Sıçanlarda indometazinle oluşturulan gastrik mukoza ülserleri üzerine K+ kanal açıcılarının etkileri

Abstract

-77- blood glucose level nor the decrease in contractile activity which let to increase an in gastric mucosal blood flow.-76- When the sensitivities of the tissues to relaxant agents are compared; nifedipine was found the most potent in all the contractions. The interpretation of protective effects of K+ channel openers cromakalim and diazoxide on indomethacin-induced gastric mucosal injury is very complicated. To explain their effectiveness in ulcer only by the differentiation in blood glucose level does not seem possible. Because, cromakalim displayed similar protective effect in ulcer while did not produce significant difference in blood glucose level. In addition, other used antiulcer drugs did not affect blood glucose level, but they decreased significantly ulcer index. However, correcting `glucose hypothesis` suggested for indomethacin induced ulcer, glibenclamide increased the ulcer score parallel to a decrease in blood glucose level. In experiments testing ` hypercontractility hypothesis` related to indomethacin-induced ulcer, diazoxide and cromakalim succesfully reversed the contractions of serotonin, which is a possible contractile agent for gastrointestinal smooth muscle, whereas diazoxide showed low responsiveness against acetylcholine contractions. These findings indicate that protective effects of diazoxide and cromakalim in indomethacin ulcer is related only partly with the suggested hypothesis. From these findings, related with the mechanism of protective effects of K+ channel openers, it can be said that this is neither completely depend on the increase of

-77- blood glucose level nor the decrease in contractile activity which let to increase an in gastric mucosal blood flow.-76- When the sensitivities of the tissues to relaxant agents are compared; nifedipine was found the most potent in all the contractions. The interpretation of protective effects of K+ channel openers cromakalim and diazoxide on indomethacin-induced gastric mucosal injury is very complicated. To explain their effectiveness in ulcer only by the differentiation in blood glucose level does not seem possible. Because, cromakalim displayed similar protective effect in ulcer while did not produce significant difference in blood glucose level. In addition, other used antiulcer drugs did not affect blood glucose level, but they decreased significantly ulcer index. However, correcting `glucose hypothesis` suggested for indomethacin induced ulcer, glibenclamide increased the ulcer score parallel to a decrease in blood glucose level. In experiments testing ` hypercontractility hypothesis` related to indomethacin-induced ulcer, diazoxide and cromakalim succesfully reversed the contractions of serotonin, which is a possible contractile agent for gastrointestinal smooth muscle, whereas diazoxide showed low responsiveness against acetylcholine contractions. These findings indicate that protective effects of diazoxide and cromakalim in indomethacin ulcer is related only partly with the suggested hypothesis. From these findings, related with the mechanism of protective effects of K+ channel openers, it can be said that this is neither completely depend on the increase of-77- blood glucose level nor the decrease in contractile activity which let to increase an in gastric mucosal blood flow.