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Effects of a Pan Selectin Inhibitor on Renal Injury after Kidney Transplantation in Dogs
Woo, Heung-Myong The Korean Society of Veterinary Clinics 2002 한국임상수의학회지 Vol.19 No.3
Selectin은 조직 염증반응의 초기화에 관여하는 결합 단백질이며, 맥관내피에서 백혈구의 rolling과 tethering을 매개한다. 따라서 selectin inhibitor를 이용하여, 이들 selectin의 수용체인 sLex 에 대한 block을 유도함으로서 염증반응의 초기화를 억제할 수 있다는 가정하에, 본 연구에서는 장기이식 후 reperfusion에서 발생하는 손상에 대한 selectin inhibitor의 효과를 알아보았다. Beagle 견을 사용하여 신장이식을 실시하였다 공여 신장은 60분의 warm ischemia를 유도한 후 UW solution으로 관류하고 24시간동안 냉장보관하여 자가이식하였으며, 반대쪽 신장은 적출하였다. 술 후 7일동안 혈청 creatinine치를 측정하였다 2차실험으로, 12마리의 Beagle견을 사용하여 4시간의 reperfusion 후 조직학적 변화와 myeloperoxidase의 활성을 조사하였다. 각 실험의 대조군은 생리 식염수를,비교군은 TBC1269 (selectin inhibitor)를 신장 적출 전과 신장이식 수술 후 reperfusion 직전에 각각 투여하였다. 혈청 creatinine은 신장이식후 급격히 증가 하였으나, 두군 사이에 유의적인 차이는 없었다. 신장피질의 백혈구 침윤은, 4시간 reperfusion후 생리식염수를 투여받은 군에서 2배의 유의적인 증가를 보였다. 그러나, TBC 1269로 처리한 군에서는 백혈구의 침윤이 유의적인 억제를 보였으며, 허혈에의한 조직학적 변화도 유의적으로 적었다. 개의 신장이식 수술에서 Selectin의 차단은 warm renal ischemia에서 기인된 손상을 개선하지는 못하나, 백혈구의 침윤을 억제하므로 delayed graft function과 관련된 술 후 염증반응의 초기화를 억제하는 효과가 있는 것으로 사료된다. Selectins are differentially expressed carbohydrate binding proteins involved in the initiation of tissue inflammation by mediating the rolling and tethering of leukocytes on the vascular endothelium. This primary event in initiation of inflammation, as occurs during reperfusion injury, can be therapeutically targeted using selectin inhibitors, which generally block binding of sLex to E-, P-, and L-selectins. The objective of this study was to determine the role of selectins in renal ischemia/reperfusion injury after kidney transplantation. Canine kidneys were subjected to 60-min warm ischemia, flushed with UW solution, cold stored for 24 h, and autotransplanted into the nephrectomized donor. Renal autografts were monitored for 7 days by serum creatinine in the first study and by histology and myeloperoxidase activity after 4-hour reperfusion in the second study. In each study, one group of animals received TBC1269 (selectin inhibitor) and the other received saline vehicle. Serum creatinine rose quickly after transplantation and was not different between the groups. TBC1269 abolished a reperfusion-induced 2-fold increase in renal cortex neutrophil infiltration and improved histologic signs of ischemia after 4 hours of reperfusion. Selectin blockade does not improve the course of injury caused by warm renal ischemia. A minor benefit associated with the inhibition of early inflammation during reperfusion after kidney transplantation seems to occur.
상용량의 아세트아미노펜 복용 후 발생한 횡문근융해에 의한 급성신부전
김형진(Heung Jin Kim),김일두(Il Doo Kim),황영훈(Yeoung Hoon Whang),배용목(Yong Mock Bae),서길동(Gil Dong Seo),김명준(Myong June Kim),김수형(Soo Heung Kim),이인상(In Sang Lee) 대한신장학회 2000 Kidney Research and Clinical Practice Vol.19 No.1
A 21-year-young man had an episode of myalgia and chilling 3 days prior to hospital admission. He had consumed common doses of acetaminophen for one day, and was presented in the sauna room for an hour. On the next morning, he complained of dyspnea and was admitted. He presented in rhabdo-myolysis and acute renal failure with increased up-take in the proximal muscles by (99m)Tc-MPD bone scan. He was treated by hemodialysis and discharged on the twenty-eighth hospital day. Rhabdomyolysis has the variable causes. The causes of this case are two, the first cause is common doses of acetaminophen. But, there is no reports for rhabdomyolysis by common doses of acetaminophen only. However, we should consider that acetaminophen is a contributing factor in this case. The second cause is viral infection. Our patient had myalgia and chilling prior to hospital admission. Heat- stroke is well known cause of rhabdomyolysis. The mechnisms for rhabdomyolysis in this disease are hypovolemia, total body potassium deficit, and increased variable cytokines. Sauna, the last cause of our rhabdomyolysis case may have the same mechanisms with heatstroke. Our case had two causative factors, common doses of acetaminophen and sauna. These factors might be cooperated in our case of rhabdomyolysis and acute renal failure.
