Impairment of endothelial-dependent pulmonary vasorelaxation after mesenteric ischemia/reperfusion

D. A. Fullerton, J. H. Eisenach, Randall S Friese, J. Agrafojo, B. C. Sheridan, Jr McIntyre R.C.

Research output: Contribution to journalArticle

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Abstract

Background. A major hemodynamic feature of acute lung injury is pulmonary hypertension caused by pulmonary vasoconstriction. Impairment of the mechanisms of pulmonary vasorelaxation may contribute to this pulmonary vasoconstriction. This study examined the effect of mesenteric ischemia/reperfusion (I/R) on lung neutrophil accumulation and endothelial- dependent and -independent cyclic 3'-5' guanosine monophosphate-mediated pulmonary vasorelaxation in rats. Methods. Rats were studied after 1 hour of superior mesenteric artery occlusion and 2 hours of reperfusion. Lung neutrophil accumulation was determined by myeloperoxidase assay (MPO). The following mechanisms of pulmonary vasorelaxation were studied in isolated pulmonary artery rings by generating dose response curves (10-9 to 10- 6mol/L): (1) receptor-dependent, endothelial-dependent relaxation (response to acetylcholine), (2) receptor-independent, endothelial-dependent relaxation (response to the calcium ionophore, A23187), and (3) endothelial-independent relaxation (response to sodium nitroprusside [SNP]). Results. Lung MPO activity was significantly increased from 2.4 ± 0.2 units/gm lung weight in controls to 10.3 ± 0.4 after mesenteric I/R (p < 0.05). The vasorelaxation response to SNP was not different after mesenteric I/R, but vasorelaxation by both acetylcholine and A23187 were significantly impaired. Conclusions. Endothelial-dependent pulmonary vasorelaxation is significantly impaired after mesenteric I/R. Such impairment of pulmonary vasorelaxation may help tip the net balance of pulmonary vasomotor tone toward vasoconstriction and contribute to the pulmonary hypertension seen in acute lung injury.

Original languageEnglish (US)
Pages (from-to)879-884
Number of pages6
JournalSurgery
Volume120
Issue number5
DOIs
StatePublished - 1996
Externally publishedYes

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Vasodilation
Reperfusion
Lung
Vasoconstriction
Acute Lung Injury
Calcimycin
Nitroprusside
Pulmonary Hypertension
Peroxidase
Mesenteric Ischemia
Neutrophils
Superior Mesenteric Artery
Calcium Ionophores
Cholinergic Receptors
Pulmonary Artery
Acetylcholine
Hemodynamics
Weights and Measures

ASJC Scopus subject areas

  • Surgery

Cite this

Fullerton, D. A., Eisenach, J. H., Friese, R. S., Agrafojo, J., Sheridan, B. C., & McIntyre R.C., J. (1996). Impairment of endothelial-dependent pulmonary vasorelaxation after mesenteric ischemia/reperfusion. Surgery, 120(5), 879-884. https://doi.org/10.1016/S0039-6060(96)80098-5

Impairment of endothelial-dependent pulmonary vasorelaxation after mesenteric ischemia/reperfusion. / Fullerton, D. A.; Eisenach, J. H.; Friese, Randall S; Agrafojo, J.; Sheridan, B. C.; McIntyre R.C., Jr.

In: Surgery, Vol. 120, No. 5, 1996, p. 879-884.

Research output: Contribution to journalArticle

Fullerton, DA, Eisenach, JH, Friese, RS, Agrafojo, J, Sheridan, BC & McIntyre R.C., J 1996, 'Impairment of endothelial-dependent pulmonary vasorelaxation after mesenteric ischemia/reperfusion', Surgery, vol. 120, no. 5, pp. 879-884. https://doi.org/10.1016/S0039-6060(96)80098-5
Fullerton, D. A. ; Eisenach, J. H. ; Friese, Randall S ; Agrafojo, J. ; Sheridan, B. C. ; McIntyre R.C., Jr. / Impairment of endothelial-dependent pulmonary vasorelaxation after mesenteric ischemia/reperfusion. In: Surgery. 1996 ; Vol. 120, No. 5. pp. 879-884.
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abstract = "Background. A major hemodynamic feature of acute lung injury is pulmonary hypertension caused by pulmonary vasoconstriction. Impairment of the mechanisms of pulmonary vasorelaxation may contribute to this pulmonary vasoconstriction. This study examined the effect of mesenteric ischemia/reperfusion (I/R) on lung neutrophil accumulation and endothelial- dependent and -independent cyclic 3'-5' guanosine monophosphate-mediated pulmonary vasorelaxation in rats. Methods. Rats were studied after 1 hour of superior mesenteric artery occlusion and 2 hours of reperfusion. Lung neutrophil accumulation was determined by myeloperoxidase assay (MPO). The following mechanisms of pulmonary vasorelaxation were studied in isolated pulmonary artery rings by generating dose response curves (10-9 to 10- 6mol/L): (1) receptor-dependent, endothelial-dependent relaxation (response to acetylcholine), (2) receptor-independent, endothelial-dependent relaxation (response to the calcium ionophore, A23187), and (3) endothelial-independent relaxation (response to sodium nitroprusside [SNP]). Results. Lung MPO activity was significantly increased from 2.4 ± 0.2 units/gm lung weight in controls to 10.3 ± 0.4 after mesenteric I/R (p < 0.05). The vasorelaxation response to SNP was not different after mesenteric I/R, but vasorelaxation by both acetylcholine and A23187 were significantly impaired. Conclusions. Endothelial-dependent pulmonary vasorelaxation is significantly impaired after mesenteric I/R. Such impairment of pulmonary vasorelaxation may help tip the net balance of pulmonary vasomotor tone toward vasoconstriction and contribute to the pulmonary hypertension seen in acute lung injury.",
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AU - Fullerton, D. A.

