Treatment of Ischemic Ulcers of the Lower Limbs With Alprostadil (Prostaglandin E1)

2006 ◽  
Vol 2006 ◽  
pp. 210-211
Author(s):  
W.L. Garner
2004 ◽  
Vol 30 (8) ◽  
pp. 1113-1117 ◽  
Author(s):  
Paolo Tondi ◽  
Laura Gerardino ◽  
Angelo Santoliquido ◽  
Roberto Pola ◽  
Maurizio Gabrielli ◽  
...  

2004 ◽  
Vol 30 (8) ◽  
pp. 1113-1117
Author(s):  
PAOLO TONDI ◽  
LAURA GERARDINO ◽  
ANGELO SANTOLIQUIDO ◽  
ROBERTO POLA ◽  
MAURIZIO GABRIELLI ◽  
...  

2014 ◽  
Vol 13 (5) ◽  
pp. 625-629 ◽  
Author(s):  
Giovanni De Caridi ◽  
Mafalda Massara ◽  
Francesco Stilo ◽  
Francesco Spinelli ◽  
Raffaele Grande ◽  
...  

1984 ◽  
Vol 1 (1) ◽  
pp. 160-170 ◽  
Author(s):  
James J. Schuler ◽  
D.Preston Flanigan ◽  
James W. Holcroft ◽  
Joseph J. Ursprung ◽  
J.Scott Mohrland ◽  
...  

VASA ◽  
2012 ◽  
Vol 41 (2) ◽  
pp. 132-135 ◽  
Author(s):  
Krohn ◽  
Gebauer ◽  
Hübler ◽  
Beck

The mid-aortic syndrome is an uncommon clinical condition characterized by severe narrowing of the descending aorta, usually with involvement of its renal and visceral branches, presenting with uncontrollably elevated blood pressures of the upper body, renal and cardiac failure, intestinal ischemia, encephalopathy symptoms and claudication of the lower limbs, although clinical presentation is variable. In this article we report the case of an eleven-year-old patient with the initial diagnosis of a mid-aortic syndrome and present the computed tomography angiography pictures and reconstructions before and after surgical therapy.


Phlebologie ◽  
2008 ◽  
Vol 37 (05) ◽  
pp. 247-252 ◽  
Author(s):  
V. S. Brauer ◽  
W. J. Brauer

SummaryPurpose: Comparison of qualitative and quantitative sonography with the lymphoscintigraphic function test and clinical findings in legs. Patients, methods: In 33 patients a lymphoscintigraphic function test of legs combined with measurement of lymph node uptake was performed and subsequently compared with sonography. Sonographic criteria were: Thickness of cutis, thickness of subcutanean fatty tissue and presence of liquid structures or fine disperse tissue structure of lower limbs, foots and toes. Results: In 51 legs uptake values lie in the pathologic area, in four legs in the grey area and in ten legs in the normal area. The cutis thickness in the lower leg shows no significant correlation with the uptake. The determination of the thickness of the subcutanean fatty tissue of the lower leg and of the cutis thickness of the feet turned out to be an unreliable method. In 47% of the medial lower legs and in 57% of the lateral lower legs with clinical lymphoedema sonography is falsely negative. Conclusion: Early lymphoedema is only detectable with the lymphoscintigraphic function test. In the case of clinical lymphoedema clinical examination is more reliable than sonography.


1990 ◽  
Vol 29 (05) ◽  
pp. 215-220 ◽  
Author(s):  
R. Benning ◽  
K. Nagel ◽  
M. Jugenheimer ◽  
S. Fischer ◽  
S. Worthmann ◽  
...  

A new 99mTc-labelled tracer (99mTc-Sestanriibi) was used for the first time to demonstrate the perfusion of the skeletal muscle. In 16 patients with obstructive atherosclerosis of the lower limbs the change of perfusion of thigh and lower leg was studied with SPECT before and after vascular surgery (n = 11) or percutaneous transluminal angioplasty (n = 5). Comparative results of scintigraphic measurements and clinical observations (ancle-arm pressure, treadmill test) in 10 surgical patients (14 operated legs) showed correct positive or negative results in 86% (12/14).


1994 ◽  
Vol 71 (01) ◽  
pp. 091-094 ◽  
Author(s):  
M Cattaneo ◽  
B Akkawat ◽  
R L Kinlough-Rathbone ◽  
M A Packham ◽  
C Cimminiello ◽  
...  

