TY - JOUR
T1 - Antibody-mediated neutrophil depletion preserves pulmonary vasomotor function
AU - Sheridan, Brett C.
AU - McIntyre, Robert C.
AU - Meldrum, Daniel R.
AU - Cleveland, Joseph C.
AU - Agrafojo, Jeanette
AU - Eisenach, John H.
AU - Harken, Alden H.
AU - Fullerton, David A.
N1 - Funding Information:
1This work was supported by NIH Grant R29HL49398. 2To whom correspondence should be addressed at Cardiothoracic Surgery, Box C-310, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Denver, CO 80262. Fax: (303) 270-3065.
PY - 1996/4
Y1 - 1996/4
N2 - Neutrophil depletion is commonly used to examine the role of neutrophils in lung injury. However, the effect of neutrophil depletion per se on mechanisms of pulmonary vascular smooth muscle relaxation is unknown. The purpose of this study was to examine the effect of neutropenia on the following mechanisms of cGMP-mediated pulmonary vasorelaxation: (1) receptor- dependent endothelium-dependent relaxation (response to acetylcholine (ACh)), (2) receptor-independent endothelium-dependent relaxation (response to the calcium ionophore A23187), and (3) endothelium-independent relaxation (response to sodium nitroprusside (SNP)). Neutropenia (<75 neutrophils/μl) was induced with anti-neutrophil antibody serum 24 hr prior to lung harvest in five rats. Saline-injected rats were controls (n = 5). Dose-response curves to ACh, A23187, and SNP were generated in isolated pulmonary artery rings preconstricted with phenylepherine. Statistical comparison was performed using one-way ANOVA with post-hoc Bonferroni-Dunn, and P < 0.05 was accepted as significant. Relaxation to ACh, A23187, and SNP was complete in both control and neutropenic rats. Thus, antibody-mediated depletion does not impair endothelial-dependent or -independent cGMP-mediated pulmonary vasorelaxation.
AB - Neutrophil depletion is commonly used to examine the role of neutrophils in lung injury. However, the effect of neutrophil depletion per se on mechanisms of pulmonary vascular smooth muscle relaxation is unknown. The purpose of this study was to examine the effect of neutropenia on the following mechanisms of cGMP-mediated pulmonary vasorelaxation: (1) receptor- dependent endothelium-dependent relaxation (response to acetylcholine (ACh)), (2) receptor-independent endothelium-dependent relaxation (response to the calcium ionophore A23187), and (3) endothelium-independent relaxation (response to sodium nitroprusside (SNP)). Neutropenia (<75 neutrophils/μl) was induced with anti-neutrophil antibody serum 24 hr prior to lung harvest in five rats. Saline-injected rats were controls (n = 5). Dose-response curves to ACh, A23187, and SNP were generated in isolated pulmonary artery rings preconstricted with phenylepherine. Statistical comparison was performed using one-way ANOVA with post-hoc Bonferroni-Dunn, and P < 0.05 was accepted as significant. Relaxation to ACh, A23187, and SNP was complete in both control and neutropenic rats. Thus, antibody-mediated depletion does not impair endothelial-dependent or -independent cGMP-mediated pulmonary vasorelaxation.
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U2 - 10.1006/jsre.1996.0176
DO - 10.1006/jsre.1996.0176
M3 - Article
C2 - 8606514
AN - SCOPUS:0029863390
SN - 0022-4804
VL - 62
SP - 74
EP - 78
JO - Journal of Surgical Research
JF - Journal of Surgical Research
IS - 1
ER -