• Journal of Periodontal and Implant Science
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• v.29 no.1
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• pp.1-14
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• 1999

Ursodeoxycholic acid(UDCA) is a hydrophilic gall bladder acid and has been used as a effective drug for liver disease related to in1munity. This drug inhibits secretions of IL-2, IL-4, and $IFN-{\gamma}$ from T-cells and production of immunoglobulin from B-cells. Also it has been reported that UDCA inhibits production of IL-1 related to the progression of periodontal disease and activation of collagenases. The purpose of the present study was to elucidate the effects of UDCA on inhibition of periodontal disease progression using clinical, microbiological and histometrical parameters. Twelve pure bred, 16 month-old-beagle dogs were used in the study. After ligature-induced periodontal diseases were formed, experimental drugs were applied twice a day and then the results of clinical, microbiological, and histometrical parameters were measured at baselie(initiation of experiment) , 4weeks and 8weeks. The gel with UDCA(concentration 0.5%, 5% 3 dogs in each) was applied to experimental group, chlorhexidine to positive control group(3dogs) and the gel without UDCA(base) to negative control group. After induction of general anesthesia, the maxillary 2nd, 3rd premolars and 1st molar and the mandibular 2nd, 3rd, 4th premolars and 1st molar were ligated in one side selected randomly and were not ligated in the opposite side. The plaque index(PI), gingival index(GI), pocket depth(PD) and gingival crevicular fluid(GCF) volum were measured clinically. The PI and GI were measured at 3 buccal points of all experimental teeth and the GCF was measured only at the 3rd premolar in the maxilla and the 4th premolar in the mandible. In the microbiological study, the samples extracted from the 3rd premolar of the maxilla and the 4th premolar of the mandible at the center of buccal surface were analyzed aerobics, anaerobics and Streptococcus colony forming units, After clinical and microbiological examination at 8weeks, the dogs were sacrificed by carotid artery perfusion. The samples were fixed and sectioned including interproximal area, and the distance from cementoenamel junction(CEJ) to alveolar crest was measured. The results were that PI, GI and PD increased until 4 weeks and decreased at 8 weeks in three groups but the differences between all the groups were not significant. The 0.5% UDCA in non-ligated group showed remarkable decrease of GCF. The experimental group applied 5% UDCA decreased the number of aerobics and anaerobics. The distance from CEJ to alveolar crest was greater in the negative control group on both ligated and non-ligated sides, but the differences were not significant stastically.

• Journal of Chest Surgery
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• v.34 no.9
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• pp.653-661
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• 2001

Background: Retrograde cerebral perfusion(RCP) is one of the methods used for brain protection during aortic arch surgery. The author previously published the data, however, for the safety of it, there still remains many controversies. The author performed RCP and checked various parameters to clarify the possibility of early detection of cerebral injury. Material and Method: The author used pigs(Landrace species) weighing 25 to 30kg and performed RCP for 120 minutes. After weaning of cardiopulmonary bypass, we observed pigs for another 120 minutes. Rectal temperature, jugular venous oxygen saturation, central venous pressure were continuously monitored, and the hemodynamic values, histological changes, and serum levels of neuron-specific enolose(NSE) and S100$\beta$ protein were checked. Central venous pressure during RCP was maintained in the range of 20 to 25 mmHg. Result: Flow rates(ml/min) during RCP were 224.3$\pm$87.5(20min), 227.1$\pm$111.0(40min), 221.4$\pm$119.5(60min), 230.0$\pm$136.5(80min), 234.3$\pm$146.1(100min), and 184.3$\pm$50.5(120min). Serum levels of NSE did not increase after retrograde cerebral perfusion. Serum levels of S100$\beta$ protein(ng/ml) were 0.12$\pm$0.07(induction of anesthesia), 0.12$\pm$0.07(soon after CPB), 0.19$\pm$0.12(20min after CPB), 0.25$\pm$0.06(RCP 20min), 0.29$\pm$0.08(RCP 40min), 0.41$\pm$0.05(60min), 0.49$\pm$0.03(RCP 80min), 0.51$\pm$0.10(RCP 100min), 0.46$\pm$0.11(RCP 120min), 0.52$\pm$0.15(CPBoff 60min), 0.62$\pm$0.15(60min after rewarming), 0.76$\pm$0.17(CPBoff 30min), 0.81$\pm$0.20(CPBoff 60min), 0.84$\pm$0.23(CPBoff 90min) and 0.94$\pm$0.33(CPBoff 120min). The levels of S100$\beta$ after RCP were significantly higher than thosebefore RCP(p<0.05). The author could observe the mitochondrial swellings using transmission electron microscopy in neocortex, basal ganglia and hippocampus(CA1 region). Conclusion: The author observed the increase of serum S100$\beta$ after 120 minutes of RCP. The correlation between its level and brain injury is still unclear. The results should be reevaluated with longterm survival model also considering the confounding factors like cardiopulmonary bypass.

