ABSTRACT
Objective To study the clinical characteristics, respond of treatment and prognosis in infants with atrial tachycardia (AT). Methods The clinical data of 23 infants with AT from August 2014 to November 2016 were retrospectively analyzed. The respond of treatment and prognosis were observed. Results Of all the 23 infants with AT, incessant AT was in 5 cases, and paroxysmal AT was in 18 cases. There were 13 infants diagnosed with AT combined with cardiac insufficiency, and among them, 5 cases were combined with tachycardia induced cardiomyopathy (TIC). Echocardiography showed that atrial septal defect in 3 cases, patent foramen oval in 6 cases, ventricular septal defect in 1 case, ventricular septal defect combined with patent foramen oval in 2 cases, ventricular septal defect combined with atrial septal defect in 1 case, and ventricular septal defect combined with coarctation of the aorta in 1 case. The curative effect was excellent in 11 cases, effective in 8 cases, and ineffective in 4 cases at discharge. There was no statistical difference in curative effect between patients with normal cardiac function and cardiac insufficiency at discharge (P＞0.05). The infants were followed up for 12 months, AT disappeared in 19 cases, 1 case progressed to sick sinus syndrome, and 3 cases were lost in follow-up. Conclusions AT can be insidious in infants, but with a favorable prognosis if treated with cardiotonic drugs and antiarrhythmic drugs during the short and mid-term follow-up. Long-term follow-up should be taken to learn more about the prognosis.
ABSTRACT
Objective To evaluate the role of c-Jun N-terminal kinase (JNK) in activation of astrocytes in midbrain periaqueductal gray (PAG) of rats with neuropathic pain.Methods A total of 72 pathogen-free male Sprague-Dawley rats,aged 9 weeks,weighing 160-200 g,were divided into 4 groups using a random number table:control group (group C,n =8),neuropathic pain group (group NP,n =40),dimethyl sulfoxide control group (group DS,n =12) and JNK inhibitor SP600125 group (group SP,n=12).Neuropathic pain was produced by chronic constriction injury (CCI).At 14 days after CCI,10 nmol JNK inhibitor SP600125 0.5 μl was intraperitoneally injected into the PAG in group SP,and 10％ dimethyl sulfoxide 0.5 μl was given instead in group DS.Eight rats were selected in group C,before CCI and at 3,7,14 and 21 days after CCI in group NP,and in DS and SP groups,and the mechanical pain threshold was measured before CCI,before administration on 14 days after CCI and at 30,45,60,75 and 90 min after administration.The rats in group C were sacrificed after the end of measurement of the mechanical pain threshold,and brains were removed for determination of phosphorylated JNK (p-JNK) and glial fibrillary acidic protein expression (by Western blot) in PAG region.The rats in group NP were sacrificed after the end of measurement of the mechanical pain threshold at each time point,and brains were removed for detection of p-JNK expression in PAG region.Four rats in DS and SP groups were sacrificed after the last measurement of the mechanical pain threshold at 45 min after administration,and brains were removed for determination of glial fibrillary acidic protein expression in PAG region.Results Compared with group C,the mechanical pain threshold was significantly decreased at each time point after CCI,and the expression of p-JNK was up-regulated at 7-21 days after CCI in group NP (P＜0.01).Compared with group DS,the mechanical pain threshold was significantly increased at 30 min after administration,and GFAP expression was down-regulated at 45 min after administration in group SP (P＜ 0.01).The mechanical pain threshold was significantly higher at 30-75 min after administration than before administration in group SP (P＜0.01).Conclusion The mechanism underlying activation of astrocytes in PAG is related to activating JNK in the rats with neuropathic pain.