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Femoral artery ligation impairs skeletal muscle force production in C57Bl/6J mice
Author(s) -
Nickell Courtney Elizabeth,
Cardinal Trevor Ryan
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.573.8
Subject(s) - arteriogenesis , medicine , skeletal muscle , femoral artery , perfusion , ligation , gastrocnemius muscle , cardiology , hindlimb , revascularization , ischemia , occlusion , anesthesia , anatomy , myocardial infarction
Patients diagnosed with Peripheral Arterial Occlusive Disease (PAOD), generally caused by atherosclerotic plaque accumulation in conduit arteries, typically experience intermittent claudication, which is characterized by pain during exercise in the lower extremities due to ischemia. Perfusion distal to occluded arteries can be maintained through enlargement of natural bypass collaterals by arteriogenesis . Unfortunately, clinical trials of arteriogenesis‐ and angiogenesis‐stimulating therapies have been unsuccessful, despite clear efficacy in animal models. This may be at least partially explained by the differences in endpoints in animal models and human patients. For example, the most common assessment of ischemic revascularization in animal models is hindpaw perfusion while the most clinical endpoint is pain‐free walking distance, which depends both on vascular supply and skeletal muscle function. However, it is unclear how occlusion affects skeletal muscle performance in animal models. To better understand the natural history of the tissue response following arterial occlusion, it is necessary to determine the impact of occlusion on skeletal muscle performance using precise and quantitative methods. Therefore, we developed a muscle force production protocol following distal femoral artery ligation (FAL). Specifically, following ligation between the epigastric and popliteal branches, we measured force production in the triceps surae, i.e. gastrocnemius and soleus, in response to single, tetanic, and fatiguing stimulations in male C57Bl/6J mice. Pilot studies indicated that force production was not different between unoperated right and left hindlimbs, with maximum twitch forces of 398.6 ± 80.5mN and 389.2 ± 41.8mN, respectively, and maximum tetanic forces of 1420.7 ± 271.4mN and 1361.7 ± 246.5mN, respectively. Following protocol development, we investigated whether forces produced at day‐7 following FAL were consistently lower than those produced by a sham‐operated hindlimb. As expected, maximum twitch force was reduced in the operated hindlimb as compared to the contralateral sham operated hindlimb, 458.95 ± 28.02 mN and 504.08 ± 28.12 mN in the operated and sham hindlimbs, respectively. Similarly, maximum tetanic force production was also reduced in the operated hindlimb, 1583.8 ± 218.2 mN, as compared to 1990.7 ± 270.7 mN in the sham. Having determined that force production is impaired at day‐7 following FAL, future studies may include characterizing the time course of force production recovery and/or investigating if force production in ligated hindlimbs can be rescued with myoblast cell transplantation. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .