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Reduced endothelial nitric oxide synthase in lungs of chronically ventilated preterm lambs

Reduced endothelial nitric oxide synthase in lungs of chronically ventilated preterm lambs Abstract Nitric oxide (NO), produced in lung vascular endothelium and airway epithelium, has an important role in regulating smooth muscle cell growth and tone. Chronic lung disease, a frequent complication of premature birth, is characterized by excess abundance, tone, and reactivity of smooth muscle in the pulmonary circulation and conducting airways, leading to increased lung vascular and airway resistance. Whether these structural and functional changes are associated with diminished pulmonary expression of endothelial nitric oxide synthase (eNOS) protein is unknown. Both quantitative immunoblot analysis and semiquantitative immunohistochemistry showed that there was less eNOS protein in the endothelium of small intrapulmonary arteries and epithelium of small airways of preterm lambs that were mechanically ventilated for 3 wk compared with control lambs born at term. No significant differences were detected for other proteins (inducible NOS, α-smooth muscle actin, and pancytokeratin). Lung vascular and respiratory tract resistances were greater in the chronically ventilated preterm lambs compared with control term lambs. These results support the notion that decreased eNOS in the pulmonary circulation and respiratory tract of preterm lambs may contribute to the pathophysiology of chronic lung disease. chronic lung disease of prematurity bronchopulmonary dysplasia pulmonary vascular resistance airway resistance pulmonary circulation respiratory failure immunohistochemistry Footnotes This work was supported in part by March of Dimes Birth Defects Foundation Grant 6-FY97-0138 (to R. D. Bland), American Heart Association Grant 96014370 (to K. H. Albertine), and National Heart, Lung, and Blood Institute (NHLBI) Grants HL-62512 (to R. D. Bland) and HL-62875 (to K. H. Albertine). Studies included in this report were conducted during the tenure of a Fellowship-to-Faculty Transition Award (to A. N. MacRitchie) supported in part by the Howard Hughes Medical Institute under the Research Resources Program for Medical Schools and NHLBI Research Training Grant T35-HL-07744 for medical students (to S. C. Jensen and A. A. Freestone). Address for reprint requests and other correspondence: R. D. Bland, Dept. of Pediatrics, Univ. of Utah School of Medicine, 50 North Medical Dr., Salt Lake City, UT 84132. The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Copyright © 2001 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Lung Cellular and Molecular Physiology The American Physiological Society

Reduced endothelial nitric oxide synthase in lungs of chronically ventilated preterm lambs

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
1040-0605
eISSN
1522-1504
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Abstract

Abstract Nitric oxide (NO), produced in lung vascular endothelium and airway epithelium, has an important role in regulating smooth muscle cell growth and tone. Chronic lung disease, a frequent complication of premature birth, is characterized by excess abundance, tone, and reactivity of smooth muscle in the pulmonary circulation and conducting airways, leading to increased lung vascular and airway resistance. Whether these structural and functional changes are associated with diminished pulmonary expression of endothelial nitric oxide synthase (eNOS) protein is unknown. Both quantitative immunoblot analysis and semiquantitative immunohistochemistry showed that there was less eNOS protein in the endothelium of small intrapulmonary arteries and epithelium of small airways of preterm lambs that were mechanically ventilated for 3 wk compared with control lambs born at term. No significant differences were detected for other proteins (inducible NOS, α-smooth muscle actin, and pancytokeratin). Lung vascular and respiratory tract resistances were greater in the chronically ventilated preterm lambs compared with control term lambs. These results support the notion that decreased eNOS in the pulmonary circulation and respiratory tract of preterm lambs may contribute to the pathophysiology of chronic lung disease. chronic lung disease of prematurity bronchopulmonary dysplasia pulmonary vascular resistance airway resistance pulmonary circulation respiratory failure immunohistochemistry Footnotes This work was supported in part by March of Dimes Birth Defects Foundation Grant 6-FY97-0138 (to R. D. Bland), American Heart Association Grant 96014370 (to K. H. Albertine), and National Heart, Lung, and Blood Institute (NHLBI) Grants HL-62512 (to R. D. Bland) and HL-62875 (to K. H. Albertine). Studies included in this report were conducted during the tenure of a Fellowship-to-Faculty Transition Award (to A. N. MacRitchie) supported in part by the Howard Hughes Medical Institute under the Research Resources Program for Medical Schools and NHLBI Research Training Grant T35-HL-07744 for medical students (to S. C. Jensen and A. A. Freestone). Address for reprint requests and other correspondence: R. D. Bland, Dept. of Pediatrics, Univ. of Utah School of Medicine, 50 North Medical Dr., Salt Lake City, UT 84132. The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Copyright © 2001 the American Physiological Society

Journal

AJP - Lung Cellular and Molecular Physiology – The American Physiological Society

Published: Oct 1, 2001

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