In:
The FASEB Journal, Wiley, Vol. 26, No. S1 ( 2012-04)
Abstract:
Pulmonary vasoconstriction is an important mechanism contributing to the development of pulmonary hypertension after pulmonary embolism (PE) probably due to increased production of reactive oxygen species (ROS). Our aim was to investigate the change of NO production and to determine the effect of ROS scavenger, Tempol, on pulmonary hypertension after PE. Using the model of in vivo pulmonary embolism and isolated, perfused rat lungs we measured the perfusion pressure and its changes after sodium nitroprusside administration and after NO synthase inhibition by L‐NAME. We used 6 groups of Wistar male rats: NN : control group + sodium nitroprusside (SN) (n=5), EN : PE + SN (n=5), TN : Tempol + PE + SN (n=5), NL : control group + L‐Name (n=5), EL : PE + L‐Name (n=5), TL : Tempol + PE + L‐name (n=5). Tempol was administered before PE. PE caused higher pulmonary pressure. Tempol‐treated rats (TN, TL) had significantly lower perfusion pressure than the animals without Tempol (EN, EL). The decrease of perfusion pressure after application of SN was higher in EN than in NN. Administration of L‐Name after PE (EL) increased the pressure more than in the controls (NL). PE also caused increased NOx production. ROS‐induced vasoconstriction contributed to the pulmonary hypertension after PE. Also, PE caused increased production of NO and NOx. Tempol decreased pulmonary hypertension after PE by inhibiting the free radicals production.
Type of Medium:
Online Resource
ISSN:
0892-6638
,
1530-6860
DOI:
10.1096/fasebj.26.1_supplement.lb627
Language:
English
Publisher:
Wiley
Publication Date:
2012
detail.hit.zdb_id:
1468876-1
detail.hit.zdb_id:
639186-2
SSG:
12
