Background : The present study was carried out in association with neutrophilic respiratory burst in the lung in order to clarify the pathogenesis of acute respiratory distress syndrome(ARDS) following acute severe hemorrhage. Because oxidative stress has been suggested as one of the principal factors causing tissue injury, the role of free radicals from neutrophils was assessed in acute hemorrhage-induced lung injury. Method : In Sprague-Dawley rats, hemorrhagic shock was induced by withdrawing blood(20 ml/kg of B.W) for 5 min and the hypotensive state was sustained for 60 min. To determine the mechanism and role of oxidative stress associated with phospholipase A2(PLA2) by neutrophils, the level of lung leakage, pulmonary myeloperoxidase(MPO), and the pulmonary PLA2 were measured. In addition, the production of free radicals was assessed in isolated neutrophils by cytochemical electron microscopy in the lung. Results : In hypotensive shock-induced acute lung injury, the pulmonary MPO, the level of lung leakage and the production of free radicals were higher. The inhibition of PLA2 with mepacrine decreased the pulmonary MPO, level of lung leakage and the production of free radicals from neutrophils. Conclusion : A. neutrophilic respiratory burst is responsible for the oxidative stress causing acute lung injury followed by acute, severe hemorrhage. PLA2 activation is the principal cause of this oxidative stress.
Park, Chan Ik;Park, Sung Jin;Lee, Sang Bong;Yeo, Kwang Hee;Choi, Seon Uoo;Kim, Seon Hee;Kim, Jae Hun;Baek, Dong Hoon
Journal of Trauma and Injury
/
v.29
no.3
/
pp.93-97
/
2016
Hepatic duct confluence injury, which is developed by blunt abdominal trauma, is rare. Conventionally, bile duct injury was treated by surgical intervention. In recent decades, however, there had been an increase in radiologic or endoscopic intervention to treat bile duct injury. In a hemodynamically stable patient, endoscopic intervention is considered as the first-line treatment for bile duct injury. A 40 year-old man was transferred to the emergency department of ${\bigcirc}{\bigcirc}$ trauma center after multiple blunt injuries. Contrast-enhanced abdominal computed tomography performed in another hospital showed a liver laceration with active arterial bleeding, fracture of the sacrum and left inferior pubic ramus, and intraperitoneal bladder rupture. The patient presented with hemorrhagic shock because of intra-peritoneal hemorrhage. After resuscitation, angiographic intervention was performed. After angiographic embolization of the liver laceration, emergency laparotomy was performed to repair the bladder injury. However, there was no evidence of bile duct injury on initial laparotomy. On post-trauma day (PTD) 4, the color of intra-abdominal drainage of the patient changed to a greenish hue; bile leakage was revealed on magnetic resonance cholangiopancreatography and endoscopic retrograde cholangiopancreatography (ERCP). Bile leakage was detected near the hepatic duct confluence; therefore, a biliary stent was placed into the left hepatic duct. On PTD 37, contrast leakage was still detected but both hepatic ducts were delineated on the second ERCP. Stents were placed into the right and left hepatic ducts. On PTD 71, a third ERCP revealed no contrast leakage; therefore, all stents were removed after 2 weeks (PTD 85). ERCP and biliary stenting could be effective treatment options for hemodynamically stable patients after blunt trauma.
The in vivo and in vitro buffer capacities of true plasma and tissue buffer capaciies were compared on dogs. Intracellular pH was determined on skeletal muscle by a modification of the method of Schloerb and Grantham using $C^{14}$ DMO. The in vivo curve for plasma or extracellular fluid has a much lower slope than the in vitro curve. The in vivo slope of skeletal muscle in the dog is approximately 20 sl. The slope for skeletal muscle in vivo falls between the in vitro and in vivo slopes of true plasma. It appears that intracellular hydrogen ion varies linearly with extracellular hydrogen ion when $CO_2$ tension is changed. Both hydrogen ion gradient and Hi/He ratio vary in skeletal muscle, with an increase in $CO_2$ tension. Infusion of 0.3N HCl gave two distinct patterns, the $H_i-H_e$ gradient decreased; and it would appear that very little hydrogen ion as such penetrated to the inside of the cells during the time of observation. Although lactic acid presumably enters the cell and the same of larger load was given as was used for hydrochloric acid, only very mild intracellular acidosis resulted, ostensibly due to metabolism of this substrate. Gluconic acid produced a more severe acidosis, both intracellularly and extracellularly, but with both of these acids the hydrogen ion gradient decreased and the $H_i/H_e$ ratio also decreased. The experiments on the dogs with hemorrhagic shock the hydrogen ion increase producing the acidosis originates inside the cells. Even so, the hydrogen ion gradient increased only very slightly in the acute experiments. This may suggest that even over short intervals of time skeletal muscle cells have a capacity to pump out hydrogen ions at a rate which maintains approximately the normal $H_i/H_e$ gradient when the source of the hydrogen ion is in the interior of the cell.
