Immediate Remote Ischemic Postconditioning Reduces Brain Nitrotyrosine Formation in a Piglet Asphyxia Model

Figure 2

Effect of RIPostC treatment on nitric oxide synthases. (a–c) nNOS levels remain unaffected by RIPostC treatment 48 hours after HI. (a) Representative nNOS staining from the hippocampus at 48 hours after HI in HI alone (upper panel) and HI + RIPostC (lower panel). (b) Mean nNOS scores across multiple brain regions in HI alone and in RIPostC-treated piglets. (c) Overall brain nNOS scores 48 hours after HI. (d–f) RIPostC treatment significantly reduced overall iNOS levels in the brain 48 hours after HI. (d) Representative micrographs of iNOS staining from the hippocampus at 48 hours after HI in HI alone (upper panel) and HI + RIPostC (lower panel). (e) Mean iNOS scores across multiple brain regions in HI alone and in RIPostC-treated piglets. (f) Overall brain iNOS scores 48 hours after HI showing significant reduction in iNOS semiquantitative scoring for the RIPostC-treated group (). (g–i) RIPostC treatment was associated with a significant increase in endothelium-derived NO 48 hours after HI injury. (g) Representative eNOS immunohistochemistry from the hippocampus at 48 hours after HI in HI alone (upper panel) and HI + RIPostC (lower panel). (h) Mean eNOS scores across multiple brain regions in HI alone and in RIPostC-treated piglets. (i) Overall significant increase in brain eNOS semiquantitative scores in RIPostC-treated piglets 48 hours after HI. (a, d, g) For comparison, naïve tissue is shown in the left column. Data are expressed as mean ± SEM in ANOVA, per group, and . dCTX1–3 = dorsal cortex 1–3; mCTX = midtemporal cortex; PYR = pyriform cortex; THAL = thalamus; Caudt = caudate; PTMN = putamen; IC = internal capsule; PvWM = periventricular white matter.

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