Assessing the impact of cerebral injury after cardiac surgery: will determining the mechanism reduce this injury? William A Baumgartner, MD, Peter L.

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Presentation transcript:

Assessing the impact of cerebral injury after cardiac surgery: will determining the mechanism reduce this injury? William A Baumgartner, MD, Peter L Walinsky, MD, Jorge D Salazar, MD, Elaine E Tseng, MD, Malcolm V Brock, MD, John R Doty, MD, J.Mark Redmond, MD, Mary E Blue, PhD, Maura A Goldsborough, Juan C Troncoso, MD, Michael V Johnston, MD The Annals of Thoracic Surgery Volume 67, Issue 6, Pages 1871-1873 (June 1999) DOI: 10.1016/S0003-4975(99)00445-2

Fig 1 Proposed mechanism of neuronal cell injury and death after hypoxia and ischemia. An excessive amount of glutamate overactivates NMDA receptors. This causes an intracellular influx of calcium resulting in the production of a variety of agents, including nitric oxide synthase (NOS). This leads to the production of nitric oxide (NO), which acts as a neurotoxin, resulting in cellular death. The Annals of Thoracic Surgery 1999 67, 1871-1873DOI: (10.1016/S0003-4975(99)00445-2)

Fig 2 In vivo measurement of NOS activity as citrulline concentration (μM) over time (Reproduced with permission by Tseng EE, et al [8]). The Annals of Thoracic Surgery 1999 67, 1871-1873DOI: (10.1016/S0003-4975(99)00445-2)