1. Delayed inhaled carbon monoxide mediates the regression of established neointimal lesions 
Michael Madigan, MD, Fateh Entabi, MD, Brian Zuckerbraun, MD, Patricia Loughran, PhD, Edith Tzeng, MD 
Journal of Vascular Surgery 
Volume 61, Issue 4, Pages (April 2015)
DOI: /j.jvs
Copyright © Terms and Conditions

2. Fig 1
Effect of delayed administration of inhaled carbon monoxide (CO) on established neointimal lesions. A, Representative photomicrographs of balloon-injured rat carotid arteries at 2 weeks postinjury, 4 weeks postinjury, and 2 weeks postinjury followed by 2 weeks of inhaled CO treatment (250 parts per million [ppm] for 1 hour daily). The autofluorescence demonstrates the elastin layers as well as the neointimal layer (10× magnification). B, Quantification of the neointimal lesion size as represented by intimal area/medial area ratio. The data are represented as mean with standard error of the mean with n = 8-10 animals per treatment group (P < .05 vs 2- and 4-week control groups).
Journal of Vascular Surgery  , DOI: ( /j.jvs )
Copyright © Terms and Conditions

3. Fig 2
Proliferative activity in the injured carotid arteries treated with air or delayed inhaled carbon monoxide (CO). Representative photomicrographs of sections of injured carotid arteries that were treated with 1 hour of inhaled CO (250 parts per million [ppm]) daily for 3 days (40× magnification). This treatment was started 2 weeks postballoon injury. Control animals were maintained in room air and the carotid arteries collected at the same time point (2 weeks + 3 days). Proliferation was detected by Ki67 staining (white cells, labeled by white arrows) and was quantified as a percent of total cells in the arterial wall as determined by DAPI nuclear staining (blue). Quantification was performed on three sections per carotid artery, five to seven animals per treatment group.
Journal of Vascular Surgery  , DOI: ( /j.jvs )
Copyright © Terms and Conditions

4. Fig 3
Apoptosis within the injured carotid arteries treated with air or delayed inhaled carbon monoxide (CO). A, Representative photomicrographs of sections of injured carotid arteries that were treated with 1 hour of inhaled CO (250 parts per million [ppm]) daily for 3 days. This treatment was started 2 weeks postballoon injury. Control animals were maintained in room air and the carotid arteries collected at the same time point (2 weeks + 3 days). Sections were stained for terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) for apoptosis (red cells), DAPI for nuclei (blue cells), and elastin (green). Vessels were imaged at 10× magnification. B, Quantification of apoptosis in the carotid arteries 3 days after initiating inhaled CO treatment is presented as percent of total cells within the arterial wall *P < .05; data collected from three sections per animals, five to seven animals per treatment group.
Journal of Vascular Surgery  , DOI: ( /j.jvs )
Copyright © Terms and Conditions

5. Fig 4
Autophagy in the carotid artery following carbon monoxide (CO) treatment. Autophagy was determined by microtubule-associated protein light chain 3 (LC3) staining. LC3 I is represented by diffuse cellular staining (red), while LC3II is represented by more punctate staining. The punctate staining indicates the localization of LC3 to autophagosome membranes during autophagy. Representative photomicrographs reveal diffuse LC3 staining with scattered cells with more punctate staining indicating cells undergoing autophagy (n = 4 rats per treatment group; 40× magnification).
Journal of Vascular Surgery  , DOI: ( /j.jvs )
Copyright © Terms and Conditions