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857 results on '"Caputi, Achille P."'

71. Tumor necrosis factor induces E-selection production in splanchnic artery occlusion shock

Author

Altavilla, Domenica, Squadrito, Francesco, Canale, Patrizia, Ioculano, Mariapatrizia, Campo, Giuseppe M., Squadrito, Giovanni, Saitta, Antonino, and Caputi, Achille P.

Subjects
Arterial occlusions -- Research, Leukocytes -- Observations, Tumor necrosis factor -- Analysis, Biological sciences
Abstract

Use of cloricromene significantly enhances survival of splanchnic artery occlusion (SAO) shocked rats, indicating that tumor necrosis factor and E-selectin are involved in SAO. Cloricromene treated sham-shocked rats survived the five hours observation period whereas SAO shock rats showed a high shock state and all rats died within two hours. The levels of sE-selectin in sham-shocked rats remained the same during the observation. In cloricromene treated SAO shocked rats sE-selectin levels increased significantly.

Published
1995

77. Role of tumor necrosis factor-alpha in acute hypovolemic hemorrhagic shock in rats

Author

Zingarelli, Basilia, Squadrito, Francesco, Altavilla, Domenica, Calapai, Gioacchino, Rosa, Massimo Di, and Caputi, Achille P.

Subjects
Tumor necrosis factor -- Analysis, Hemorrhagic shock -- Physiological aspects, Biological sciences
Abstract

Tumor necrosis factor-alpha (TNF-alpha) functions as a mediator of acute hypovolemic hemorrhagic shock and causes vascular hyporeactivity during the shock in rats. Mean arterial blood pressure is stabilized by the shock by extracting blood continuously from iliac catheter vessels. Hypocontractile nature of aortas of shocked rats to phenylephrine is corrected by administering anti TNF-alpha.

Published
1994

98. Pharmacological inhibition of leukotrienes in an animal model of bleomycin-induced acute lung injury

Author

Crimi Nunzio, Sortino Mariangela, Muià Carmelo, Gili Elisa, Mazzon Emanuela, Genovese Tiziana, Failla Marco, Caputi Achille P, Cuzzocrea Salvatore, and Vancheri Carlo

Subjects
Diseases of the respiratory system, RC705-779
Abstract

Abstract Leukotrienes are increased locally in idiopathic pulmonary fibrosis. Furthermore, a role for these arachidonic acid metabolites has been thoroughly characterized in the animal bleomycin model of lung fibrosis by using different gene knock-out settings. We investigated the efficacy of pharmacological inhibition of leukotrienes activity in the development of bleomycin-induced lung injury by comparing the responses in wild-type mice with mice treated with zileuton, a 5-lipoxygenase inhibitor and MK-571, a cys-leukotrienes receptor antagonist. Mice were subjected to intra-tracheal administration of bleomycin or saline and were assigned to receive either MK-571 at 1 mg/Kg or zileuton at 50 mg/Kg daily. One week after bleomycin administration, BAL cell counts, lung histology with van Gieson for collagen staining and immunohistochemical analysis for myeloperoxidase, IL-1 and TNF-α were performed. Following bleomycin administration both MK-571 and zileuton treated mice exhibited a reduced degree of lung damage and inflammation when compared to WT mice as shown by the reduction of:(i) loss of body weight, (ii) mortality rate, (iii) lung infiltration by neutrophils (myeloperoxidase activity, BAL total and differential cell counts), (iv) lung edema, (v) histological evidence of lung injury and collagen deposition, (vi) lung myeloperoxidase, IL-1 and TNF-α staining. This is the first study showing that the pharmacological inhibition of leukotrienes activity attenuates bleomycin-induced lung injury in mice. Given our results as well as those coming from genetic studies, it might be considered meaningful to trial this drug class in the treatment of pulmonary fibrosis, a disease that still represents a major challenge to medical treatment.

Published
2006
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