• Biomolecules & Therapeutics
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• 제5권3호
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• pp.223-227
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• 1997

The protective effect of human urinary trypsin inhibitor(UTI) on acute hemorrhagic shock in beagle dog was studied. Hemorrhagic shock was experimentally induced in thoracotomized beagle dogs by removing blood and maintaining low arterial blood pressure for 30 min, and then blood removed was entirely transfused back into the dogs within one hour. When the blood was transfused, UTI was administered together to check the potential protective effect of UTI on hemorrhagic shock. The arterial blood pressure recovery was accelerated slightly by UTI treatment. Blood pH and $P_{a co2}$ returned to normal level in shorter time in the UTI treatment group. These data suggest that UTI may have protective effects on experimentally induced hemorrhagic shock.

• Korean Journal of Acupuncture
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• 제33권2호
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• pp.58-66
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• 2016

Objectives : In order to find a possible non-invasive manipulation tool for maintenance of the cardiovascular functions in hemorrhagic shock, this study was aimed at evaluating effects of acupoints acupressure on the changes in blood pressure and heart rate from an animal model of hemorrhagic shock. Methods : In adult Sprague-Dawley rats, hemorrhagic shock was induced by a withdrawal of arterial blood from the femoral artery with volume of 0.8 ml per 100 g of body weight using peristaltic syringe pump. We applied the acupressure with a pressure oscillator to tail as a control and 2 different acupoints of sobu(HT8), youngchun(KI1) under 3 different conditions : 1) normal arterial blood pressure without bleeding, 2) at the beginning of bleeding, and finally 3) hemorrhagic shock. Results : Under normal arterial blood pressure without hemorrhage, there was a significant increase in systolic and diastolic blood pressures by the acupressure to the tail, HT8 and especially KI1 for 30 sec compared with before acupressure. Under hemorrhagic shock condition, the tail acupressure had minimal changes in cardiovascular parameters. Either the HT8 or KI1 acupressure resulted in a significant increase in arterial pressure but did not heart rate. At the beginning of bleeding, tail acupressure failed to change the reduction of arterial pressure and heart rate. However, there was a significant increase in blood pressure and heart rate following either the HT8 or especially KI1 acupressure. Conclusions : HT8 and KI1 acupressure affected cardiovascular signs but tail acupressure did not in rat model of hemorrhagic shock. These experimental data suggest that a acupressure with a pressure oscillator to HT8 or KI1 can be one of alternative emergency manipulations to ameliorate compromised cardiovascular functions under hemorrhagic shock condition.

• 대한전자공학회:학술대회논문집
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• 대한전자공학회 2009년도 정보 및 제어 심포지움 논문집
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• pp.132-134
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• 2009

Hemorrhagic shock is a common cause of death in emergency rooms. Since the symptoms of hemorrhagic shock occur after shock has considerably progressed, it is difficult to diagnose shock early. The purpose of this study was to improve early diagnosis of hemorrhagic shock using a survival prediction model in rats. We measured ECG, blood pressure, respiration and temperature in 45 Sprague-Dawley rats, and then obtained a logistic regression equation predicting survival rates. Area under the ROC curves was 0.99. The Hosmer-Lemeshow goodness-of-fit chi-square was 0.86(degree of freedom=8, p=0.999). Applying the determined optimal boundary value of 0.25, the accuracy of survival prediction was 94.7%

• 대한전자공학회:학술대회논문집
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• 대한전자공학회 2008년도 하계종합학술대회
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• pp.1075-1076
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• 2008

Hemorrhagic shock is a common cause of death in emergency rooms. The objective evaluation of hemorrhagic shock is very important for early diagnosis and treatment. The purpose of this study is to understand its mechanism by analyzing the changes of bio-signals in hemorrhagic shock using controlled hemorrhage of SD rats. In this study, we constructed a hemorrhagic integrated system to control bleeding and to simultaneously measure bio-signals such as ECG, blood pressure, temperature, and respiration. In order to verify the system, we measured the bio-signals mentioned above while hemorrhagic shock was induced by withdrawing blood (2.5ml/100g/15min) from a femoral vein for 10 rats.

