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- 주제어 : ureteral pressure (검색결과 2 건)
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요관압 상승시 신혈류량 조절에 prostaglandin이 미치는 효과
민영기,양훈모,김종규,이석호 순천향의학연구소 2001 Journal of Soonchunhyang Medical Science Vol.7 No.1
Higher ureteral pressure than in normal condition causes increase in renal blood flow (RBF) and partial impairment of the autoregulation of RBF. Higher ureteral pressure increased renal prostaglandin production, it is not clear whether or not it is also responsible for partial impairment of the autoregulation of RBF. Therefore, we investigated the role which prostaglandin play in the autoregulation of RBF, studying the interaction between ureteral pressure and RBF autoregulation may reveal the role of prostaglandin in tubuloglomerular feedback. For the purpose of this experiment, six anesthetized mongrel dogs were prepared for the measurements of RBF, mean systemic and renal arterial pressure (RAP) and the manipulation of ureteral pressure to 0 cmH20, 20 cmH20 and 40 cmH20. The autoregulation curves were determined during both control and elevation of the ureteral pressure, before and after the pretreatment with indomethacin, a cyclooxygenase inhibitor. The desired ureteral pressure was achieved by vertically elevating the water-filled reservoir connected to the ureteral catheter to 20 cm and 40 cm above the kidney level. In response to the elevation of the ureteral pressure, RBF increased from 167±11 ml/min to 185±8 ml/min, 204±11 ml/min respectively and the renal arterial pressure and the systemic arterial pressure didn't change significantly. During 0 mmHg of ureteral presure threshold pressure of RBF autoregulation was 59±3 mmHg. On the other hand, during 20 cmH20, 40 cmH20 of ureteral pressure, the autoregulation curves shifted upward and rightward from control, threshold pressure is elevated by 74±3 mmHg. The pretreatment of the dogs with indomethacin failed to affect the lower limit of RBF autoregulation during both control (63±5 mmHg) and the elevated ureteral pressure (77±5 mmHg). Since RBF failed to increase in response to the elevated ureteral pressure, RBF autoregulation curves obtained during the elevated ureteral pressure shifted only rightward from indomethacin control. The results indicate that the increased intrarenal level of prostaglandin by increased ureteral pressure or prostaglandin-induced vasodilation does not appear to bear any relation to the reduction in the autoregulatore capacity during elevated ureteral pressure. It seems that the partial impairment of the autoregulation during acute ureteral obstruction is due to the consumption of tubuloglomerular feedback mechanism at 0 mmHg of ureteral pressure and that prostaglandin is neither mediator nor effector of tubuloglomerular feedback mechanism.
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오상향,남기석,이상오,박상일,최은,이양균 순천향의학연구소 2001 Journal of Soonchunhyang Medical Science Vol.7 No.1
Objective : To investigate the pathogenesis of anemia and serum protein alteration in patient with pressure ulcer and proper management method. Method : Eleven patients with pressure ulcer were investigated. To investigate the change of anemia and serum protein between pre- and post-treatment of pressure ulcer, we measured hemoglobin, hematocrit, serum iron, ferritin, transferrin, mean corpuscular volume(MCV), red cell count, serum albumin and globulin before and after healing of pressure ulcer. Result : There was significant increases of hemoglobin, hematocrit, red cell count, MCV, serum iron, ferrtin and transferrin after healing of pressure ulcer(p<0.05). The serum ablumin and A/G ratio were increased significantly(p<0.05). The total globulin and α1-globulin were decreased significantly(p<0.05). There was no statically significant relationship between the ulcer size and the degree of anemia and hypoalbuminemia. Conclusion : This research suggested that anemia and serum protein alteration in patient with pressure ulcer are thought result from chronic inflammatory process. So, anemia and alteration of protein does not require any treatment such as transfusion, iron and albumin supply.
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