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Kyuseok Kim 3 Articles
Sulforaphane Post-treatment Had No Protective Effects in Paraquat-intoxicated Rats
Gui Sang Jang, Jae Hyuk Lee, Kyuseok Kim, You Hwan Jo, Joong Eui Rhee, Kyoungbun Lee, Chan Jong Park, Chang Woo Kang, Soohoon Lee, Joonghee Kim
J Trauma Inj. 2013;26(1):6-13.
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AbstractAbstract PDF
PURPOSE
Sulforaphane is a naturally-occurring isothiocyanate abundant in broccoli. It has been suggested as a promising antioxidant. In this study, the therapeutic effect of sulforaphane in paraquat intoxication was investigated.
METHODS
Paraquat was administered via the tail vein, after which sulforaphane or a vehicle (4% DMSO) was administered intraperitoneally 15 minutes after paraquat administration. Histological injury, lipid peroxidation, plasma cytokine (IL-6, IL-10), and nitric oxide were measured. In addition, the effect of sulforaphane on survival in paraquat-intoxication was observed.
RESULTS
Regarding histological injury, lipid peroxidation, and plasma cytokine and nitric-oxide response, sulforaphane administration showed no protective effects in paraquat-intoxicated rats. Rather, it increased mortality (log rank p=0.03) and caused lipid peroxidation, as well as plasma cytokine and nitric-oxide production, to be increased.
CONCLUSION
Sulforaphane had no therapeutic effect on paraquat-intoxicated rats; rather, it increased mortality.
Summary
Effect of Therapeutic Hypercapnia on Systemic Inflammatory Responses in Hemorrhagic Shock in Rats
Kyeong Won Kang, You Hwan Jo, Kyuseok Kim, Jae Hyuk Lee, Joong Eui Rhee
J Korean Soc Traumatol. 2012;25(1):17-24.
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AbstractAbstract PDF
PURPOSE
This study was performed to investigate whether therapeutic hypercapnia could attenuate systemic inflammatory responses in hemorrhagic shock in rats.
METHODS
Male Sprague-Dawley rats were mechanically ventilated and underwent pressure-controlled (mean arterial pressure: 38+/-1 mmHg) hemorrhagic shock. At 10 minutes after the induction of hemorrhagic shock, the rats were divided into the normocapnia (PaCO2=35-45 mmHg, n=10) and the hypercapnia (PaCO2=60-70 mmHg) groups. The PaCO2 concentration was adjusted by using the concentration of inhaled CO2 gas. After 90 minutes of hemorrhagic shock, rats were resuscitated with shed blood for 10 minutes and were observed for 2 hours. The mean arterial pressure (MAP) and the heart rate were monitored continuously, and the results of arterial blood gas analyses, as well as the plasma concentrations of interleukin (IL)-6, IL-10, and nitrite/nitrate were compared between the normocapnia and the hypercapnia groups.
RESULTS
The MAP and the heart rate were not different between the two groups. The plasma concentration of IL-6 was significantly lower in the hypercapnia group than in the normocapnia group (p<0.05). The IL-10 concentration was not different and the IL-6 to IL-10 ratio was significantly lower in the hypercapnia group compared to the normocapnia group. The plasma nitrite/nitrate concentration of the hypercapnia group was lower than that of the normocapnia group.
CONCLUSION
Therapeutic hypercapnia attenuates systemic inflammatory responses in hemorrhagic shock.
Summary
The Effect of Hypothermia on Lung Inducible Nitric Oxide Synthase Gene Expression in Intestinal Ischemia-Reperfusion Injury
Kyuseok Kim, Jeong Hun Lee, Gil Joon Suh, Yeo Kyu Youn, Young Joon Kang, Min A Kim, Sang Ki Cho, Hyo Keun Shin
J Korean Soc Traumatol. 2006;19(1):14-20.
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AbstractAbstract PDF
PURPOSE
Although hypothermia has been used in many clinical situations, such as post cardiopulmonary resuscitation, stroke, traumatic brain injury, septic shock, and hemorrhagic shock, the mechanism by which it works has not been clearly elucidated. We aimed to evaluate the effect of hypothermia on the plasma nitric oxide (NO) concentration, lung iNOS expression, and histologic changes in intestinal ischemia-reperfusion (IR).
METHOD
Male Sprague-Dawley rats were randomly divided into the hypothermia group (HT, n=8, 27~30 degrees C) and the normothermia group (NT, n=8, 36~37 degrees C). They underwent 30 min of intestinal ischemia by clamping the superior mesenteric artery, which was followed by 1.5 h of reperfusion. They were then sacrificed. The acute lung injury (ALI) score, the plasma NO concentration, and lung iNOS gene expression were measured.
RESULTS
Compared with the HT group, the NT group showed severe infiltrations of inflammatrory cells, alveolar hemorrhages, and interstitial hypertrophies in lung tissues. There were significant differences in the ALI scores between the NT and the HT groups (8.7 +/- 1.5/HPF in NT vs 5.8 +/- 1.2/HPF in HT, p=0.008). Although the plasma NO concentration was slightly lower in the HT group, there was no significant difference between the two groups (0.80 +/- 0.24 micromol/L in NT vs 0.75 +/- 0.30 micromol/L in HT, p=0.917). Lung iNOS gene expression was stronger in the NT group than in the HT group. The band density of the expression of iNOS in lung tissues was significantly increased in the NT group compared to the HT group (5.54 +/- 2.75 in NT vs 0.08 +/- 0.52 in HT, p=0.002).
CONCLUSIONS
This study showed that hypothermia in intestinal IR reduces inflammatory responses, ALI scores, and iNOS gene expression in lung tissues. There was no significant effect of hypothermia on the plasma NO concentration.
Summary

J Trauma Inj : Journal of Trauma and Injury