Two polyethylene tubes were inserted into the esophagus of anesthetized rabbit in order to record the fluctuation of the intraluminal pressure through the orifices located near the tips of the tubes. The orifice of the first tube was 10 cm apart from the incisor of the rabbit and the orifice of the second tube was 5 cm below that of the first one. The tubes were filled with saline solution running at various rates ranging from 1.5 ml/min. to 4.2 ml/min. The tubes were connected to the pressure transducers and the electrical signals were recorded by the physiograph. When the peristaltic wave approached to the orifice a rise in the pressure was recorded, returning to the base line when the portion of the orifice was quiescent. The frequency of the peristaltic motion and the velocity of the wave were studied in connection with the flow rate of saline solution through the tubes and in the case of massive acute hemorrhage. The results obtained were as follows: 1. There was reflux of fluid induced during the procedure of the experiment. This outwrad flow through the pharynx seemed to elicite swallowing reflexes. Accordingly, the frequency of peristalsis of the esophagus was largely dependent on the flow rate of the fluid through the inserted tubes. By the flow rate of 1.5 ml/min., 2.5 ml/min., or 4.2 ml/min., the frequencies of the peristalsis were revealed to be $8.6{\pm}3.6/10min.,\;14.5{\pm}4.8/10min.\;or\;21.1{\pm}6.3/10min.,$ respectively. The velocity of peristalsis also coincided with the enhanced motility of the esophagus, showing $6.6{\pm}1.5\;cm/sec.,\;8.9{\pm}3.9\;cm/sec.,\;or\;12.4{\pm}4.6\;cm/sec.,$ respectively. 2. By acute hemorrhage, amounting to 2% of the body weight, the frequency of the peristalsis increased to twofold of the control and the propagation velocity also increased by 52 percent. 3. Retransfusion of the shed blood resulted in divergent responses. In some cases there were noticable ameliorations of the effects brought by acute hemorrhage, and in the others there were still increasing tendenies of the motility after the transfusion. 4. Some speculation was made about the possibility of a kind of relationship between the irreversibility of the hemorrhagic shock and the absence of responses by transfusion. 5. The peristalsis persisted even after complete disconnection at the midportion of the esophagus, reaffirming the view of a central regulation of the spatiotemporally coordinated motility, peristalsis.
Background : The central physiological derangement of hemorrhagic fever with renal syndrome (HFRS) caused by hantaan virus (HTNV) is a vascular dysfunction, manifested by hemorrhage, impaired vascular tone and increased vascular permeability. Platelet activating factor (PAF), whose actions are mediated through a specific receptor, is a potent bioactive lipid. PAF has diverse biological functions in the vascular system, such as increasing vascular permeability, adhesion of leukocytes to the endothelium and reduction of cardiac output, which result in hypotension and shock. The goal of the present study was to investigate whether PAF is involved in the pathogenesis of HFRS. For this purpose, we evaluated the effect of HTNV on the expression of PAF receptor (PAF-R) and on the activity of PAF-acetylhydrolase (PAF-AH) instead of PAF because PAF is rapidly degraded by PAF-AH in vivo. Materials and methods : To evaluate the expression of PAF-R, we performed reverse-transcription PCR, western blot and FACS analyses using HTNV-infected human umbilical vein endothelial cells (HUVECs) and non-infected (control) HUVECs. In addition, we measured the activity of plasma PAF-AH in HFRS patients and normal healthy persons. Results : The mRNA and protein expression of PAF-R was increased in HTNV-infected HUVECs compared with control HUVECs at 2 and 3 days post-infection (d.p.i.). FACS analysis showed that HTNV induced the surface expression of PAF-R in HUVECs from 2 d.p.i. The activity of plasma PAF-AH was 2.5-fold lower in HFRS patients than in normal healthy persons. Conclusion : Increased PAF-R expression by HTNV might increase the responsiveness to PAF in endothelial cells. Reduced PAF-AH activity in the blood of HFRS patients might delay PAF degradation. These results suggest that changes in PAF-R and PAF-AH by HTNV might influence to PAF activity and might be involved in the vascular dysfunction of HFRS.
