flunarizine and Edema

The effect of flunarizine in the treatment of post-phlebitic syndrome (PPS) and venous leg ulcers was studied in 42 patients in a double-blind, placebo-controlled trial over a period of 3 months. During the first month the dose of flunarizine or the matching placebo was 1 capsule of 5 mg twice-daily, and during the following 2 months 1 capsule of 5 mg once-daily. Most of the subjective symptoms such as heaviness in the legs, pain, paraesthesia, cramps at night, and swelling of the ankles considerably improved during treatment with flunarizine and were slightly improved in the placebo group. The ulcer surface area decreased after 3 months' treatment with flunarizine by 68.3% (p < 0.001), and after treatment with placebo by 20.5% (p > 0.05). In 15 patients treated with flunarizine and 1 with placebo the ulcers vanished completely. An improvement in the photoplethysmographic record of the lower legs in the flunarizine group was observed, as shown by increase in the index recovery time, while there were no significant changes in the placebo group. The results show that the favorable effect of flunarizine in the treatment of PPS and venous leg ulcers might be due largely to an improvement in subcutaneous circulation of the lower legs. Flunarizine may be an important adjunct to the conservative management of the complications caused by chronic venous insufficiency.

Topics: Adult; Aged; Aged, 80 and over; Double-Blind Method; Edema; Female; Flunarizine; Humans; Leg Ulcer; Male; Middle Aged; Pain; Phlebitis; Photoplethysmography

This study aimed to explore the role and mechanism(s) of flunarizine hydrochloride in the intracerebral hemorrhage (ICH) rats. The 32 adult male Sprague Dawley (SD) rats were randomly assigned into four groups: control group, sham group, ICH group, and FLU + ICH group. The effects of flunarizine hydrochloride were assessed on the basis of hematoma volume, blood-brain barrier (BBB) integrity, and brain water content in the ICH rat models. The role of flunarizine hydrochloride in cell recovery was assessed by behavioral scores, quantitative real-time polymerase chain reaction (qRT-PCR), and western blot assay. Involvement of PI3K/AKT pathway in exerting the effect of flunarizine hydrochloride was also determined. Results showed that the hematoma volume, BBB integrity, and brain water content were significantly decreased in the FLU + ICH group. Cell apoptosis significantly increased in the ICH model group, while flunarizine hydrochloride decreased this increase. The expressions of glial cell line-derived neurotrophic factor (GDNF), neuroglobin (NGB), and p-AKT were increased after flunarizine hydrochloride treatment in ICH rats. In conclusion, flunarizine hydrochloride has protective effects against ICH by reducing brain injury, cell apoptosis, and the activation of P13K/AKT pathway. These findings provide a theoretical basis for the treatment of flunarizine hydrochloride in ICH.

Topics: Animals; Apoptosis; Behavior, Animal; Blood-Brain Barrier; Brain; Brain Injuries; Calcium Channel Blockers; Cerebral Hemorrhage; Edema; Flunarizine; Glial Cell Line-Derived Neurotrophic Factor; Globins; Hematoma; Male; Nerve Tissue Proteins; Neuroglobin; Neurons; Neuroprotective Agents; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-bcl-2; Rats, Sprague-Dawley; Water