These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: [Preventive effect of endothelial nitric oxide synthase gene transfer on chronic hypoxic pulmonary hypertension in rats].
    Author: Jin Q, Zhang TZ, Chen WM, Zhou J, Liu XJ.
    Journal: Zhongguo Wei Zhong Bing Ji Jiu Yi Xue; 2009 Apr; 21(4):222-5. PubMed ID: 19374790.
    Abstract:
    OBJECTIVE: To investigate the preventive effect of endothelial nitric oxide synthase (eNOS) gene transfer on chronic hypoxic pulmonary hypertension (CHPH) in rats. METHODS: Twenty-four male Wistar rats were randomly divided into four groups with 6 rats in each group: normoxia group (group N), hypoxia group (group H), hypoxia with LacZ group (group H-LacZ) and hypoxia with eNOS group (group H-eNOS). AdCMVceNOS, AdCMVLacZ or normal saline (NS) was injected intratracheally 3 days before the beginning of exposure to normoxia or hypoxia. Rats in group H-eNOS received 50 microl of AdCMVceNOS (5 x 10(12)pfu/L), rats in group H-LacZ received equal dose of AdCMVLacZ, rats in group N and group H received equal dose of NS. Hemodynamic parameters [including mean systemic arterial pressure (MSAP), heart rate (HR) and mean pulmonary arterial pressure (MPAP)], pulmonary vascular remodeling (percentage of muscularized arteries in small pulmonary vessels) and right ventricular hypertrophy (ratio of right ventricle to left ventricle + septum weight) were measured after 2 weeks of exposure to normoxia or hypoxia. The expression of eNOS, cyclic guanosine monophosphate (cGMP) and nitric oxide (NO) level were also measured in lungs. RESULTS: The MPAP, right ventricular hypertrophy index and pulmonary vascular remodeling in rats in group H-eNOS were obviously lower than those in group H and H-LacZ, but higher than that in group N (all P<0.01). There was no significant difference with regard to HR and MSAP in rats in all groups (all P>0.05). The eNOS protein in group H and H-LacZ was obviously higher than that in group N, but obviously lower than that in group H-eNOS (all P<0.01). The NO level in rat lungs in group H and H-LacZ was obviously lower than that in group N, and value in group H-eNOS was higher than that in the other groups (P<0.05 or P<0.01). With regard to cGMP in rat lungs, there was no significant difference among group N, H and H-LacZ (all P>0.05), but they were all obviously lower than that in group H-eNOS (all P<0.01). CONCLUSION: Intratracheal eNOS gene transfer upregulates the activity of eNOS protein, elevates the level of NO/cGMP in lungs, and alleviates CHPH in rats.
    [Abstract] [Full Text] [Related] [New Search]