Limb Collaterals

Schoop, W

doi:10.1007/978-1-4615-3092-3_15

Cited by 7 publications

(13 citation statements)

References 10 publications

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“…In such cases, limb loss is uncommon and early symptoms of arterial insufficiency are rapidly reversed [4,31]. In commenting on the clinical situation, both Schoop [80] and Longland [54] noted that a threat of necrosis subsequent to acute arterial occlusion only occurs for certain sections of large transport arteries. Surgical texts note that arterial occlusion at the most common sites in the lower extremity is relatively well tolerated due to the pre‐existing collateral network [8,50,62,68].…”

Section: To What Extent Is the Human Vasculature Capable Of Compensatmentioning

confidence: 99%

“…Collateral circulations were described for the major arteries including the thoracic and abdominal aorta, common carotid, external iliac, subclavian, brachial, and femoral arteries. Major pre‐existing arterial anastomoses in the femoral‐popliteal system include arterial branches from the hypogastric trunk, external iliac, superficial iliac circumflex, and genicular arteries [34,80]. Longland noted the abundance of small arterial anastomoses in skeletal muscle in his address to the Royal College of Surgeons of England in 1953 [54].…”

Section: How Does the Vasculature Compensate For Major Arterial Occlumentioning

confidence: 99%

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Marvels, Mysteries, and Misconceptions of Vascular Compensation to Peripheral Artery Occlusion

et al. 2010

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Peripheral arterial disease is a major health problem and there is a significant need to develop therapies to prevent its progression to claudication and critical limb ischemia. Promising results in rodent models of arterial occlusion have generally failed to predict clinical success and led to questions of their relevance. While sub-optimal models may have contributed to the lack of progress, we suggest that advancement has also been hindered by misconceptions of the human capacity for compensation and the specific vessels which are of primary importance. We present and summarize new and existing data from humans, Ossabaw miniature pigs, and rodents which provide compelling evidence that natural compensation to occlusion of a major artery (i) may completely restore perfusion, (ii) occurs in specific pre-existing small arteries, rather than the distal vasculature, via mechanisms involving flow-mediated dilation and remodeling (iii) is impaired by cardiovascular risk factors which suppress the flow-mediated mechanisms and (iv) can be restored by reversal of endothelial dysfunction. We propose that restoration of the capacity for flow-mediated dilation and remodeling in small arteries represents a largely unexplored potential therapeutic opportunity to enhance compensation for major arterial occlusion and prevent the progression to critical limb ischemia in the peripheral circulation.

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Section: To What Extent Is the Human Vasculature Capable Of Compensatmentioning

confidence: 99%

Section: How Does the Vasculature Compensate For Major Arterial Occlumentioning

confidence: 99%

Marvels, Mysteries, and Misconceptions of Vascular Compensation to Peripheral Artery Occlusion

et al. 2010

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“…The interconnection between the a. thoracica interna and the a. epigastrica inferior bypasses any obstruction in the descending thoracic aorta down to the iliac arteries. Obstruction of the abdominal aorta also may result in the recruitment of the mesenteric arterial network (106). The preexistent collateral arterial network in the knee region as well as the intercon-nections between the radial and the ulnar arteries, and between the digital arteries of each digit of the upper and the lower extremities have become standard textbook knowledge for medical students (125).…”

Section: The Discovery Of the Collateral Circulation And Of Preexistementioning

confidence: 99%

Arteriogenesis The Development and Growth of Collateral Arteries

2003

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In patients with atherosclerotic vascular diseases, collateral vessels bypassing major arterial obstructions have frequently been observed. This may explain why some patients remain without symptoms or signs of ischemia. The term "arteriogenesis" was introduced to differentiate the formation of collateral arteries from angiogenesis, which mainly occurs in the ischemic, collateral flow-dependent tissue. Many observations in various animal models and humans support that the remodeling of preexisting collateral vessels is the mechanism of collateral artery formation. This remodeling process seems to be mainly flow-mediated. It involves endothelial cell activation, basal membrane degradation, leukocyte invasion, proliferation of vascular cells, neointima formation (in most species studied), and changes of the extracellular matrix. The contribution of ischemia to arteriogenesis is still unclear, but arteriogenesis clearly can occur in the absence of any significant ischemia. It is questionable, whether collateral arteries also form de novo in ischemic vascular diseases. A better understanding of the mechanisms of arteriogenesis will be important for the design of more effective strategies for the treatment of patients with ischemic vascular diseases.

