1985 Volume 13 Issue 4 Pages 1043-1049
We evaluated the plasma levels of thromboxane B2 (Tx B2) and 6-keto PG F1α in both healthy controls and diabetic subjects before and after forearm ischemia, and the effects of trapidil on prostaglandin metabolism of these subjects. Our observations were listed as follows.
(1) Before ischemia, plasma levels of Tx B2 and 6-keto PG F1α were 101.4±75.0pg/ml (Mean±SEM) and 115.1±14.6pg/ml in controls, and 181.4±161.4pg/ml and 65.2±9.0pg/ml in diabetics, respectively. In diabetics, plasma levels of 6-keto PG F1α was significantly lower than in controls (p<0.01).
(2) After ischemia, plasma levels of Tx B2 and 6-keto PG F1α were 177.1±136.2pg/ml and 227.4±10.5pg/ml in diabetics, respectively. In diabetics, forearm ischemia did not induce the increase in plasma level of 6-keto PG F1α significantly, and was significantly lower than those in controls (p<0.05).
(3) After trapidil treatment in diabetics, plasma levels of Tx B2 did not change significantly. Plasma levels of 6-keto PG F1α was 82.7±22.8pg/ml before ischemia, and 127.7±23.1pg/ml after ischemia. After ischemia, plasma levels of 6-keto PG F1α was significantly higher than those before treatment (p<0.01).
The results indicate that the secretion of prostacyclin to forearm ischemia is decreased in diabetics. These abnormalities may play an important role in the pathogenesis and/or development of diabetic micro- and macro-angiopathy. Trapidil, known as coronary vasodilator, would be useful for its promoting effect of prostacyclin production, although further study would be needed to elucidate the detailed mechanisms.