• Journal of Trauma and Injury
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• 제25권1호
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• pp.17-24
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• 2012

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: $38{\pm}1$ mmHg) hemorrhagic shock. At 10 minutes after the induction of hemorrhagic shock, the rats were divided into the normocapnia ($PaCO_2$=35-45 mmHg, n=10) and the hypercapnia ($PaCO_2$=60-70 mmHg) groups. The $PaCO_2$ concentration was adjusted by using the concentration of inhaled $CO_2$ 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.

• Journal of Veterinary Science
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• 제21권1호
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• pp.6.1-6.12
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• 2020

Currently, the optimal resuscitation fluid remains debatable. Therefore, in the present study, we designed a trometamol-balanced solution (TBS) for use as a resuscitation fluid for hemorrhagic shock. Hemorrhagic shock was induced in 18 male Wistar-Kyoto rats, which were assigned to normal saline (NS), Ringer's solution (RS), and TBS groups. During the hemorrhagic state, their hemodynamic parameters were recorded using an Abbott i-STAT analyzer with the CG4+ cartridge (for pH, pressure of carbon dioxide, pressure of oxygen, total carbon dioxide, bicarbonate, base excess, oxygen saturation, and lactate), the CG6+ cartridge (for sodium, potassium, chloride, blood glucose, blood urea nitrogen, hematocrit, and hemoglobin), and enzyme-linked immunosorbent assay kits (calcium, magnesium, creatinine, aspartate aminotransferase, alanine aminotransferase, bilirubin, and albumin). Similar trends were found for the parameters of biochemistries, electrolytes, and blood gas, and they revealed no significant changes after blood withdrawal-induced hemorrhagic shock. However, the TBS group showed more effective ability to correct metabolic acidosis than the NS and RS groups. TBS was a feasible and safe resuscitation solution in this study and may be an alternative to NS and RS for resuscitation in hemorrhagic shock patients without liver damage.

• 전자공학회논문지SC
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• 제48권4호
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• pp.1-9
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• 2011

쇼크(shock)란 조직에 필요한 산소 요구량과 공급 간의 불균형에 의해 유발되는 임상증후군을 말한다. 환자의 치료효과와 생존율 향상을 위해서 쇼크의 조기 진단은 매우 중요하다. 그러나 현재 쇼크 진단에 사용되는 맥박, 혈압 등 생체 징후의 경우 출혈 정도를 제대로 반영하지 못하여 환자에 대한 처치가 늦어질 수 있다. 따라서 쇼크의 조기 진단을 위한 많은 연구들이 진행되어 왔으며, 조직의 저산소증, 대사성 산증을 반영해주는 지표인 젖산 농도와 관류 측정의 유용성이 입증된 바 있다. 본 연구에서는 흰쥐를 대상으로 정량적 출혈을 유도한 후, 젖산 농도 측정과 laser Doppler flowmeter를 통해 관류를 측정하였으며, 지혈 후 젖산 농도/관류의 비(ratio)를 생존 예측을 위한 새로운 지표로써 제안하였다. 새로 제안된 지표를 통한 생존예측을 ROC 커브 방법에 적용한 결과, 민감도 90.0%, 특이도 96.7%, 정확도 94.0%를 보였으며, 생존군과 사망군 간 새로운 지표의 유의한 차이도 가장 조기에 보여주었다. 향후 임상 적용 연구를 통해 새롭게 제안한 지표의 임상 적용이 가능하다면, 쇼크 환자를 조기 진단하고 치료효과를 높일 수 있을 것으로 생각된다.

• 대한약리학회지
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• 제2권1호
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• pp.99-109
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• 1966

It has been known that the pronounced hypotension resulting from hemorrhage gives rise to compensatory stimulation of the adrenosympathetic system, which leads to an increase of liberation of catecholamines from sympathetic nervous system and adrenal medulla. It is obvious, therefore, that numerous physiological and biochemical changes during the hemorrhagic hypotention might be mediated through the increased liberation of catecholamines. Although an extensive studies have been reported on changes of protein and carbohydrate metabolism in hemorrhagic shock a few studies on the changes of lipid metabolism have been reported. Levenson(1961) observed a marked increase of serum lipids content during hemorrhagic shock and also noticed a marked elevation of serum free fatty acids. He suggested that these effects were due to mobilization and accelerated metabolic breakdown of lipids which might be resulted by sympathetic stimulation as a cause. To elucidate the mechanism of this, author studied the change of serum free fatty acids and blood sugar with relation to catecholamines during experimentally induced hemorrhagic shock in dog. Healthy male mongrel dogs weighing approximately 15kg were used. Under the general anesthesia with pentobarbital, rapid hemorrhage was produced from the femoral artery maintaining blood pressure level of 40 mmHg measured by the manometer connected with the opposite femoral artery throughout the experiment. Serum free fatty acids(FFA) and blood sugar were measured by the methods of Dole(1956) and Folin-wu,(1920) respectively. Tissue catecholamine was measured by Shore and Olin method(1958) using Aminco-Bowman spectrophotofluorometer.