간경변증에 있어서 초음파검사상 문맥의 크기와 간정맥 계압의 상관관계에 관한 연구
최흥재(Heung Jai Choi),박인서(In Suh Park),문영명(Young Myong Moon),전재윤(Chae Yoon Chon),김두식(Doo Sik Kim),정재복(Jae Bok Chung) 대한소화기학회 1985 대한소화기학회지 Vol.17 No.1
N/A Diagnosis of portal hypertension can be made clinically by observing the esophageal varices, splenomegaly and/or ascites, but it is impossible in case without such clinical finding. For the measurement of portal pressure, wedged hepatic venous pressure, splenic pulp pressure, umblical vein pressure, mesentic vein pressure and direct punture of portal vein at laparotomy have been used, but these methods have not been frequently applied because their procedures are complicated and risky. After introduction of ultrasound in the field of clinical medicine, the portal vein size is easily visualized and the diagnosis of portal hypertension has been made by observing the portal venous system without difficulty. But the normal size of portal and splenic veins which are very important diagnostic criteria in ultrasound examination are not clearly defined and the diagnostic rate by the size of portal and splenic veins are reported by several authors with variable results. In this study we measured the diameter of splenic and portal vein with realtime ultrasonography in inspiratory and expiratory phase and checked the wedged hepatic venous pressure in 29 patients with liver cirrhosis and 14 persons without liver diease for control to see the normal range of diameter of vessels and the relationship between portal pressure and size of vessels. The results are as follows: l) The means of the diameter of splenic and portal veins of 14 control persons in inspira- tory phase were 0.49+-0.166cm and 0.79+-0.209cm and in expiratory phase 0.37% +-0.127cm and 0.67+-0.181cm respectively. The mean wedged hepatic venous pressure in control was 2. 1<1. 013 mmHg. 2) The means of the diameter of splenic and portal vein of 29 patients with liver cirrhosis in inspiration were 1.04+-0.233 cm and 1.30+-0.220 cm and expiration 0.96+-0.281 and 1.21+-0.231cm respectively. The mean wedged hepatic venous pressure in patients group was 14.0+-8.19 mmHg. 3) The upper criteria of normal diameter(mean+2SD) of splenic vein were 0.8cm in inspiration and 0.6 cm in expiration and of portal vein l. 2 cm in inspiration and 1. 0 cm in expiration. The splenic vein was within normal criteria in 13 out of 14 normaI persons in inspiration and expiration. The portal vein was in normal criteria in all in inspiration and in 13 in expiration. 4) In liver cirrhosis the wedged hepatic venous pressure was high (over 5 mmHg) in 24 cases and within normal limits in 5 cases. The size of splenic vein was larger than normal criteria in 2 cases from 5 with normal wedged hepatic venous pressure in inspiration and expiration and in 19 cases from 24 with high wedged hepatic venous pressure in inspiration and 22 cases in expiration. The size of portal vein was larger than normal criteria in 2 cases from 5 with normal wedged hepatic venous pressure in inspiration and 4 in expiration, and 17 cases from 24 with high wedged hepatic venous pressure in inspiration, and 21 cases in expiration, 5) The diagnostic efficacy of size of vessels on ultrasonography for portal hypertension was as follows. The sensitivity of splenic vein was 79.2% In inspihatory phase and 91.7% in expiratory phase and that of portal vein was 70.8% in inspiratory phase and 89.5 in expitatory phase. The specificity of splenic vein was 84.2% in inspiratory and expiratory phase and that of portal vein was 89.5% in inspiratory phase and 73.7% in expiratory phase. The positive predictability of splenic vein was 86.4% in inspiratory phase and 88.0% in expiratory phase and that of portal vein was 89.5% in inspiratory phase and 80.8% in expiratory phase. The negative predictability of splenic vein was 76.2% in inspiratory phase and 88.9% in expiratory phase and that of portal vein was 70.5% in inspiratory phase and 83.4% in expiratory phase. 6) The correlation coefficiencies between wedged hepatic venous pressure and the diameter of splenic and portal vein in control and diseased group were under 0.5, but in total the correlation coeffi