Document Detail

Pulmonary hypertension in a murine model of the acquired immunodeficiency syndrome.
MedLine Citation:
PMID:  8025749     Owner:  NLM     Status:  MEDLINE    
Rapidly accumulating evidence suggests that a proportion of patients with acquired immunodeficiency syndrome (AIDS) develop hypertensive pulmonary vascular disease reminiscent of primary pulmonary hypertension. As an initial step to explore the link between AIDS and hypertensive pulmonary vascular disease, the present study determined whether pulmonary hypertension is present in a well-characterized murine model of retrovirus-induced immunodeficiency. In agreement with previous reports, mice infected with the LP-BM5 murine leukemia virus developed polyclonal B and T cell activation followed by progressive and severe B and T cell immunodeficiency. At 12 wk postinfection, when persistent immunodeficiency was established, mice were anesthetized, and right ventricular systolic pressure was determined in open-chest, mechanically ventilated animals. Mean right ventricular systolic pressure was 14.7 +/- 1.3 mm Hg in control animals and was increased significantly to 22.5 +/- 3.2 mm Hg in virus-infected mice. Right ventricular hypertrophy was also present in infected mice as evidenced by a 27% increase in the ratio of right to left ventricular weights; there were no group-dependent differences in the left ventricular to total-body weight ratio. Morphometric evaluation indicated that medial thickness in muscularized pulmonary arteries, expressed as a percentage of the external diameter, was 9.6 +/- 0.4% in control lungs and increased to 14.4 +/- 0.5% in lungs from infected animals. Qualitative histopathologic analysis suggested increased perivascular collagen deposition in lungs from infected animals relative to control animals. Unlike AIDS patients with pulmonary hypertension, infected mice did not exhibit plexiform lesions or intimal fibrosis of the pulmonary arteries.(ABSTRACT TRUNCATED AT 250 WORDS)
M N Gillespie; C L Hartsfield; W N O'Connor; D A Cohen
Related Documents :
8997619 - Nitric oxide regulation of tp receptor-mediated pulmonary vasoconstriction in the anest...
1153409 - Comparison of the effects of prostaglandins f1alpha, f2alpha, f1beta, and f2beta on the...
10490569 - Early therapeutic experience with the endothelin antagonist bq-123 in pulmonary hyperte...
3921279 - Dose requirements and hemodynamic effects of transdermal nitroglycerin compared with pl...
3297489 - Thromboxane synthesis inhibition reverses group b streptococcus-induced pulmonary hyper...
3923869 - Acute cardiopulmonary effects of nitroglycerin in canine oleic acid pulmonary edema.
7148649 - Frequency analysis approach to the origin of the first and second heart sounds.
18398329 - Pulse pressure or dipping pattern: which one is a better cardiovascular risk marker in ...
6624679 - Noninvasive determination of systolic, diastolic and end-systolic blood pressure in neo...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of respiratory and critical care medicine     Volume:  150     ISSN:  1073-449X     ISO Abbreviation:  Am. J. Respir. Crit. Care Med.     Publication Date:  1994 Jul 
Date Detail:
Created Date:  1994-08-10     Completed Date:  1994-08-10     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9421642     Medline TA:  Am J Respir Crit Care Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  194-9     Citation Subset:  AIM; IM; X    
Division of Pharmacology and Experimental Therapeutics, College of Pharmacy, Lexington, Kentucky.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Hypertension, Pulmonary / complications*,  pathology,  physiopathology
Lung / pathology
Mice, Inbred C57BL
Murine Acquired Immunodeficiency Syndrome / complications*,  pathology,  physiopathology
Grant Support

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Mechanism by which the prone position improves oxygenation in acute lung injury.
Next Document:  Dose-responsive increases in pulmonary fibrosis after inhalation of asbestos.