• The Korean Journal of Physiology
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• 제2권1호
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• pp.47-52
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• 1968

Twenty white rabbits anesthetized with nembutal (30 mg/kg) were employed in this experiment. Five of them served as controls; the remaining rabbits as experimental group were subjected to irreversible hemorrhagic shock. Shock was induced by bleeding the animals until mean blood pressure decreased to a level of 50-40 mmHg. This level of pressure was maintained for 3-4 hours, after which the drawn blood was reinfused. The reinfusion of blood caused the elevation of arterial pressure almost the control level for some minutes, after which a gradual and progressive decline of blood pressure became evident. This decline was thought to be the result from irreversible hemorrhagic shock. When mean blood pressure declined to less than 50 mmHg, chest was opened and samples of arterial blood and left ventricular muscle were taken. Left ventricular muscle and blood plasma were analyzed for potassium, sodium, chloride and water content. Blood glucose concentration was determined by Somogyi-Nelson's method. Extracellular and intracellular myocardial water and electrolyte content were calculated on the basis that electrolytes are distributed between plasma water and interstitial water according to Gibbs-Donnan equilibrium. In this calculation extracellular water was substituted for Na space. The findings obtained were as follows: 1. The concentration of blood glucose was 87mg% in the controls and it rose to 222 mg% in shock (P<0.01). 2. Plasma potassium elevated significantly from 3.3 mEq/l in controls to 8.0 mEq/l in shock (P<0.01), while small decreases in sodium (151-146 mEq/l) and chloride (102-96 mEq/l) were observed (P<0.3, P<0.1), 3. The changes of blood water content (83.1-84.3%) and cardiac water content (77.5-78.3 gm/100gm WT) were observed. 4. In control animals myocardial potassium levels which averaged 30.2 mEq/100 gmDT rose significantly to 40.3 mEq/100 gmDT in shock (P<0.01), while moderate decreases in sodium(16.3-14.3 mEq/100 gmDT) were observed in shock. 5. The calculated transmembrane resting potential of left ventricular muscle of control animals averaged 95 mV, while rabbits in shock averaged 77 mV. (P <0.01). The findings of this experiment do not correspond with the conclusions that myocardial depression seems to be the cause of irreversible hemorrhagic shock, because the excitability of heart muscle is elevated. From the point of view that the lowered transmembrane resting potential, the cause of death in terminal stage of irreversible hemorrhagic shock may be ventricular fibrillation. It can't be said, however, that the lowered transmembrane resting potential is responsible for the transition from reversible to irreversible hemorrhagic shock. The marked increase in blood glucose suggested that glycogenolysis in the liver is favorably active in shock.

• Journal of Trauma and Injury
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• 제27권4호
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• pp.204-207
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• 2014

Non-occlusive mesenteric ischemia (NOMI) encompasses all forms of mesenteric ischemia with patent mesenteric arteries. NOMI is commonly caused by decreased cardiac output resulting in hypoperfusion of peripheral mesenteric arteries. We report a case of NOMI secondary to hemorrhagic shock and rhabdomyolysis due to trauma. A 42-year-old man presented to our trauma center following a pedestrian trauma. On arrival, he was drowsy and in a state of hemorrhagic shock. He was found to have multiple fractures, both lung contusion and urethral rupture. An initial physical examination and abdominal computed tomography (CT) scan revealed no evidence of intra-abdominal injury. High doses of catecholamine were administered for initial 3 days due to unstable vital sign. On day 25 of hospitalization, follow-up abdominal CT scan demonstrated that short segment of small bowel loop was dilated and bowel wall was not enhanced. During exploratory laparotomy, necrosis of the terminal ileum with intact mesentery was detected and ileocecectomy was performed. His postoperative course was uneventful and is under rehabilitation.