Suppression of Vascular Injury at the Arthus Reaction Site by a Complement Inhibitor, 5,5',5"-(1,3,6-Naphthalene-triyl- tris[sulfonylimino])-tris(1,3-benzenedisulfonic Acid) Hexasodium Salt

1991 ◽  
Vol 8 (1) ◽  
pp. 50-59 ◽  
Author(s):  
M.Y.M. (a, c) Abdel Mawla ◽  
K.P. (b) Dingemans ◽  
M. (c) Amer ◽  
G.T. (a) Venneker ◽  
M. (a) van Meegen ◽  
...  
Keyword(s):  
Vascular Injury ◽  
Reaction Site ◽  
Complement Inhibitor ◽  
Arthus Reaction

Suppression of Complement-Mediated Vascular Injury at Arthus Reaction Sites by Complement Inhibitors

Complement ◽  
1986 ◽  
Vol 3 (1) ◽  
pp. 40-48 ◽  
Author(s):  
S.S. Asghar ◽  
K.P. Dingemans ◽  
A. Kammeijer ◽  
W.R. Faber ◽  
M.Y.M. Abdel Mawla
Keyword(s):  
Vascular Injury ◽  
Arthus Reaction ◽  
Complement Inhibitors

Diagnostic workup and endovascular treatment of popliteal artery trauma

VASA ◽  
2019 ◽  
Vol 48 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Cheong J. Lee ◽  
Rory Loo ◽  
Max V. Wohlauer ◽  
Parag J. Patel
Keyword(s):  
Vascular Injury ◽  
Gold Standard ◽  
Imaging Techniques ◽  
Computed Tomographic Angiography ◽  
Vascular Trauma ◽  
Endovascular Techniques ◽  
Computed Tomographic ◽  
Arterial Injuries ◽  
Arterial Trauma ◽  
Peripheral Arterial

Abstract. Although management paradigms for certain arterial trauma, such as aortic injuries, have moved towards an endovascular approach, the application of endovascular techniques for the treatment of peripheral arterial injuries continues to be debated. In the realm of peripheral vascular trauma, popliteal arterial injuries remain a devastating condition with significant rates of limb loss. Expedient management is essential and surgical revascularization has been the gold standard. Initial clinical assessment of vascular injury is aided by readily available imaging techniques such as duplex ultrasonography and high resolution computed tomographic angiography. Conventional catheter based angiography, however, remain the gold standard in the determination of vascular injury. There are limited data examining the outcomes of endovascular techniques to address popliteal arterial injuries. In this review, we examine the imaging modalities and current approaches and data regarding endovascular techniques for the management popliteal arterial trauma.

Pharmacometabonomics of Ginseng Extracts on Vascular Injury Induced by Chronic Homocysteine Treatment.

Planta Medica ◽  
2012 ◽  
Vol 78 (05) ◽  
Author(s):  
E Lui ◽  
J Hou ◽  
K Zhong ◽  
J Hu ◽  
B Barrett ◽  
...  
Keyword(s):  
Vascular Injury

Antiplatelet Effect of FK633, a Platelet Glycoprotein Ilb/IIIa Antagonist, on Thrombus Formation and Vascular Patency after Thrombolysis in the Injured Hamster Carotid Artery

1997 ◽  
Vol 77 (03) ◽  
pp. 562-567 ◽  
Author(s):  
Takehiro Kaida ◽  
Hiroyuki Matsuno ◽  
Masayuki Niwa ◽  
Osamu Kozawa ◽  
Hideo Miyata ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Carotid Artery ◽  
Vascular Injury ◽  
Bleeding Time ◽  
Thrombus Formation ◽  
Separate Experiment ◽  
Platelet Glycoprotein ◽  
Neointima Formation ◽  
Vascular Patency ◽  
Injured Artery

SummaryThe antithrombotic and restenosis-preventing effects of FK633, an inhibitor of platelet aggregation via binding to the glycoprotein (GP) Ilb/IIIa receptor, were studied. IC50 value of FK633 against platelet aggregation ex vivo induced by 2.5 |iM adenosine diphosphate (ADP) was 5.4 X 10"7 M as determined using hamster platelet rich plasma. The inhibitory effect was also investigated in vivo on thrombus formation at the carotid arterial wall injured by a modified catheter. As a control, the left carotid artery was injured and the time required to develop a thrombotic occlusion (3.9 ±1.1 min, mean ± S.E.M., n = 18) was determined. Then, the right carotid artery of the same animal was injured while a continuous intravenous (i.v.) infusion of FK633 was administered at doses of 0 (saline), 0.1,0.3 or 1.0 mg/kg/h. The time to occlusion was dose-dependently prolonged. In a separate experiment, 10% of the total tPA dose (0.52 mg/kg) was injected into the injured artery as a bolus and the remaining was infused i.v. at a constant rate for 30 min. When FK633 (0.3 or 1.0 mg/kg/h) was infused together with tPA, late patency of the reperfused artery was much improved as compared with that of treatment with tPA alone. Bleeding time, measured at the end of the tPA infusion, was markedly prolonged when the higher dose of FK633 (1.0 mg/kg/h) was coadministered, however coadministration of the lower dose of FK633 (0.3 mg/kg/h) was almost without prolongation on the bleeding time, despite a significant effect on the vascular patency after thrombolysis. Next, neointima formation was evaluated 2 weeks after the vascular injury. When FK633 (0.3 mg/kg/h) was continuously infused i. v. by an implanted osmotic pump for 3,7 or 14 days after the vascular injury, the neointimal area formation was significantly suppressed in the treatment groups for 7 or 14 days. These findings suggest that FK633 inhibits platelet activation in the injured artery and improves vascular patency after thrombolysis with tPA with a concomitant suppression of neointima formation.

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