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dc.contributor.authorBrown, Margaret D.
dc.contributor.authorKelsall, C.J.
dc.contributor.authorMilkiewicz, M.
dc.contributor.authorAnderson, Stephen I.
dc.contributor.authorHudlicka, Olga
dc.date.accessioned2008-03-18T11:21:09Z
dc.date.available2008-03-18T11:21:09Z
dc.date.issued2005
dc.identifier.citationMicrocirculation, 2005, 12(4): 373-381
dc.identifier.issn1073-9688
dc.identifier.pmid16020083
dc.identifier.doi10.1080/10739680590934817
dc.identifier.urihttp://hdl.handle.net/2436/20980
dc.description.abstractOBJECTIVES: To develop a model of peripheral arterial disease (PAD) in rat skeletal muscle with sustained impairment of microcirculatory perfusion, and to ascertain whether increased muscle activity can reverse the impairment. METHODS: Three weeks after iliac ligation in rats, the ipsilateral femoral artery was ligated (double ligation, DL), and in some animals, muscle activity was increased by electrical stimulation for 2 weeks (10 Hz, 15 min on, 85 mins off, 7 times per day). Diameter changes of precapillary arterioles to vasoactive agonists and capillary perfusion (flow intermittency, capillary red cell velocity [V(rbc)], and diameters) were measured in extensor digitorum longus muscle and compared with 5 weeks iliac only ligation (single ligation, SL) and controls. Total muscle endothelial nitric oxide synthase (eNOS) was estimated by Western blotting. RESULTS: Whereas single ligation increased intermittency of capillary flow with little effect on V(rbc) and shear stress, DL completely eliminated increases in V(rbc) and shear stress after muscle contractions. Arterial dilation to sodium nitroprusside was attenuated similarly in SL and DL; in SL, acetylcholine induced constriction and bradykinin an attenuated dilation, but in DL vessels were unresponsive to either. Chronic stimulation returned all microcirculatory parameters in DL to normal and increased levels of eNOS protein by 75%. CONCLUSIONS: Femoral artery ligation following iliac ligation impairs arteriolar vasodilator capacity, capillary perfusion, and shear-dependent function of microcirculatory endothelium more than iliac ligation alone and is more representative of long-standing ischemia in PAD. Chronic intermittent electrical stimulation can normalize these derangements.
dc.language.isoen
dc.publisherTaylor & Francis (Informa Healthcare)
dc.relation.urlhttp://www.informaworld.com/smpp/title~content=t713723262
dc.subjectArterioles
dc.subjectCapillary perfusion
dc.subjectCapillary shear stress
dc.subjectEndothelial-dependent dilation
dc.subjectIschemia
dc.subjectSkeletal muscle
dc.subject.meshAnimals
dc.subject.meshDisease Models, Animal
dc.subject.meshElectric Stimulation
dc.subject.meshEndothelium, Vascular
dc.subject.meshFemoral Artery
dc.subject.meshMicrocirculation
dc.subject.meshMuscle Contraction
dc.subject.meshMuscle, Skeletal
dc.subject.meshNitric Oxide Synthase
dc.subject.meshNitric Oxide Synthase Type III
dc.subject.meshPeripheral Vascular Diseases
dc.subject.meshRats
dc.subject.meshRats, Sprague-Dawley
dc.subject.meshVasodilation
dc.titleA new model of peripheral arterial disease: sustained impairment of nutritive microcirculation and its recovery by chronic electrical stimulation.
dc.typeJournal article
dc.identifier.journalMicrocirculation
html.description.abstractOBJECTIVES: To develop a model of peripheral arterial disease (PAD) in rat skeletal muscle with sustained impairment of microcirculatory perfusion, and to ascertain whether increased muscle activity can reverse the impairment. METHODS: Three weeks after iliac ligation in rats, the ipsilateral femoral artery was ligated (double ligation, DL), and in some animals, muscle activity was increased by electrical stimulation for 2 weeks (10 Hz, 15 min on, 85 mins off, 7 times per day). Diameter changes of precapillary arterioles to vasoactive agonists and capillary perfusion (flow intermittency, capillary red cell velocity [V(rbc)], and diameters) were measured in extensor digitorum longus muscle and compared with 5 weeks iliac only ligation (single ligation, SL) and controls. Total muscle endothelial nitric oxide synthase (eNOS) was estimated by Western blotting. RESULTS: Whereas single ligation increased intermittency of capillary flow with little effect on V(rbc) and shear stress, DL completely eliminated increases in V(rbc) and shear stress after muscle contractions. Arterial dilation to sodium nitroprusside was attenuated similarly in SL and DL; in SL, acetylcholine induced constriction and bradykinin an attenuated dilation, but in DL vessels were unresponsive to either. Chronic stimulation returned all microcirculatory parameters in DL to normal and increased levels of eNOS protein by 75%. CONCLUSIONS: Femoral artery ligation following iliac ligation impairs arteriolar vasodilator capacity, capillary perfusion, and shear-dependent function of microcirculatory endothelium more than iliac ligation alone and is more representative of long-standing ischemia in PAD. Chronic intermittent electrical stimulation can normalize these derangements.


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