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Olprinone improves diaphragmatic contractility and fatigability during abdominal sepsis in a rat model

Olprinone improves diaphragmatic contractility and fatigability during abdominal sepsis in a rat model. Miyakawa, H.; Oishi, K.; Hagiwara, S.; Kira, S.; Kitano, T.; Iwasaka, H.; Noguchi, T. (Department of Anesthesiology, Faculty of Medicine, Oita University, Oita, Japan). Acta Anaesthesiologica Scandinavica, 48(5), 637-641 (English) 2004 Blackwell Publishing Ltd. CODEN: AANEAB.Several reagents with their cas registry numbers 106730-54-5 and 9003-99-0 are used here. ISSN: 0001-5172. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Respiratory failure with diaphragmatic fatigability is common in patients suffering sepsis or septic shock. However, the development and progress of diaphragmatic fatigability remains poorly understood, and no method has been established to treat fatigability. In this study, we hypothesize that neutrophil activation contributes to the development of diaphragmatic fatigability. We also sought to investigate whether a phosphodiesterase inhibitor, olprinone, improves diaphragmatic fatigability assocd. with abdominal sepsis and inhibits an increase in myeloperoxidase activity in diaphragmatic muscle. Male Wistar rats were randomly assigned to a sham group, coecal legation perforation group (CLP), and a phosphodiesterase inhibitor (PDE) pretreated group. At 16 h after surgical procedure, the left hemidiaphragm was removed for the measurement of diaphragmatic contractility and fatigability. In addn., for the measurement of serial changes in myeloperoxidase activity, the right hemidiaphragm was also removed at 4, 8 or 16 h after the surgical procedure in each group. In a septic model involving rats, we obsd. that diaphragmatic muscles were fatigable and myeloperoxidase activity increased. We also demonstrated that i.p. administration of olprinone improves diaphragmatic fatigability and inhibits an increase in myeloperoxidase activity induced by abdominal sepsis. Olprinone represents a potential therapy for cases of respiratory failure with diaphragmatic fatigability resulting from inhibition of neutrophil activation. .

Olprinone, a phosphodiesterase III inhibitor, reduces gut mucosal injury and portal endotoxin level during acute hypoxia in rabbits

Olprinone, a phosphodiesterase III inhibitor, reduces gut mucosal injury and portal endotoxin level during acute hypoxia in rabbits. Satoh, Tomoyuki; Morisaki, Hiroshi; Ai, Kimiaki; Kosugi, Shizuko; Yamamoto, Michiko; Serita, Ryohei; Kotake, Yoshifumi; Takeda, Junzo (Department of Anesthesiology and General Intensive Care Unit, Keio University School of Medicine, Tokyo, Japan). Anesthesiology, 98(6), 1407-1414 (English) 2003 Lippincott Williams & Wilkins. CODEN: ANESAV. ISSN: 0003-3022. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Preservation of gut integrity has become a therapeutic goal to obviate bacterial translocation in the critically ill. The authors examd. whether olprinone, a phosphodiesterase III inhibitor, protected functional and structural integrity of gut mucosa against acute progressive hypoxia. Thirty-two animals were randomly allocated to a control group (n = 12), a low-dose group (0.2 mg × kg-1 × min-1 olprinone; n = 10), or a high-dose group (0.6 mg × kg-1 × min-1 olprinone; n = 10) after preparatory surgery. Ascending aortic and portal blood flow, intramural pH of the ileum, and portal endotoxin levels were measured at normoxia and through three stages of progressive hypoxia (fraction of inspired oxygen = 0.17, 0.13, and 0.10). At normoxia, ascending aortic flow in the high-dose group was approx. 20% higher than in the control and low-dose groups. During progressive hypoxia, both ascending aortic and portal flow in the control group were depressed, whereas olprinone infusion attenuated such alterations and redistributed blood to the splanchnic area in a dose-dependent manner. On the contrary, the redn. of intramural pH of the ileum and the elevation of portal endotoxin levels obsd. in the control group were significantly minimized in both the low- and high-dose groups to a similar extent during acute hypoxia. Histopathol. alterations of gut mucosa obsd. 9036-21-9 and 106730-54-5 which are cas registry numbers of substances are two of reagents here. in the control group were minimized by olprinone infusion dose-independently, accompanied by redn. of mortality rate of the animals. Olprinone slows progression of intestinal mucosal acidosis and gut barrier dysfunction, concurrently with preservation of microscopic structures, through both flow-dependent and -independent mechanisms under acute hypoxia. Such properties of olprinone may serve to protect the host under insult. .