Search

The facial nerve was transected in rats at different postnatal ages, from birth to early adulthood. NADPH-diaphorase histochemistry was performed to analyze the induction of nitric oxide synthase, the synthetic enzyme of the free radical nitric oxide, in injured facial motoneurons. In addition,in situnick-end labeling of DNA fragmentation (TUNEL technique) was performed after axotomy at birth, to verify the occurrence of apoptosis in the damaged facial motoneurons. A striking age-dependency was found in the induction of nitric oxide synthase activity in axotomized facial motoneurons. NADPH-diaphorase positivity was not detectable in these neurons 1 and 2 days after axotomy at birth, when apoptotic changes were evident and marked. In addition, NADPH-diaphorase staining was hardly detectable in the facial nucleus 4 days after axotomies at birth, when extensive motoneuron loss was evident. NADPH-diaphorase positivity was instead induced in the facial motoneurons axotomized from the end of the first postnatal week to adulthood, when the nerve cell loss was less severe than in newborns. However, the time course of the enzyme activity induction varied considerably in relation to the animals' age. These findings are discussed in relation to the role of nitric oxide in motoneuron death or protective response to injury and of oxidative stress in neurodegeneration.

Purpose: The coexistence of mitral regurgitation (MR) and severe aortic stenosis is a common problem in elderly patients that limits the indication for percutaneous aortic prosthesis (TAVI). However, recent publications indicate a decrease in MR after TAVI because of the improvement of left ventricle (LV) hemodynamic conditions. The aim of our study was to investigate clinical and echocardiographic predictors of MR after TAVI. Methods: We included patients undergoing TAVI from May 2008 to November 2012. It was performed a 3D transesophageal echocardiogram during the procedure and a transthoracic echocardiogram before discharge and 12 months after implantation. We studied the etiology of MR before procedure, LV ejection fraction, chambers volume, pulmonary hypertension and tricuspid regurgitation, as well as clinical and technical variables related to the procedure. Results: 90 patients underwent TAVI successfully (Table). At the beginning, 21% of patients had MR at least grade III/IV. After TAVI, 84.4% of patients showed no change in MR degree, 12.2% improved and only 3.3% worsened. Variables related with MR worsening were rheumatic MR etiology, history of atrial fibrillation (AF) and the coexistence of significant tricuspid regurgitation (TR) in the baseline study (p <0.04, p <0.01; p <0.03, respectively). Conclusions: In patients undergoing TAVI, the rheumatic etiology of MR, the previous history of AF and significant TR coexistence were factors related to MR worsening after the procedure.   Baseline characteristics. N = 90Age81.9 ± 6.9Women49 (54.4%)LVEF56 % ± 11.6Previous stroke16 (18%)Previous AF36 (42.4%)Baseline creatinine serum level1.3 mg/dl ± 0.5EuroSCORE16.8 ± 9.2Transfemoral approach71 (79.8%)Transapical approach18 (20.2%) LVEF: ejection fraction of the left ventricle. AF: atrial fibrillation

In the isolated perfused rat heart the main released purine catabolite is uric acid. Furthermore purine nucleosides and bases added to the perfusion buffer are oonverted into uric acid at the passage through the coronary circulation. In the human heart a low xanthine oxidase activity has been observed, however few data are available on the release of uric acid. In this work we have determined the purine catabolites by HPLC in deproteinated blood samples collected from the aorta and coronary sinus in human patients submitted to routine cardiac catheterization, whole blood concentration of uric acid increased from 105 ± 21 uM in aortic blood to 189 ± 25 uM in coronary sinus blood, while the concentrations of xanthine and hypoxanthine were slightly decreased or in a few patients were unchanged. Only trace amounts of inosine and adenosine could be detected. The amount of the released uric acid is consistent with the xanthine oxidase activity in human heart. From these results it appears that in the human heart under rest conditions uric acid is the main purine catabolite and that the purine output exceeds the reuptake. In basal conditions the net purine output (including uric acid) should correspond to myocardial de novo synthesis of purine nucleotides. The formation of uric acid must be taken into account in the study of purine metabolism also in human heart.