Smoking-Induced Dopamine Release Studied with 11CRaclopride PET / 대한핵의학회잡지

PURPOSE: It has been postulated that dopamine release in the striatum underlies the reinforcing properties of nicotine. Substantial evidence in the animal studies demonstrates that nicotine interacts with dopaminergic neuron and regulates the activation of the dopaminergic system. The aim of this study was to visualize the dopamine release by smoking in human brain using PET scan with [11C]raclopride. MATERIALS AND METHODS: Five male non-smokers or ex-smokers with an abstinence period longer than 1 year (mean age of 24.4+/-1.7 years) were enrolled in this study. [11C]raclopride, a dopamine D2 receptor radioligand, was administrated with bolus-plus- constant infusion. Dynamic PET was performed during 120 minutes (3x20s, 2x60s, 2x120s, 1x180s and 22x300s). Following the 50 minute-scanning, subjects smoked a cigarette containing 1 mg of nicotine while in the scanner. Blood samples for the measurement of plasma nicotine level were collected at 0, 5, 10, 15, 20, 25, 30, 45, 60, and 90 minute after smoking. Regions for striatal structures were drawn on the coronal summed PET images guided with co-registered MRI. Binding potential, calculated as (striatal-cerebellar) /cerebellar activity, was measured under equilibrium condition at baseline and smoking session. RESULTS: The mean decrease in binding potential of [11C]raclopride between the baseline and smoking in caudate head, anterior putamen and ventral striatum was 4.7 %, 4.0 % and 7.8 %, respectively. This indicated the striatal dopamine release by smoking. Of these, the reduction in binding potential in the ventral striatum was significantly correlated with the cumulated plasma level of the nicotine (Spearman's rho=0.9, p=0.04). CONCLUSION: These data demonstrate that in vivo imaging with [11C]raclopride PET could measure nicotine-induced dopamine release in the human brain, which has a significant positive correlation with the amount of nicotine administered by smoking.

Prenatal Diagnosis of Complete Atrioventricular Septal, Defect:Clinical Outcome of 35 Cases

PURPOSE: Prenatal diagnosis of congenital heart disease has been made by fetal echocardiography and its clinical impact on the outcome of complete atrioventricular septal defect(AVSD) cases has been analysed. METHODS: A retrospective study was performed for the fetal cases for complete AVSD diagnosed, confirmed postnatally or at second study and/or at autopsy and/or follow up at CHA hospital between January 1993 and December 2001. The outcome of complete AVSD has been analysed, and the associated anomalies & chromosomal defects has been described. RESULTS: There were 450 cases of significant CHD that had been diagnosed prenatally during the study period. Of whom 35 cases had complete AVSD, and 32 cases had complete AVSD associated with visceral heterotaxy. In the cases with complete AVSD who with chromosomal study, 53.8% had Down syndrome and an additional 7.7% had other chromosomal anomaly. Associated cardiac malformation was 34.2%. Extracardiac anomaly without chromosomal defect was founded in 5 cases(14%) included polydactyly, hydrocephalus, duodenal atresia, omphalocele, cleft lip and single umbilical artery. Among 35 fetal complete AVSD cases, 29 cases of complete AVSD has been terminated, 1 case died in utero, 1 case died at neonatal period and 4 cases were referred to cardiac center for planned delivery. The most common factors of termination were extracardiac and chromosomal anomaly. CONCLUSION: Among the significant CHD, incidence rate of complete AVSD was 7.8%. And the most of the complete AVSD has been terminated. 4 cases(11.4%) were referred to the cardiac center for planned delivery. The rate of termination was 82.9%. Fetal diagnosis of complete AVSD greatly increased the rate of termination.