Altered brain activation to colorectal distention in visceral hypersensitive maternal-separated rats.

BACKGROUND: Early life trauma can predispose to increased visceral pain perception. Human neuroimaging studies emphasize that altered brain processing may contribute to increased visceral sensitivity. The aim of our study was to evaluate brain responses to painful visceral stimuli in maternal-separated rats before and after acute stress exposure in vivo. METHODS: H(2)(15)O microPET scanning was performed during colorectal distention in maternal-separated rats before and after water avoidance stress. Brain images were anatomically normalized to Paxinos space and analyzed by voxel-based statistical parametric mapping (SPM2). Colorectal induced visceral pain was assessed by recording of the visceromotor response using abdominal muscle electromyography. KEY RESULTS: Colorectal distention (1.0-2.0 mL) evoked a volume-dependent increase in visceromotor response in maternal-separated rats. Stress [water avoidance (WA)] induced an increased visceromotor response to colorectal distention in awake and anesthetized rats. In pre-WA rats, colorectal distention evoked significant increases in regional blood flow in the cerebellum and periaquaductal gray (PAG). Colorectal distention post-WA revealed activation clusters covering the PAG as well as somatosensory cortex and hippocampus. At maximal colorectal distention, the frontal cortex was significantly deactivated. CONCLUSIONS & INFERENCES: WA stress induced increased pain perception as well as activation of the somatosensory cortex, PAG, and hippocampus in maternal-separated rats. These findings are in line with human studies and provide indirect evidence that the maternal separation model mimics the cerebral response to visceral hypersensitivity in humans.

Assessment of systemic inflammatory response (SIR) in patients undergoing radiofrequency ablation or partial liver resection for liver tumors.

INTRODUCTION: Local therapies for liver tumors are considered to be safe. However, cryoablation (CA) has been associated with an exaggerated systemic inflammatory response (SIR). Aim of this study was to assess the degree of SIR after radiofrequency ablation (RFA) in comparison with major (MR) or minor (mR) liver resection. MATERIAL AND METHODS: Thirty-nine patients were treated with RFA (n = 11), MR (n = 10) or mR (n = 18). SIR parameters [white blood count (WBC) and C-reactive protein (CRP)], proinflammatory mediators [IL-6, TNF-alpha and sPLA2], liver damage parameters [AST/ALT] and platelet counts were determined at different time points. The volume of ablated liver was calculated on the first CT after RFA in order to correlate ablated liver volume with liver enzyme release and SIR. All data are expressed as median values with quartiles [25%, 75%]. RESULTS: RFA induced a moderate SIR, as demonstrated by a significant elevation of CRP (77 mg/L vs 3 mg/L), IL-6 (96 pg/ml vs 4 pg/ml) and sPLA2 (41 ng/ml vs 7 ng/ml, p < 0.05). Peak point values of SIR (WBC and CRP at 24 vs 48 h and 48 vs 72 h) and proinflammatory response parameters (24 vs 48 h) occurred earlier after RFA than after mR or MR. Time-to-time comparison revealed even increased levels of CRP (77 mg/L [59, 160]) 24h after RFA when compared to patients undergoing major or minor resection (50 mg/L [28, 66] and 59 mg/L [24, 91], respectively) and increased levels of IL-6 (67 pg/ml [42, 131]) 4 h after RFA when compared to patients undergoing minor resection (29 pg/ml [20, 55]). Postoperative levels of AST and LDH correlated significantly with the ablated liver volume 1h after RFA (RC = 0.860 and RC = 0.868, respectively, p < 0.05). CONCLUSION: RFA induced a moderate SIR of the same magnitude as in patients undergoing partial liver resection. None of the patients showed signs of an exaggerated SIR, as has been reported after cryoablation.