1 The aim of this study was to investigate the involvement of peroxynitrite, reactive metabolite originating from nitric oxide and superoxide, in preconditioning of the ischaemic myocardium in rat isolated hearts. 2 Isolated hearts perfused with Krebs-Henseleit solution were preconditioned either by 3 min of coronary artery occlusion (CAO) or by peroxynitrite administration at three dierent concentrations (0.1, 1, 10 mM) for 3 min, followed by 10 min reperfusion and 30 min of CAO. Peroxynitrite, at 1 mM concentration, decreased the incidence of VT from 100% (n=14) to 62% (n=13) and abolished the occurrence of VF (50% in the control group). 3 N-2-mercaptopropionylglycine (MPG, 1 mM ± 10 mM) produced a concentration-dependent inhibition of peroxynitrite signals in luminol chemiluminescence and 67+1% inhibition was observed at 100 mM (n=7). MPG (at 300 mM, n=7) added to the perfusate 10 min prior to ischaemic preconditioning or peroxynitrite infusion and maintained until CAO, signi®cantly reversed the bene®cial eects of the ischaemic and peroxynitrite-treated groups. MPG administration in the peroxynitrite-treated group increased the incidence of VT from 62% (n=13) to 100% (n=10) and total VF from 0% (n=0) to 67% (n=10). Similarly, MPG elevated the incidence of VT from 50% (n=10) to 100% (n=8) in the ischaemic preconditioned group. On its own, MPG did not aect the severity of cardiac arrhythmias. 4 These results suggest that endogenously produced peroxynitrite plays a signi®cant role in the antiarrhythmic eect of ischaemic preconditioning in the rat isolated hearts.
We hypothesized that sex hormones may affect motility disorders because these diseases occur more often in women than in men, and symptoms often occur or worsen after ovulation. Luteinizing hormone (LH) is predominantly secreted by the anterior pituitary midway through the menstrual cycle; it results in the development of the corpus luteum. LH levels also increase after bilateral gonadectomy. LH and human chorionic gonadotropin (hCG) bind to the same receptor, but rats lack hCG. To assess how LH and hCG influence myoelectric activity of the small intestine and to test the specificity of the LH receptor, we implanted electrodes on the jejunum of female rats. LH (0.1 or 0.5 NIH units) was administered intraperitoneally to intact and gonadectomized rats and 0.5 NIH units to rats that had been both hypophysectomized and gonadectomized; intact animals were treated with 100 units USP of hCG. Recordings were made with the rats in fasted and in fed states, and their intestinal motility was analysed. The most striking effects of LH, hypophysectomy, and hCG were the same: phase III of the migrating myoelectric complex was markedly fragmented and its duration lengthened (P < 0.0001). Gonadectomy alone and gonadectomy with hypophysectomy also increased fragmentation and phase III duration (P < 0.01 or better). LH receptors respond similarly to LH and hCG, and both hormones alter myoelectric activity of the rat small intestine in comparable ways.
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