1. Nitric oxide mediates neurologic injury after hypothermic circulatory arrest 
Elaine E Tseng, MD, Malcolm V Brock, MD, Mary S Lange, MA, Juan C Troncoso, MD, Charles J Lowenstein, MD, Mary E Blue, PhD, Michael V Johnston, MD, William A Baumgartner, MD 
The Annals of Thoracic Surgery 
Volume 67, Issue 1, Pages (January 1999)
DOI: /S (98)

2. Fig 1
In vivo measurement of NOS activity as citrulline concentration (μmol/L) over time. Peak levels of citrulline were plotted over three time periods: HCA, reperfusion CPB 2 to 8 hours after HCA. (∗ = p < 0.05, 2 to 8 hours versus baseline. ∗∗ = p < 0.05, 17477AR versus untreated HCA control [Ctl] group.)
The Annals of Thoracic Surgery  , 65-71DOI: ( /S (98) )

3. Fig 2
Nitric oxide synthase (NOS) activity (pmol 14C-citrulline · mg protein−1 · min−1) in the dorsolateral neocortex in untreated control dogs, HCA dogs at 72 hours, and 17477AR-treated dogs at 72 hours after HCA.∗p < 0.05 compared with untreated HCA dogs.
The Annals of Thoracic Surgery  , 65-71DOI: ( /S (98) )

4. Fig 3
Tympanic membrane temperatures (°C) during cooling CPB, HCA, rewarming CPB, and recovery.
The Annals of Thoracic Surgery  , 65-71DOI: ( /S (98) )

5. Fig 4
Neurologic deficit score of HCA dogs versus 17477AR-treated dogs over time. (∗ = p < 0.05, 17477AR versus HCA alone.)
The Annals of Thoracic Surgery  , 65-71DOI: ( /S (98) )

6. Fig 5
Treatment with 17477AR reduced necrosis 72 hours after HCA, as seen by hemotoxylin and eosin–stained sections of the CA1 region of the hippocampus (40× magnification): (A) normal untreated control dog; (B) HCA dog at 72 hours (arrows indicate necrosis); (C) dog treated with 17477AR after HCA.
The Annals of Thoracic Surgery  , 65-71DOI: ( /S (98) )