Potential effectiveness of minidose aspirin combined with dilazep in anti-platelet therapy.

Abstract

The anti-platelet aggregating action of minidose aspirin and its combined effect with dilazep were examined in healthy male volunteers. A quantitative and dose-dependent decrease in platelet aggregability was observed on a single oral administration of 30 mg, 100 mg and 300 mg of aspirin and also on the repeated oral administration of 10 mg and 30 mg three times a day for 5 days. Administration of 100 mg of dilazep in combination with 30 mg or 100 mg of aspirin produced an anti-platelet effect equivalent to a 3-fold dose of aspirin alone. In the repeated administration test, the t. i. d. admin istration of aspirin 10 mg+ dilazep 100 mg was confirmed to be close to the ideal in the balance between anti-platelet action and the reduced production of PGI2.

Effect of the antiplatelet drug dilazep dihydrochloride on urinary podocytes in patients in the early stage of diabetic nephropathy.

“…Dilazep dihydrochloride is also known to have a vasodilating effect in coronary, cerebral, and renal vessels and is often used in patients with ischemic heart disease, cerebral ischemia, or renal dysfunction (22). Here we report that dilazep dihydrochloride treatment reduced microalbuminuria and the number of urinary podocytes, probably by suppressing platelet hypersensitivity, suppressing decreases in anionic charge, and/or increasing renal blood flow (23)(24)(25). However, the precise mechanisms are still unclear.…”

Dilazep, a nucleoside transporter inhibitor, modulates cell cycle progression and DNA synthesis in rat mesangial cells in vitro

“…1995 ), and (b) suppression of platelet adhesion and coagulation and the maintenance of the glomerular filtration rate as a result of increased renal blood flow ( Nagase et al . 1985 , Yasunaga et al . 1988 ).…”

“…However, only a few mechanisms have been proposed for the effects of dilazep on diseases of the kidney. These include (a) suppression of the decrease in anionic charge in the glomerular basement membrane (Yamamoto et al 1995), and (b) suppression of platelet adhesion and coagulation and the maintenance of the glomerular ®ltration rate as a result of increased renal blood ¯ow (Nagase et al 1985, Yasunaga et al 1988. The former can improve proteinuria and the latter should suppress mesangial cell proliferation by inhibiting plateletderived growth factor released from platelets (Iida et al 1988, Silver, Jaffer & Abboud 1989, Floege et al 1992.…”

Effects of antiplatelet drug dilazep dihydrochloride on anionic sites and extracellular matrix (ecm) components in glomerular basement membrane of stz‐induced diabetic rats

“…Several pharmacological effects of dilazep dihydrochloride have been reported as follows: (I) suppression of platelet adhesion and coagulation, (2) suppression of phospholipase activity of platelets. (3) increase of red blood cell flexibility, (4) suppression of decreases of anionic charge in the GBM, and (5) maintenance of glomerular filtration rate (GFR) due to increased renal blood flow (6,16,17). However, there has been no report on preventive effects of dilazep dihydrochloride on the glomerular anionic sites in STZ-induced diabetic rats.…”