A subacute toxicity study of cis-Malonato[(4R,5R)-4,5-bis(aminomethyl)-2-isopropyl-1,3-dioxolane]platinum(II)(SKI 2053R) was carried out to obtain information on its toxicological profiles, and to determine the maximum tolerated dose in beagle dogs. Four groups of beagle dogs (2M and 2F per group, 0,0.5,1.0,2.0mg/kg/day)were given 15 i.v. injections of SKI 2053R. In order to compare the toxic effects of SKI 2053R with those of cisplatin, one group was treated with cisplatin(0.7mg/kg/day)according to the same treatment schedule. The dosing schedule was divided into 3 courses of 5 consecutive days with 23-day dose-free intervals between each course. After completion of the treatments, remaining dogs were necropsied under established guidelines. Three of four dogs in the high dose group and one of four dogs in the middle dose group treated with SKI 2053R died of hypovolemic shock secondary to hemorrhagic and ulcerative enterocolitis. No toxicity-related mortality occurred in the low dose group of SKI 2053R. No survivor was observed in the group of cisplatin. Clinical signs including vomiting, diarrhea, anorexia and loss body weight were apparent in dogs given either cisplatin or high and middle doses of SKI 2053R. Severe thrombocytopenia and leukocytopenia were observed in the high dose group of SKI 2053R and cisplatin-treatment group, while toxicities as bone marrow suppression were reversible. The significant elevation of serum ALP values in group of SKI 2053R(2.0 mg/kg/day and 1.0mg/kg/day) and cisplatin(0.7mg/kg/day)was observed. Slight proteinuria waa observed in high and middle dose level groups of SKI 2053R. In histopathological examinations, pathological alterations of liver, kidney and spleen were noted dose-dependantly in dogs treated with SKI 2053R, and there was no overt sign of toxicity in low dose group of SKI 2053R. Compared to SKI 2053R, more severe durg-related toxicities occurred in dogs treated with cisplatin. It waw estimated that maximum tolerated dose of SKI 2053R in this treatment schedule was 0.5~0.7mg/kg/day. In conclusion, overall toxic potential of SKI 2053R was approximately 3 times lower than that of cisplatin with respect of lethality.
Background : For unknown reasons, the serum ferritin concentrations are higher in patients with acute lung injury. A pretreatment with aspirin reduces the acute lung injury in rats subjected severe hemorrhage, and increases the rate of ferritin synthesis in vitro. This study investigated the effect of aspirin on the serum ferritin changes in rats subjected to severe hemorrhage. Methods : Hemorrhagic shock was induced by withdrawing blood (20 ml/kg of B.W.) through the femoral artery for 5 min. The rats were pretreated with aspirin (10 mg/kg, i.v.) 30 min before hemorrhage. Results : The protein content and leukocyte count in the bronchoalveolar lavage fluid, lung tissue myeloperoxidase activities were significantly higher after hemorrhage. The aspirin pretreatment prevented these changes. The serum and lavage fluid ferritin concentrations were elevated higher after hemorrhage. These were also attenuated by the aspirin pretreatment. Conclusion : The changes in the serum and lung lavage ferritin level might be closely related to the severity of hemorrhage-induced acute lung injury. Therefore, the serum and lavage ferritin concentrations can be a useful biomarker for patients with precipitating conditions.
Dengue virus is a typical mosquito-borne virus, and the half of the world's population is exposed to infection. Dengue virus causes relatively mild symptoms such as dengue fever. However, when not treated properly, it is known to cause severe symptoms such as dengue hemorrhagic fever and dengue shock syndrome with a mortality rate of over 20%. Development of dengue virus detection technology is very important because it is reported that early diagnosis of dengue fever can lower the mortality rate to less than 1%. In this study, patent search related to dengue virus detection technology was conducted in Korea, USA, Europe, Japan, and China. The quantitative analysis of 69 validated patents from the searched patents was conducted by country, year, and patent holder. In addition, in-depth analysis was carried out by classifying into three categories: molecular diagnostics, immuno-diagnostics, and cell culture-based diagnostics from all validated patents. From these results, we analyzed the patent trend related to dengue virus detection and dengue fever diagnosis technology and discussed the features and limitations of molecular diagnostics and immuno-diagnostics at present level. Furthermore, we discussed the direction of technology development and future prospects to overcome limitations.
