Experimental methods in the pathogenesis of limb ischemia

Barie, Philip S.; Mullins, Richard J.

doi:10.1016/0022-4804(88)90059-5

Cited by 43 publications

(21 citation statements)

References 87 publications

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“…We used nonparticulate 99m Tc-04 as a radioisotope instead of particulate 99m Tc-MAA. The 99m Tc-MAAs that other authors used for determining regional distribution of blood flow are larger particles than capillaries and thus are trapped in the first capillary bed they encounter and distributed in proportion to the perfusion (14,17,21). But, the 99m Tc-04 that we used are not particles, so we could get a radioisotopic angiogram for 1 min and evaluate regional dynamic distribution of blood flow.…”

Section: Discussionmentioning

confidence: 99%

“…The simple ligation of iliac or femoral arteries could not produce adequate ischemia at rest (11-13, 15, 16). The multiple ligation of branches of the iliac, common femoral, and deep femoral arteries shows only a short time of ischemia in a dog model (17). Aortic ligation produces variable results depending on the experimental animals, and it is impossible to use a contralateral limb as a control (18,19).…”

Section: Introductionmentioning

confidence: 99%

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An experimental model of ischemia in rabbit hindlimb

et al. 2001

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An Experimental Model of Ischemia in Rabbit HindlimbThis study was performed to establish an experimental model of ischemia for the investigation of new treatment modality of limb-threatening ischemia. We produced ischemia in the hindlimbs of 8 New Zealand white rabbits. Under general anesthesia, the left femoral artery was exposed, freed, and excised from distal external iliac artery to proximal popliteal and saphenous arteries. And then both hindlimbs were serially examined to assess the ischemia according to the time table until postoperative 6 weeks. We assessed clinical observation, blood pressure, radioisotopic perfusion scan, and angiography. Clinical ischemic changes of the operated feet were observed in 63%. The blood pressure of left calves was measurable on postoperative day 3 (p <0.05, vs preoperative day 2) and then gradually increased to reach a plateau in postoperative week 6. Radioisotopic arterial perfusion showed similar profiles as in blood pressure. Angiography of ischemic hindlimbs demonstrated a few collateral vessels arising from the internal iliac artery with the reconstitution of the posterior tibial artery in postoperative week 2. In postoperative week 6, collaterals remained the same in number. However, these became dilated and tortuous and showed reconstitution in distal hindleg. In conclusion, this is a reproducible, measurable, and economical animal model of hind limb ischemia.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

An experimental model of ischemia in rabbit hindlimb

et al. 2001

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“…In mild and structural adaptation o f resistance vessels [6,7]. Fur thermore, generation o f a collateral circulation can restore blood supply to the ischemic region [8][9][10], Collateral ves sels and normal vascular beds are not comparable, as col lateral vessels are hyperreactive to substances like sero tonin [11,12], thromboxane A2 analogues [ 13] and nor adrenaline [ 14], This is probably due to differences in vas cular structure and sensitivity of receptor-linked mecha nisms.…”

Section: Introductionmentioning

confidence: 99%

“…The col lateralized circulatory beds may be hyperreactive to vaso constrictors in comparison to normal beds due to an increased vessel wall thickness o f collaterals [10,12] or due to a diminished innervation o f collateral vessels, which results in hypersensitivity o f postsynaptic receptors [14].…”

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confidence: 99%

Increased Responsiveness of the Vascular Bed to Angiotensin I, Angiotensin II and Phenylephrine in Acute and Chronic Ischemic Hindlimbs in Rats

Nelissen-Vrancken

Leenders²,

Boudier³

et al. 1992

J Vasc Res

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Ischemia activates several compensatory mechanisms to restore blood supply. To investigate possible changes in the reactivity of blood vessels after acute and chronic ischemia of skeletal muscle, the response (resistance changes) of the vascular bed to angiotensin II (AII) and phenylephrine (PE) in a hindlimb perfusion model were studied in control, acutely ischemic (45 min) and chronically ischemic (4 weeks) spontaneously hypertensive rats. Furthermore, the effects of angiotensin I (AI) were studied to investigate the involvement of local angiotensin-I-converting enzyme (ACE) in adaptive responses. Ischemia was induced by partial occlusion of the left common iliac artery. Both in acute and chronic ischemia, the reactivity (maximal resistance change) of the vascular bed in the ischemic hindlimb to AI, AII and PE was increased only in severe ischemia (residual flow < 40%), whereas the sensitivity (ED50) was not influenced. The increase in reactivity was comparable for AI and AII, implying that local ACE seems not to be involved. These results suggest that severe ischemia of skeletal muscle results in nonselective hyperreactivity of the vascular bed, which may be due to alterations of receptor-linked mechanisms or ultrastructural changes of blood vessels.

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“…however such blood flow is inadequate to maintain aerobic metabolism (Klenerman and Crawley 1977). Reactive hyperemia and arterial vasodilatation follow brief periods of tissue ischemia (Romanus 1977, Larsson and Lewis 1978, Santavirta et al 1978, Kennedy et al 1981, Klenerman et al 1982, Barie and Mullins 1988, Authier 1988. Tissue edema follows reperfusion after thirty minutes to four hours of skeletal muscle ischemia (Paletta et al 1960, Miller et al 1979, Klenerman et al 1982, Korthius et al 1985, Silver et al 1986, Suva1 et al 1987, Dreyfuss and Smith 1988, Gidlof 1988, Soussi 1989.…”

Section: Mechanisms Of Tourniquet-induced Muscle Injurymentioning

confidence: 99%

Tourniquet-induced neuromuscular injury

Pedowitz

1991

Acta Orthopaedica Scandinavica

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Experimental methods in the pathogenesis of limb ischemia

Cited by 43 publications

References 87 publications

An experimental model of ischemia in rabbit hindlimb

An experimental model of ischemia in rabbit hindlimb

Increased Responsiveness of the Vascular Bed to Angiotensin I, Angiotensin II and Phenylephrine in Acute and Chronic Ischemic Hindlimbs in Rats

Tourniquet-induced neuromuscular injury

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