SummaryNormal human platelets aggregated by thrombin undergo the release reaction and are not readily deaggregated by the combination of inhibitors hirudin, prostaglandin E1 (PGE1) and chymotrypsin. Released adenosine diphosphate (ADP) plays an important role in the stabilization of thrombin-induced human platelet aggregates. Since ticlopidine inhibits the platelet responses to ADP, we studied thrombin-induced aggregation and deaggregation of 14C-serotonin-labeled platelets from 12 patients with cardiovascular disease before and 7 days after the oral administration of ticlopidine, 250 mg b.i.d. Before and after ticlopidine, platelets stimulated with 1 U/ml thrombin aggregated, released about 80–90% 14C-serotinin and did not deaggregate spontaneously within 5 min from stimulation. Before ticlopidine, hirudin (5× the activity of thrombin) and PGE1 (10 μmol/1) plus chymotrypsin (10 U/ml) or plasmin (0.06 U/ml), added at the peak of platelet aggregation, caused slight or no platelet deaggregation. After ticlopidine, the extent of platelet deaggregation caused by the same inhibitors was significantly greater than before ticlopidine. The addition of ADP (10 μmol/1) to platelet suspensions 5 s after thrombin did not prevent the deaggregation of ticlopidine-treated platelets. Thus, ticlopidine facilitates the deaggregation of thrombin-induced human platelet aggregates, most probably because it inhibits the effects of ADP on platelets.


1990 ◽  
Vol 63 (01) ◽  
pp. 076-081 ◽  
Author(s):  
Pascale Gaussem ◽  
Sophie Gandrille ◽  
Pascale Molho-Sabatier ◽  
Loïc Capron ◽  
Jean-Noël Fiessinger ◽  
...  

SummaryUsing a monoclonal antibody-based assay, we measured the fibrin degradation product release in the supernatant of plasma clots obtained before and after venous occlusion (VO) in 30 patients with definite or suspected vascular thrombosis (19 definite and 2 suspected deep vein thrombosis, 6 recurrent superficial thrombophlebitis, 3 arterial occlusions of lower limbs). tPA and PAI-1 concentrations were determined using ELISA assays; the post-occlusion values were corrected for haemoconcentration. The increase in tPA during VO was correlated with haemoconcentration (r = 0.74), but 3 patients had ineffective VO (<2% increase in proteins). The fibrinolytic response to VO was evaluated using the shortening of the time necessary for the release of 200 μg of fibrin degradation products per mg of fibrinogen (Δ T 200). Two among the 27 patients with effective VO were bad responders with a Δ T 200 <3 h (whereas all the others had Δ T 200 >10 h). These patients had respectively a deficient tPA release (Δ tPA = 1 ng/ml) and an elevated PAI-1 level at rest (33 ng/ml). Several other patients were bad responders in terms of tPA release or of shortening of the euglobulin clot lysis time but they had a normal Δ T 200. This plasma clot test reflects the ability of free tPA to bind to fibrin (the amount of which depends on the level of tPA and PAI-1), and may be useful in the diagnosis of a hypofibrinolytic state.


1973 ◽  
Vol 30 (01) ◽  
pp. 138-147 ◽  
Author(s):  
Christopher R. Muirhead

SummaryThe filter loop technique which measures platelet aggregation in vivo in the flowing-blood of the rat was compared to the optical density technique of Born which is carried out in vitro with platelet rich plasma. Using these two experimental models the effect on platelet aggregation of three known inhibitors sulfinpyrazone, dipyridamole and prostaglandin E1, and a novel compound 5-oxo-l-cyclopentene-l-heptanoic acid (AY-16, 804) was determined.The effects on platelet aggregation of the known inhibitors were consistent with information in the literature. Prostaglandin E1 was the most potent inhibitor in both techniques; sulfinpyrazone inhibited aggregation in both models but was less potent than prostaglandin E1. AY-16, 804 exhibited activity in vitro and in vivo similar to that of sulfinpyrazone. Dipyridamole did not inhibit platelet aggregation in vivo and did not inhibit aggregation in vitro in concentrations at which it remained soluble.The filter loop technique is a suitable model for measuring platelet aggregation in the flowing blood of the rat. It is a relatively simple method of determining aggregation and easily adapted to other species.


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