Background: Major vascular injuries can jeopardize a patient's life or imperil limb survival. We performed this study to establish an optimal management plan for vascular injuries. Material and Method: We retrospectively reviewed 26 cases of vascular injury that were treated at Pusan National University Hospital from May, 1999 to September, 2004. The age and sex distribution, the locations and causes of vascular injury, the diagnostic tools, the degree of injuries, clinical manifestations, the treatment modality and complications were reviewed. Result: The mean age was 39.5 years (range: $12{\sim}86$) and the male to female ratio was 22 : 4. The injuries were in 6 descending thoracic aortas, 4 femoral arteries, 4 popliteal veins and so on. The causes of injury were iatrogenic in 8 cases, traffic accident in 7, stab injury in 6 and industrial accident in 5. The most commonly used diagnostic tools were CT and angiography. The degrees of arterial injury were pseudoaneurysm in 10 cases, partial severance in 5, complete severance in 3 and thrombosis in 3. The degrees of venous injury were partial severance in 6 cases, complete severance in 2 and arteriovenous fistula in 2. The clinical manifestations were absence of pulse in 8 cases, coldness in 7, chest pain in 6, swelling in 5, bleeding in 5 and so on. The most frequently used type of revascularization was graft interposition in 11 cases. Two arteriovenous fistulae were repaired by endovascular procedure. There was one case of mortality due to multi-organ failure after hemorrhagic shock, There were three major amputations, and two of them were due to delayed diagnosis and treatment. Conclusion: A system for the early diagnosis and treatment is essential for improving limb salvage and patient mortality. As a consequence of the widespread application of endovascular procedures, the incidence of iatrogenic injuries has recently increased. Educating physicians is important for the prevention of iatrogenic injury. Easy communication and cooperation for earlier involvement of a vascular surgeon is also an important factor.
Pathophysiological mechanism of hemorrhagic fever with renal syndrome (HFRS) is not fully understood. Major clinical findings of HFRS patients are widespread hemorrhage, acute renal failure and shock. Basic lesion is vascular injury with microvascular hemorrhage and relatively little inflammation. According to autopsy findings, renal medulla shows focal hemorrhage, tubular necrosis and interstitial mononuclear infiltrates. The predominant cell type in the renal and pulmonary interstitium is a fibroblast and it participates in the healing process at the injury site by secreting a large amount of extracellular matrix proteins. Cultured human lung fibroblasts and Mongolian gerbil fibroblasts were known to be good host cells for the hantaan virus. It is possible that not only the endothelial cell but also the fibroblast is a target of Hantaan virus and the fibroblast might be involved in the pathogenesis and the healing process in HFRS. Integrins are adhesion molecules, and act as receptors for many extracellular matrix proteins. Recently, there are many reports that cell surface integrins influence on some viral infections or reversely viruses influence on the expression of integrins. The ${\alpha}_5{\beta}_1$ integrin is a major receptor for the fibronectin which is an important extracellular matrix protein secreted by fibroblasts. In this study, the role of ${\alpha}_5{\beta}_1$ integrin in the infection of Hantaan virus was examined by using anti-${\alpha}_5{\beta}_1$, integrin, anti-${\alpha}_5$ integrin and anti-${\beta}_1$, integrin antibodies in chicken embryo fibroblasts (CEF) and Mongolian gerbil fibroblasts(MGF). The treatment of anti-${\alpha}_5{\beta}_1$, integrin antibody in CEF reduced the virion titers 26.8% and the amount of nucleocapsid N protein 32.6% when compared with control CEF. When MGF were treated with anti-${\alpha}_5$, anti-${\beta}_1$ and anti-${\alpha}_5{\beta}_1$ integrin antibodies, virion titers were reduced by 26.5%, 29.4% and 28.7% and the amount of nucleocapsid N protein were reduced by 65.2%, 59.7% and 72.6%. These results suggested that ${\alpha}_5{\beta}_1$ integrin might act as a receptor for the Hantaan virus or blocking of ${\alpha}_5{\beta}_1$ integrin influences on the viral replication in CEF and MGF. It is also possible that the blocking of only one subunit of integrin represents similar results in that of whole molecule.
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