RESUMEN
It is known that Kiutsu state (obstruction of qi) is frequently observed in bronchial asthma. We found that Oketsu (blood stagnation) state is also observed in such patients. In the present study, we analyzed the Oketsu state in 70 asthma patients. Oketsu state was evaluated by Oketsu score (OS) by Dr. Terasawa. OS was significantly elevated in asthmatic patients, and it increased depending on the severity of the asthma. OS was no different in atopic asthma and non-atopic asthma. OS was significantly high in oral steroid treated patients. However, when the object is restricted only in the moderate state, OS was no different between the steroid treated group and the non-steroid treated group. From these results, we conclude that the Oketsu state is deeply interacted with asthma and that low dose oral steroid administration does not seem to worsen the Oketsu state in patients with asthma. We should follow the OS before and after the administration of steroids to test this hypothesis. We will investigate it in the near future.
RESUMEN
Granulocyte elastase released from activated leukocytes plays an important role in leukocyte infiltration. Since activated leukocytes have been shown to be involved in the pathogenesis of gastric mucosal lesion formation induced by indomethacin, inhibition of granulocyte elastase release from activated leukocytes may be useful in the prevention of these lesions. Rikkunsi-to and ONO-5046, a granulocyte elastase inhibitor, markedly inhibited gastric mucosal lesion formation in rats. Gastric myeloperoxidase activity was significantly increased 3 hours after indomethacin administration. This increase was significantly inhibited by Rikkunsi-to and ONO-5046. Rikkunsi-to inhibited granulocyte elastase release from activated neutrophils in vitro while cimetidine did not. Although cimetidine markedly prevented the indomethacin-induced gastric mucosal lesion formation, it did not reduce gastric myeloperoxidase activity. Therefore, unlike cimetidine, Rikkunsi-to may prevent indomethacin-induced gastric mucosal lesion formation by inhibiting neutrophil activation.