• Journal of Chest Surgery
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• v.41 no.1
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• pp.41-48
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• 2008

Background: Accurate assessment of the preload and the fluid responsiveness is of great importance for optimizing cardiac output, especially in those patients with coronary artery occlusive disease (CAOD). In this study, we evaluated the relationship between the parameters of preload with the changes in the stroke volume index (SVI) after fluid loading in patients who were undergoing coronary artery bypass grafting (CABG). The purpose of this study was to find the predictors of fluid responsiveness in order to assess the feasibility of using. certain parameters of preload as a guide to fluid therapy. Material and Method: We studied 96 patients who were undergoing CABG. After induction of anesthesia, the hemodynamic parameters were measured before (T1) and 10 min after volume replacement (T2) by an infusion of 6% hydroxyethyl starch 130/0.4 (10 mL/kg) over 20 min. Result: The right ventricular end-diastolic volume index (RVEDVI), as well as the central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP), failed to demonstrate significant correlation with the changes in the SVI (%). Only the right ventricular ejection fraction (RVEF) measured at T1 showed significant correlation. with the changes of the SVI by linear regression (r=0.272, p=0.017). However, when the area under the curve of receiver operating characteristics (ROC) was evaluated, none of the parameters were over 0.7. The volume-induced increase in the SVI was 10% or greater in 31 patients (responders) and under 10% in 65 patients (non-responders). None of the parameters of preload measured at T1 showed a significant difference between the responders and non-responders, except for the RVEF. Conclusion: The conventional parameters measured with a volumetric pulmonary artery catheter failed to predict the response of SVI following fluid administration in patients suffering with CAOD.

• Journal of the korean academy of Pediatric Dentistry
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• v.32 no.3
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• pp.416-426
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• 2005

Intravenous sedation have many advantages of rapid onset and recovery, ability of control sedation levels and duration through titration. Midazolam is most commonly used intravenous medication for sedation in pediatrics, endoscopy, oncologic procedures and so on. But in dentistry, midazolam intravenous sedation is usually for adult, and there are few reports for children. Todays, children who need sedation become more and older, intravenous sedation technique is going a matter of concern in pediatric dentistry. The purpose of this paper is to evaluate the efficacy of sedation and clinical success for different initial dosage of midazolam in intravenous sedation for pediatric dental patients. 16 healthy children (male 10, female 6), mean age $54.7{\pm}10.7$ months, who needed at least two separate treatment visits requiring local anesthesia were chosen for this study. Every children were taken 0.3mg/kg, maximum 5mg of midazolam by intramuscular route, and then 30~50% $N_2O-O_2$ for 10 minutes was given. On every visits, one of the following 2 different initial dosage was given by intravenous route : (1) Group I : 0.1mg/kg Midazolam (2) Group II : 0.2mg/kg Midazolam. Additional dosage was half of the first dose. Physiologic parameters (oxygen saturation, heart rate, respiratory rate, end-tidal carbon dioxide pressure) was recorded by ten procedure steps. Behavior was videotaped and rated using Ohio State University Behavioral Rating Scale and Automated Counting System by one investigator, blind to administered dosage. After the treatment, operator evaluated the clinical success. Physiologic parameters were stable and within normal range during treatment in both groups. The analyzed sedative effect, in behavioral evaluation, ratio of favorable Quiet was higher in group II, and clinical success rate of group II was better than group I. Induction time was rapid in group II, and recovery time was rapid in group I. And there was no statistically difference between two groups in every results.

• Journal of Chest Surgery
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• v.35 no.12
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• pp.847-853
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• 2002

We previously published the data that proved the safety of retrograde cerebral perfusion for 120 minutes. At this time, we planned to check the neuron-specific enolase and S100-$\beta$ in serum and urine to assess the possibility of early detection of cerebral injury. Material and Method: We used pigs(Landrace species) weighing 35 kg and performed RCP for 120 minutes. After the weaning of cardiopulmonary bypass, we observed the pigs for another 120 minutes. Systemic arterial pressure, central venous pressure, and serum and urine levels of neuron-specific enolose (NSE) and S100$\beta$ protein were checked. Central venous pressure during RCP was maintained in the range of 20 to 25 mmHg. Result: Serum levels of NSE(ng/$m\ell$) were 0.67$\pm$0.18(induction of anesthesia), 0.53$\pm$0.47(soon after CPB), 0.44$\pm$0.27(20min alter CPB), 0.24$\pm$0.09(RCP 20min), 0.37$\pm$0.35(RCP 40min), 0.33$\pm$0.21 (RCP 60min), 0.37$\pm$0.22(RCP 80min), 0.41$\pm$0.23(RCP 100 min), 0.48$\pm$0.26(RCP 120min), 0.42$\pm$0.29(30min after rewarming), 0.35 $\pm$0.32(60min after rewarming, 0.42$\pm$0.37(CPBoff 30min), 0.47$\pm$0.34(CPBOff 60min), 0.47$\pm$0.28(CPBOff 90min), and 0.57$\pm$0.29(CPBOff 120min). There was no statistically significant difference in levels between before and after RCP(ANOVA, p＞0.05). Urine levels of NSE also showed no statistically significant difference in levels between before and after RCP. There was no correlation between urine and serum levels of NSE(Pearson correlation, p＞0.05). Serum levels of S100$\beta$ protein(ng/$m\ell$) during the same time frames were 0.14$\pm$0.08, 0.15$\pm$0.07, 0.22$\pm$0.15, 0.23$\pm$0.07, 0.28$\pm$0.10, 0.40$\pm$0.05, 0.47$\pm$0.03, 0.49$\pm$0.12, 0.43$\pm$0.11, 0.46$\pm$0.15, 0.62$\pm$0.17, 0.77$\pm$0.21, 0.78$\pm$0.23, 0.77$\pm$0.23, and 0.82$\pm$0.33. There was statistically significant difference in levels between before and after RCP(ANOVA, p＜0.05). Urine levels of NSE also showed statistically significant difference in levels between before and after RCP(ANOVA, p＜0.05). There was significant correlation between urine and serum levels of NSE(Pearson correlation, p＜0.05). Conclusion: The author observed the increase in serum and urine levels of S100$\beta$ after 120 minutes of RCP. Significant correlation between serum and urine levels was observed. The results were considered to be the fundamental data that could correlate this study with human-based study.