Pathophysiological Mechanisms of Chronic Venous Disease and Implications for Venoactive Drug Therapy.

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ischemia 5 angiologydiseases
thrombosis 1 angiologydiseases
vascular disease 1 angiologydiseases

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ischemia 22284 models, MPFF treatment was shown to reduce leukocyte adhesion to vascular endothelium. In a hamster ischemia -reperfusion model, neutrophil adhesion in post-capillary venules was lower in animals pre-treated with
ischemia 22480 pre-treated with MPFF than in control animals [[71],[72]]. Similar findings were obtained in two rat ischemia -reperfusion models employing the cremaster muscle and mesentery vein [[73]] (Figure 2).One mechanism
ischemia 27897 of its constituent flavonoids, significantly reduced the number of leaky capillary sites produced by ischemia -reperfusion [[91]]. In a rabbit model of sclerotherapy, MPFF treatment for 21 days prior to initiation
ischemia 41072 reduce leukocyte adhesion and activation in different models of venous inflammation induced either by ischemia -reperfusion or by transient venous hypertension [[71],[73],[75],[76],[77]]. In humans, venoactive drugs
ischemia 45037 flux of rolling leukocytes (C), and microvascular protein leakage (D) in rat cremaster muscles. I/R = ischemia /reperfusion. Statistically different from * control (nonischemic conditions) and + vehicle: p < 0.05.
thrombosis 25278 may also reduce endothelial cell activity in CVD, which is an important trigger of inflammation and thrombosis . In patients with C2 to C5 CVD, MPFF treatment for 60 days reduced plasma ICAM-1 concentrations by 32%
vascular disease 41869 ulcer healing time. Inappropriate endothelial activation in CVD is a mechanism common to other cardio vascular disease s and diabetes. Drugs that specifically target endothelial dysfunction in these diseases may also be

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