PURPOSE: To investigate the neuroprotective effect of growth hormone(GH) on neuronal cell necrosis and apoptosis at 1 week and 3 weeks after hypoxic ischemic brain injury. METHODS: Sprague-Dawley rats, seven-day-old, were used. Rats were anesthetized with ether less than 5 minutes. The right carotid artery was cut between double ligation. And then, rats were allowed to recover for 30 minutes followed by exposure to 8% oxygen at 37 degrees C for 2 hours for hypoxic ischemic insult. The study group was divided into 2 groups, control group(N=3) and GH treated group(N=3). GH treated group received intraperitoneal injection of GH 1 IU 2 hours after hypoxic ischemic insult following daily adminstration as same dose for 5 days. Rats were decapitated at 1 week and 3 weeks after hypoxic ischemic brain injury. After then, right hippocampal CA1 and CA3 neurons of rat brains were examined. RESULTS: Necrosis was significantly less in GH treated group than control group, and was more prominent at 3 weeks in both groups. The apoptosis was not found in GH treated and control group. CONCLUSION: GH has a neuroprotective effect on neuronal cell deaths(especially necrosis) from 1 week to 3 week after hypoxic ischemic insult in neonatal rat.
Animals ; Apoptosis ; Brain Injuries* ; Brain* ; Carotid Arteries ; Control Groups ; Ether ; Growth Hormone* ; Injections, Intraperitoneal ; Ligation ; Necrosis ; Neurons ; Neuroprotective Agents* ; Oxygen ; Rats* ; Rats, Sprague-Dawley

PURPOSE: Treatment of Kawasaki disease with intravenous gamma globulin(IVGG), together with aspirin, has been dernonstrated to be safe and effective in preventing coronary artery lesion and systemic inflarnmation, but optimal IVGG dosage and administration method are still controversial. We compared the therapeutic efficacy and clinical response of single IVGG 1g/kg to that of IVGG lg/kg for comparable risk group of Kawasaki disease. METHODS: We conducted a prospective study involving 63 children with Kawasaki disease requiring IVGG treatment(Harada score> or =4) at Chungnam National University Hospital from February 1996 to January 1999. The children were assigned to receive IVGG either as a single infusion of 1g/kg(A group, 32 person) or 2g/kg(B group, 31 person) and aspirn(100mg/kg/day through acute phase, then 3 to 5mg/kg/day for 8 weeks of duration). RESULTS: There were no significant difference between the two groups according to clinical and laboratry data, including coronary artery lesions(group A, 31.3% and group B, 29.0%) before treatment. After IVGG treatment ratio of complication with coronary artery lesion(group A 1/32=3.1% and group B, 2/31=6.5%) and that of retreatment(group A, 4/32=12.5%, group B, 2/31=6.5%), duration of fever(group A, 1.3+/-1.6 days and group B, 0.7+/-1.4 days), hospital stay(group A, 7.0+/-1.4 days and group B, 6.5+/-2.0 days), laboratory finding and side effects of IVGG were not significantly different(P>0.05). The total dosage of IVGG was significantly lower in group A than group B(group A, 1.16+/-0.37g/kg, 375,421+/-207,351won and group B, 2.10+/-0.40g/kg, 641,498+/-274,750won (P<0.05). CONCLUSION: The therapeutic efficacy and clinical response of single 1g/kg therapy are comparable to that of single 2g/kg therapy.
Aspirin ; Child ; Chungcheongnam-do ; Coronary Vessels ; gamma-Globulins* ; Humans ; Mucocutaneous Lymph Node Syndrome* ; Prospective Studies

PURPOSE: To investigate the effect of intraperitoneal injection of IGF-I after hypoxic ischemic brain injury on neuronal cell necrosis, apoptosis and expression of proapoptotic and antiapoptotic proteins bax and bcl-2, respectively. METHODS: The right carotid artery was cut between the double ligation. Then allowed to recover for 30 minutes followed by exposure to 8% oxygen at 37degree C for 2 hours. Devided 2 groups, control group(N=30) and IGF-I treated group(N=30). IGF-I treated group received IGF-I 20 microg 2 hours after hypoxic ischemic injury intraperitoneally. Rates were decapitated at 24 hours and 72 hours following hypoxic ischemic brain injury. After then, right hippocampal CA1 and CA3 neuronsof rat brains were examined. RESULTS: The apoptosis and necrosis was significantly less in IGF-I treated group than control group and necrosis was more prominent in CA1 neurons than CA3 neurons. Necrosis was slightly decreased at 72 hours in both groups(P<0.05). The apoptosis was more prominent at 24 hours than 72 hours after hypoxic ischemic injury(P<0.05). Bax protein expression was prominent in control group, especially at 72 hours(P<0.05) and less in the IGF-I treated group than control group. Bcl-2 protein expression was not detected in both group. CONCLUSION: The results from this study suggest that exogenous systemic IGF-I had a neuroprotective effect by inhibition of up-regulation of bax protein expression after hypoxic ischemic brain injury.
Animals ; Apoptosis ; bcl-2-Associated X Protein ; Brain Injuries* ; Brain* ; Carotid Arteries ; Control Groups ; Injections, Intraperitoneal ; Insulin-Like Growth Factor I* ; Ligation ; Necrosis ; Neurons ; Neuroprotective Agents ; Oxygen ; Rats* ; Up-Regulation