Pulmonary protection by leukotriene synthesis inhibitor BAY X1005 against lipopolysaccharide-induced injury (part 2)

General acceptance of sLTs as major mediators of LPS-induced shock, strengthened by the likelihood that their transcellular synthesis occurs in the pulmonary vascular bed, prompted us to explore whether BAY X1005, a new, potent, selective LT synthesis inhibitor that binds to FLAP and demonstrates systemic anti-inflammatory and antiallergic properties (10,11), can protect blood-perfused lungs against LPS-induced increase in pulmonary arterial perfusion pressure (PAP) and reduce pneumotoxicity of LPS.

ANIMALS AND METHODS
Mongrel rabbits (3.5 to 4 kg body weight) were anesthetized with sodium pentobarbitone (30 mg/kg intravenously). Heparin (5000 U) was administered intravenously, and the rabbits were exsanguinated through a cannula inserted in the carotid artery. Drained blood was collected for later use in lung perfusion.

The trachea, pulmonary artery and left atrium were can-nulated, and the preparation was connected to a recirculating perfusion circuit (total of 130 mL) consisting of a heated (37°C) open reservoir, a bubble-drop depulsator, a heat exchanger and a roller pump. After the residual blood was flushed from the pulmonary circulation, perfusion was initiated via the pulmonary artery with a Krebs-Henseleit bicarbonate solution containing 0.02% bovine albumin and bubbled with 95% oxygen and 5% carbon dioxide. If you have a medical condition that requires serious treatment for less money, you will appreciate this affordable my canadian pharmacy that offers only best quality medications with fast guaranteed delivery.

This entry was posted in Lung injury and tagged BAYX1005, Leuko-trienes, Leukotriene synthase inhibitors, Lipopolysaccharide, Lung injury, Septic shock.