Inhaled nitric oxide prevents pulmonary endothelial dysfunction after mesenteric ischemia-reperfusion

David A. Fullerton, John H. Eisenach, Robert C. McIntyre, Randall S Friese, Brett C. Sheridan, Gates B. Roe, Jeanette Agrafojo, Anirban Banerjee, Alden H. Harken

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

This study examined the effect of inhaled nitric oxide (NO) on lung neutrophil accumulation and endothelial-dependent and -independent guanosine 3',5'-cyclic monophosphate (cGMP)-mediated mechanisms of pulmonary vasorelaxation after mesenteric ischemia-reperfusion (I/R) in mechanically ventilated rats. Inhaled NO (20 ppm) was administered in two protocols: 1) throughout mesenteric I/R and 2) during mesenteric reperfusion alone. Concentration-response curves were generated (10-9 to 10-6 M) for acetylcholine (ACh), A23187, and sodium nitroprusside (SNP) in isolated pulmonary arterial rings preconstricted with phenylephrine. Lung neutrophil accumulation [myeloperoxidase assay (MPO)] was significantly increased from 2.4 ± 0.2 units/g lung wt in controls to 10.3 ± 0.4 after 1 h of superior mesenteric artery occlusion and 2 h of reperfusion. Lung MPO activity was not different from controls in rats receiving inhaled NO either 1) during mesenteric I/R or 2) during mesenteric reperfusion alone. The concentration- response curves demonstrated significant impairment of pulmonary vasorelaxation by endothelial-dependent mechanisms (response to ACh and A23187) but not endothelial-independent pulmonary vasorelaxation (response to SNP) after mesenteric I/R. This pulmonary vasomotor dysfunction was prevented by administration of inhaled NO during either mesenteric I/R or during mesenteric reperfusion alone. We conclude that inhaled NO prevents lung neutrophil accumulation and pulmonary vascular endothelial dysfunction after mesenteric I/R.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume271
Issue number2 15-2
StatePublished - Aug 1996
Externally publishedYes

Fingerprint

Reperfusion
Nitric Oxide
Lung
Vasodilation
Neutrophils
Calcimycin
Nitroprusside
Peroxidase
Acetylcholine
Mesenteric Ischemia
Superior Mesenteric Artery
Cyclic GMP
Phenylephrine
Blood Vessels

Keywords

  • A23187
  • acetylcholine
  • guanosine 3',5'-cyclic monophosphate
  • neutrophil
  • pulmonary vascular endothelium
  • smooth muscle
  • sodium nitroprusside

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Cell Biology
  • Physiology
  • Physiology (medical)

Cite this

Inhaled nitric oxide prevents pulmonary endothelial dysfunction after mesenteric ischemia-reperfusion. / Fullerton, David A.; Eisenach, John H.; McIntyre, Robert C.; Friese, Randall S; Sheridan, Brett C.; Roe, Gates B.; Agrafojo, Jeanette; Banerjee, Anirban; Harken, Alden H.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 271, No. 2 15-2, 08.1996.

Research output: Contribution to journalArticle

Fullerton, DA, Eisenach, JH, McIntyre, RC, Friese, RS, Sheridan, BC, Roe, GB, Agrafojo, J, Banerjee, A & Harken, AH 1996, 'Inhaled nitric oxide prevents pulmonary endothelial dysfunction after mesenteric ischemia-reperfusion', American Journal of Physiology - Lung Cellular and Molecular Physiology, vol. 271, no. 2 15-2.
Fullerton, David A. ; Eisenach, John H. ; McIntyre, Robert C. ; Friese, Randall S ; Sheridan, Brett C. ; Roe, Gates B. ; Agrafojo, Jeanette ; Banerjee, Anirban ; Harken, Alden H. / Inhaled nitric oxide prevents pulmonary endothelial dysfunction after mesenteric ischemia-reperfusion. In: American Journal of Physiology - Lung Cellular and Molecular Physiology. 1996 ; Vol. 271, No. 2 15-2.
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