AU - Eisenach, J. H.

AU - Friese, Randall S

AU - Agrafojo, J.

AU - Sheridan, B. C.

AU - McIntyre R.C., Jr

PY - 1996

Y1 - 1996

N2 - Background. A major hemodynamic feature of acute lung injury is pulmonary hypertension caused by pulmonary vasoconstriction. Impairment of the mechanisms of pulmonary vasorelaxation may contribute to this pulmonary vasoconstriction. This study examined the effect of mesenteric ischemia/reperfusion (I/R) on lung neutrophil accumulation and endothelial- dependent and -independent cyclic 3'-5' guanosine monophosphate-mediated pulmonary vasorelaxation in rats. Methods. Rats were studied after 1 hour of superior mesenteric artery occlusion and 2 hours of reperfusion. Lung neutrophil accumulation was determined by myeloperoxidase assay (MPO). The following mechanisms of pulmonary vasorelaxation were studied in isolated pulmonary artery rings by generating dose response curves (10-9 to 10- 6mol/L): (1) receptor-dependent, endothelial-dependent relaxation (response to acetylcholine), (2) receptor-independent, endothelial-dependent relaxation (response to the calcium ionophore, A23187), and (3) endothelial-independent relaxation (response to sodium nitroprusside [SNP]). Results. Lung MPO activity was significantly increased from 2.4 ± 0.2 units/gm lung weight in controls to 10.3 ± 0.4 after mesenteric I/R (p < 0.05). The vasorelaxation response to SNP was not different after mesenteric I/R, but vasorelaxation by both acetylcholine and A23187 were significantly impaired. Conclusions. Endothelial-dependent pulmonary vasorelaxation is significantly impaired after mesenteric I/R. Such impairment of pulmonary vasorelaxation may help tip the net balance of pulmonary vasomotor tone toward vasoconstriction and contribute to the pulmonary hypertension seen in acute lung injury.

AB - Background. A major hemodynamic feature of acute lung injury is pulmonary hypertension caused by pulmonary vasoconstriction. Impairment of the mechanisms of pulmonary vasorelaxation may contribute to this pulmonary vasoconstriction. This study examined the effect of mesenteric ischemia/reperfusion (I/R) on lung neutrophil accumulation and endothelial- dependent and -independent cyclic 3'-5' guanosine monophosphate-mediated pulmonary vasorelaxation in rats. Methods. Rats were studied after 1 hour of superior mesenteric artery occlusion and 2 hours of reperfusion. Lung neutrophil accumulation was determined by myeloperoxidase assay (MPO). The following mechanisms of pulmonary vasorelaxation were studied in isolated pulmonary artery rings by generating dose response curves (10-9 to 10- 6mol/L): (1) receptor-dependent, endothelial-dependent relaxation (response to acetylcholine), (2) receptor-independent, endothelial-dependent relaxation (response to the calcium ionophore, A23187), and (3) endothelial-independent relaxation (response to sodium nitroprusside [SNP]). Results. Lung MPO activity was significantly increased from 2.4 ± 0.2 units/gm lung weight in controls to 10.3 ± 0.4 after mesenteric I/R (p < 0.05). The vasorelaxation response to SNP was not different after mesenteric I/R, but vasorelaxation by both acetylcholine and A23187 were significantly impaired. Conclusions. Endothelial-dependent pulmonary vasorelaxation is significantly impaired after mesenteric I/R. Such impairment of pulmonary vasorelaxation may help tip the net balance of pulmonary vasomotor tone toward vasoconstriction and contribute to the pulmonary hypertension seen in acute lung injury.

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