Effect of tooth pulp and periaqueductal central gray stimulation on the expression of genes encoding the selected neuropeptides and opioid receptors in the mesencephalon, hypothalamus and thalamus in rats.

Nociceptive stimulation has been considered to affect the expression of genes encoding endogenous neuropeptides and their receptors. The effect of electric stimulation of the tooth pulp and/or periaqueductal gray (PAG) in rats on mRNA levels of the selected neuropeptides and opioid receptors (ORs) was investigated in comparison with control group, without stimulation. The levels of mRNA for the selected neuropeptides: galanin (GAL), vasopressin (AVP), oxytocin (OT), substance P (SP), somatostatin (SOM), vasoactive intestinal peptide (VIP), endomorphin-2 (EM-2), and opioid receptors: MOR, DOR and KOR in mesencephalic, hypothalamic and thalamic tissues were determined by real-time PCR. It was demonstrated that in the control group expression of the tested neuropeptides was at a very low level in the mesencephalon and thalamus, but at the higher level in the hypothalamus. The highest expression of ORs was observed in the mesencephalon. Nociceptive tooth pulp stimulation had the strongest effect in the hypothalamus, elevating mRNA levels of all tested neuropeptides except SOM. Electric stimulation of PAG either did not change or down-regulated mRNA levels of the neuropeptides in the cerebral structures. Simultaneous stimulation of PAG and tooth pulp either did not affect mRNA levels of the investigated neuropeptides or caused their slight decrease versus tooth pulp stimulation. The noxious stimulation of tooth pulp increased also the levels of OR mRNAs, while stimulation of PAG had the opposite effect. The above results demonstrated that tooth pulp stimulation significantly up-regulated the mRNA levels for a number of neuropeptides and all three types of ORs in the rat brain, which would result in more potent antinociception. In contrast, PAG stimulation down-regulated the mRNA levels of several neuropeptides and ORs in the cerebral tissues, which would cause decreased synthesis of ORs. The obtained results represent a new insight into the mechanism of orofacial pain.

[Atrioventricular nodal and atrioventricular reentrant tachycardia in a patient with Ebsteinanomaly--the role of percutaneous RF ablation, surgery and Amplatzer septal occluder]. / Dwie postacie czestoskurczu nawrotnego u chorej z zespolem Ebsteina przyczyna ekwiwalentów zespolu MAS.Rola przezskórnej ablacji, operacji i zapinki Amplatza.

We present a case of a twelve-year-old girl with Ebstein's anomaly, atrial septal defect and two forms of tachycardia. From the first year the patient suffered from episodes of tachycardia. A few months prior to admission, episodes of palpitations became more frequent, periodically incessant and difficult to interrupt, despite amiodarone treatment. During the tachycardia the patient deteriorated with severe cyanosis, hypotension and often with syncope. During sinus rhythm ECG showed RA enlargement and preexcitation. During the documented tachycardia with rate 160-170/min, the ECG showed right bundle branch block (QRS=160 ms) with right axis deviation. An echocardiogram demonstrated dislodgment of septal tricuspid leaflet 30 mm with a high degree of right ventricle atrialisation, moderate tricuspid insufficiency, and ASD with bidirectional shunt. During the EP study two forms of tachycardia were induced: orthodromic atrioventricular reentrant tachycardia, and atrioventricular nodal reentry tachycardia. Both tachycardias were successfully ablated. Four months later the patient underwent TV replacement with aortic homograft, Glenn anastomosis and ASD closure with fenestration. During the next 18 months, the patient was in better general condition, but still was cyanotic especially during exercise (SAT 76%). An Amplatzer occluder was implanted on the 'residual' atrial septal defect. During the 24-month follow-up period, the patients has been in a good general condition, showing good exercise tolerance with no cyanosis or arrhythmia.