[Effect of products released by activated neutrophils on pulmonary arterial pressure].
Using organ perfusing methods, the effect of activated neutrophils on pulmonary arterial pressure was examined. Lung of the rats were perfused with warm (37 degrees C) Krebs solution in constant flow rate. Perfusing pressure was obviously increased when adding activated PMN to the perfusate and permeability of pulmonary capillaries increased too. Elastase and oxygen free radical (OFR) were released by activated PMN. Human neutrophil elastase (HNE) and oxygen free radical produced from the reaction between xanthine and xanthine oxidase could inhibit PGI2 production by cultured bovine pulmonary arterial endothelial cells. OFR increased the tension of rabbit pulmonary arterial ring, and this effect was independent on endothelial cells. Results suggested that activated neutrophils and products released by them could directly cause the constriction of pulmonary arterial smooth muscle or inhibit PGI2 production which would increase the tension of pulmonary vessels. All this may play role in pathogenesis of pulmonary hypertension.
Yan
Y Z
YZ
Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000818:Animals; D001794:Blood Pressure; D005609:Free Radicals; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology*; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular; D009504:Neutrophils / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism; D010196:Pancreatic Elastase / Q000378:metabolism*; D011651:Pulmonary Artery / Q000502:physiology*; D051381:Rats
D005609:Free Radicals; D015121:6-Ketoprostaglandin F1 alpha; D010196:Pancreatic Elastase; D010100:Oxygen