Functional and Morphological Assessment of Rat Aorta Stored in University of Wisconsin and Eurocollins Solutions

Abebe, Worku; Cavallari, Nicola; Agrawal, Devendra K.; Rowley, J M; Thorpe, Patricia E.; Hunter, William J.; Edwards, John D.

doi:10.1097/00007890-199310000-00006

Cited by 38 publications

(27 citation statements)

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“…A functional assessment found Euro-Collins to be more damaging than UW after 24 h of storage (28). This correlates with both our results and those of Abebe (51). A phase-contrast study of cultured endothelial cells found that UW did not result in any observable change, whereas Collins solutions resulted in more prominent nuclei (29).…”

Section: Many Of the Nuclei In The 24-h Euro-collins Stored Groupsupporting

confidence: 93%

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Cold Storage Preservation and Warm Ischaemic Injury to Isolated Arterial Segments: Endothelial Cell Injury

Neil¹,

Lynch

Hardie

et al. 2002

American Journal of Transplantation

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Injury to endothelial cells is thought to be important to the development of the vascular lesion of chronic rejection. It was the aim of this study to develop a semiquantitative method to assess endothelial injury in arterial grafts and to document the injury produced by cold storage preservation and additional warm ischaemia. Twelve-and 24-h cold preservation of rat aortic segments, together with an additional 1 h of warm ischaemia, were assessed. Electron micrographs of representative endothelial cells were scored for cytoplasmic, nuclear and mitochondrial injury.

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Section: Many Of the Nuclei In The 24-h Euro-collins Stored Groupsupporting

confidence: 93%

“…Similar findings were seen with Euro-Collins solution storage of rat aorta by Abebe and colleagues (51). They also showed that the endothelial cells were no longer functional, being unable to produce nitric oxide, supporting our interpretation of irreversible cell injury.…”

Section: Many Of the Nuclei In The 24-h Euro-collins Stored Groupsupporting

confidence: 90%

Cold Storage Preservation and Warm Ischaemic Injury to Isolated Arterial Segments: Endothelial Cell Injury

Neil¹,

Lynch

Hardie

et al. 2002

American Journal of Transplantation

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“…The hSV specimens (mean patient age 71.5 ± 3.7 yrs) left over from the bypass surgical procedure were used for the study. Specimens were collected fresh in ice-cold University of Wisconsin solution, which is used to maintain cellular and tissue integrity in the organs for transplantation [11]. The hSV conduits were immediately brought to the laboratory where all of the procedures were carried out under sterile conditions.…”

Section: Specimen Collection Processing and Culture Of Smooth Musclementioning

confidence: 99%

Involvement of connexin 43 in angiotensin II-induced migration and proliferation of saphenous vein smooth muscle cells via the MAPK-AP-1 signaling pathway

Jia

Cheng

Gangahar

et al. 2008

Journal of Molecular and Cellular Cardiology

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Proliferation and migration of vascular smooth muscle cells (VSMCs) lead to intimal thickening and influence the long-term patency of venous graft post coronary arterial bypass graft. There is increasing evidence that connexins are involved in the development of intimal hyperplasia and restenosis. We assessed connexin 43 (Cx43) expression and its role in angiotensin II-induced proliferation and migration of smooth muscle cells and the signal pathways involved in human saphenous vein bypass conduits. Angiotensin-II significantly increased gap junctional intercellular communication and induced the expression of Cx43 in human saphenous vein SMCs in a dose-and time-dependent manner through angiotensin II type 1 receptor. The effect of angiotensin-II was blocked by siRNA of ERK 1/2, p38 MAPK and JNK, respectively. Overexpression of Cx43 markedly increased the proliferation of saphenous vein SMCs. However, siRNA for Cx43 inhibited angiotensin-II-induced proliferation, cyclin E expression and migration of human saphenous vein SMCs. In dual-luciferase reporter assay, angiotensin-II markedly activated AP-1 transcription factor, which was significantly attenuated by a dominant negative AP-1 (A-Fos) with subsequent inhibition of angiotensin-II-induced transcriptional expression of Cx43. These data demonstrate the role of Cx43 in the proliferation and migration of human saphenous vein SMCs and angiotensin-II induced Cx43 expression via mitogen-activated protein kinases (MAPK)-AP-1 signaling pathway.

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“…Pearl et al [26] observed, in fact, a loss of endothelial-dependent vasodilatation due to a reduced hand, Evora et al [27] showed, using a protocol designed to eliminate the variable of infusion pressure, showed that UWs does not impair endothelium-depen-Allopurinol 0.136 g/L 1 dent relaxation to acetylcholine and endothelium-inde-Hydroxyethyl starch 50 g/L pendent smooth muscle relaxation to sodium nitroprus-Insulin 40 U/L Penicillin G 200,000 U side of rat aorta stored up to 24 hr [28].…”

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confidence: 99%

Functional and Morphological Evaluation of Canine Veins Following Preservation in Different Storage Media

Cavallari

Abebe

Mingoli

et al. 1997

Journal of Surgical Research

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Functional and Morphological Assessment of Rat Aorta Stored in University of Wisconsin and Eurocollins Solutions

Cited by 38 publications

References 0 publications

Cold Storage Preservation and Warm Ischaemic Injury to Isolated Arterial Segments: Endothelial Cell Injury

Cold Storage Preservation and Warm Ischaemic Injury to Isolated Arterial Segments: Endothelial Cell Injury

Involvement of connexin 43 in angiotensin II-induced migration and proliferation of saphenous vein smooth muscle cells via the MAPK-AP-1 signaling pathway

Functional and Morphological Evaluation of Canine Veins Following Preservation in Different Storage Media

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