To evaluate the mechanisms involved in onset of pulmonary edema and the stress due to mechanical ventilation, we used 18 anaesthetised mechanically ventilated pigs, divided into three groups. Group 1 was ventilated with increasing tidal volumes (VT). Group 2 was treated with E. coli LPS (20 microng/kg/h i.v.) for 180 min and was ventilated with basal VT. Group 3 was ventilated with increasing VT and treated with LPS as Group 2. At 180 min of experimental time, Group 1 and 3 received L-NAME (10 mg/kg i.v.), an inhibitor of nitric oxide (NO) synthases. Our results show that increasing VT counterbalances the pulmonary hypertension due to endotoxic shock and, favouring NO release, improves endothelial capillary permeability, preventing edema formation
Analisi dei meccanismi responsabili dell’edema polmonare / S. Mazzola, B. Ciminaghi, M. Albertini, M.G. Clement. - In: ATTI DELLA SOCIETA' ITALIANA DELLE SCIENZE VETERINARIE. - ISSN 1721-1980. - 56:(2002), pp. 63-64. ((Intervento presentato al 56. convegno LVI Congresso SISVet tenutosi a Giardini Naxos, Messina nel 2002.
Analisi dei meccanismi responsabili dell’edema polmonare
S. MazzolaPrimo
;M. AlbertiniPenultimo
;M.G. ClementUltimo
2002
Abstract
To evaluate the mechanisms involved in onset of pulmonary edema and the stress due to mechanical ventilation, we used 18 anaesthetised mechanically ventilated pigs, divided into three groups. Group 1 was ventilated with increasing tidal volumes (VT). Group 2 was treated with E. coli LPS (20 microng/kg/h i.v.) for 180 min and was ventilated with basal VT. Group 3 was ventilated with increasing VT and treated with LPS as Group 2. At 180 min of experimental time, Group 1 and 3 received L-NAME (10 mg/kg i.v.), an inhibitor of nitric oxide (NO) synthases. Our results show that increasing VT counterbalances the pulmonary hypertension due to endotoxic shock and, favouring NO release, improves endothelial capillary permeability, preventing edema formationPubblicazioni consigliate
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