml (100 g)-1 min-1, which was 18 % of the maximal flow established during reactive hyperaemia. SRS-O2 saturation fell both in muscle (from 66 +/- 2 % at rest to 57 +/- 3 %, P < 0.05) and in peritendinous regions (58 +/- 4 to 52 +/- 4 %, P < 0.05) during exercise along with a rise in leg vascular conductance and microvascular haemoglobin volume, despite elevated systemic vascular resistance. 4. The parallel rise in calf muscle and peritendinous blood flow and fall in O2 saturation during exercise indicate that blood flow is coupled to oxidative metabolism in both tissue regions. Increased leg vascular conductance accompanied by elevated microvascular haemoglobin volume reflect vasodilatation in both muscle and peritendinous regions. However, peak exercise peritendinous blood flow reaches only approximately 20 % of its maximal blood flow capacity.
PURPOSE: We conducted a retrospective study of the distribution of sonographically detected abnormalities in the heels of patients who had a clinical diagnosis of Achilles tendinosis. METHODS: One hundred eighteen symptomatic heels in 73 patients who had a clinical diagnosis of chronic Achilles tendinosis were examined over a 12-month period by the same experienced sonologist. The distribution of altered tendon architecture and features suggesting retrocalcaneal bursitis or Achilles paratendinosis were evaluated. RESULTS: Sonograms of 118 symptomatic heels demonstrated that 96 (81%) had abnormalities confined to the proximal two thirds of the Achilles tendon, 9 (8%) had abnormalities in the distal third alone, and 13 (11%) had abnormalities at both sites. Of the 109 heels with proximal two-third Achilles tendon disease, 99 (91%) had medial tendon involvement; 22 of the 99 showed diffuse tendon changes. Lateral tendon segment changes were seen in 22 (19%) of the 118 symptomatic heels. No lateral tendon segment was involved in isolation. Of the 22 heels with distal third abnormalities, 14 (64%) had sonographic evidence of Achilles paratendinitis, and 13 (59%) had sonographic evidence of Achilles tendinosis. Eighteen of the 22 had sonographic evidence of retrocalcaneal bursitis. In all cases of distal third tendinosis, the deep surface of the tendon was primarily involved. In the heels with both proximal and distal changes, superficial segment involvement of the mid-Achilles tendon was present. CONCLUSIONS: Sonography provides information that helps to accurately diagnose clinical Achilles tendinopathy and may help to determine the biomechanical processes involved in the injury.
OBJECTIVE: To investigate the early stages in the formation of bony spurs in relation to normal enthesis development. METHODS: Histologic sections of rat Achilles tendons, stained with toluidine blue or Masson's trichrome, were examined in animals ranging from 2 weeks to 1 year of age. Further material prepared for immunohistochemistry was labeled with monoclonal antibodies for laminin and type IV collagen to highlight the presence of small blood vessels at the enthesis. Sections of small spurs from the Achilles tendons of elderly humans were also examined for comparison. RESULTS: As a part of normal development, bone grows into the Achilles tendon as the calcaneus enlarges. Ossification is preceded by vascular invasion, which occurs along rows of enthesis fibrocartilage cells. Small bony spurs develop when ossification at one point on the enthesis outstrips that on either side. CONCLUSION: Bony spurs can develop in the Achilles tendon without the need for preceding microtears or any inflammatory reaction, and they form by endochondral ossification of enthesis fibrocartilage. The increased surface area created at the tendon-bone junction may be an adaptive mechanism to ensure the integrity of the interface in response to increased mechanical loads.