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M NaCl intake and water intake, and bilateral injections of the selective mu-OR antagonist D-Phe-Cys-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) in the doses of 0.5, 1, and 2 nmol into the CeA produced a dose-related decrease of 0.3 M NaCl and water intake induced by DAMGO 2 nmol into the same site. In rats treated with the diuretic furosemide (10 mg/kg b.w.) click here combined with the angiotensin-converting enzyme inhibitor captopril (5 mg/kg b.w.) injected subcutaneously, bilateral injections of DAMGO 2 nmol into the CeA increased 0.3 M NaCl intake and water intake and the blockade of mu-ORs with CTAP 1 nmol injected into the CeA reduced the increase in 0.3 M NaCl intake and water intake induced by DAMGO 2 nmol into the same site. Bilateral injections of DAMGO into the CeA did not change urinary volume, sodium urinary excretion and mean arterial pressure, but increased activity. Thus stimulating mu-ORs in the CeA increases hypertonic sodium intake, whereas antagonizing these sites inhibits hypertonic sodium intake. Together, our results implicate mu-ORs in the CeA in a positive regulation of sodium intake. (c) 2012 IBRO. Published by Elsevier Ltd.

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“Objectives: Various types of surgical and interventional procedures have been reported to cause cardiac sympathetic denervation. We aimed at evaluating the effects of coronary artery bypass grafting (CABG) in cardiac sympathetic AZD1080 innervation through meta-iodobenzyl-guanidine (MIBG) imaging.

Methods: MIBG imaging was performed in 21 patients with coronary artery disease (CAD) 1 day before and 1 week and 6 months after CABG with concomitant Microtubule Associated measurements of corrected QT interval. In each study we evaluated MIBG defect score in a 16-segment left ventricular model, MIBG-defect size (percent) from generated polar

maps, and heart/mediastinum ratio.

Results: Mean MIBG defect score and size were increased (32 +/- 9.5 vs 24 +/- 5, P < .0001, and 49.5% +/- 20.4% vs 37% +/- 8.7%, P = .004, respectively) and mean heart/mediastinum ratio was reduced (1.5 +/- 0.4 vs 1.9 +/- 0.3, P < .0001) at 1 week after CABG. At 6 months these indices had no significant differences compared with their pre-CABG values. Mean corrected QT interval demonstrated no significant changes. Increase in MIBG score in the second imaging was associated with adverse events related to arrhythmia and myocardial dysfunction during the 6-month follow-up period in a binary logistic regression model.

Conclusions: CABG is associated with clinically important but reversible reduction in cardiac sympathetic nerve function, with periprocedural effects (cardioplegia, hypothermia, ischemia, direct nerve injury) being possible mechanisms for this finding. (J Thorac Cardiovasc Surg 2012;144:210-6)”
“Inhibition of return (IOR) is a phenomenon thought to reflect a mechanism to protect the organism from redirecting attention to previously scanned insignificant locations.