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“…In various species, the preexisting vessels are the size of the smallest arteries, and they enlarge ϳ100% (14,20,35,45,56). Available clinical studies have indicated that subsequent to arterial occlusion in the peripheral circulation, the primary vessels that enlarge as collaterals are preexisting arteries (4,29,57). The largest of the preexisting vessels are typically those that become the dominant collaterals (35,45,51).…”

mentioning

confidence: 99%

Suppressed hindlimb perfusion in Rac2^−/− and Nox2^−/− mice does not result from impaired collateral growth

Distasi

Case

Ziegler

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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arteriogenesis; hindlimb ischemia; necrosis; regeneration; NADPH oxidase 2 IN THE PERIPHERAL CIRCULATION, the dilation and enlargement of preexisting vessels that form collateral pathways subsequent to arterial occlusion are the primary vascular compensations that preserve tissue viability and maintain function. These vessels dilate within seconds (25,39,45,70) and undergo expansion for weeks (20,25,45,69). In various species, the preexisting vessels are the size of the smallest arteries, and they enlarge ϳ100% (14,20,35,45,56). Available clinical studies have indicated that subsequent to arterial occlusion in the peripheral circulation, the primary vessels that enlarge as collaterals are preexisting arteries (4,29,57). The largest of the preexisting vessels are typically those that become the dominant collaterals (35,45,51). Combined anatomic and modeling studies have predicted that hindlimb flow subsequent to femoral artery occlusion is primarily determined by these collaterals (22,56). This is consistent with studies of segmental resistances that demonstrated that compensation in the collateral vessels is of significantly greater hemodynamic importance than adaptations in the distal microvasculature (43,71,75). Nevertheless, few studies investigating the mechanisms of vascular compensation subsequent to arterial occlusion in mice have specifically identified and studied these preexisting vessels that form the primary collateral pathways. Such investigations are needed because angiogenesis and collateral growth are initiated by different stimuli, and differences exist in the molecules and mechanisms that mediate these important processes (7, 11).Leukocytes, especially lymphocytes (63, 74) and macrophages (2,33,37), have been shown to have an important role in vascular compensation to hindlimb ischemia. Recent studies by Tojo et al. (66) and Urao et al. (72) have established that NADPH oxidase 2 (Nox2)-derived ROS from bone marrowderived cells (BMDCs) have an important role in neovascularization in the ischemic mouse hindlimb. The initial report (66) concluded from microsphere data that collateral growth was impaired, but did not specifically identify collateral bypass vessels or measure their diameters.To investigate the hypothesis that Nox2-derived NAD(P)H oxidase mediates primary collateral growth subsequent to arterial occlusion, the present study used Rac2-null (Rac2 Ϫ/Ϫ ) and Nox2-null (Nox2 Ϫ/Ϫ ) mice and a novel method of identifying primary hindlimb collaterals. Rac2 is expressed primarily, if not exclusively, in hematopoietic cells (38, 52) and binds to and activates Nox2-containing NAD(P)H oxidase (24,40). In addition, leukocytes from Rac2 Ϫ/Ϫ and Nox2 Ϫ/Ϫ mice have impaired function related to reduced ROS production (47,66,72). We present a method to identify the dominant or primary collateral that should be the major collateral supplying flow to

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Limb Collaterals

Cited by 7 publications

References 10 publications

Marvels, Mysteries, and Misconceptions of Vascular Compensation to Peripheral Artery Occlusion

Marvels, Mysteries, and Misconceptions of Vascular Compensation to Peripheral Artery Occlusion

Arteriogenesis The Development and Growth of Collateral Arteries

Suppressed hindlimb perfusion in Rac2^−/− and Nox2^−/− mice does not result from impaired collateral growth

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Limb Collaterals

Cited by 7 publications

References 10 publications

Marvels, Mysteries, and Misconceptions of Vascular Compensation to Peripheral Artery Occlusion

Marvels, Mysteries, and Misconceptions of Vascular Compensation to Peripheral Artery Occlusion

Arteriogenesis The Development and Growth of Collateral Arteries

Suppressed hindlimb perfusion in Rac2−/− and Nox2−/− mice does not result from impaired collateral growth

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Suppressed hindlimb perfusion in Rac2^−/− and Nox2^−/− mice does not result from impaired collateral growth