• Journal of the Korean Society of Radiology
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• v.79 no.6
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• pp.332-336
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• 2018

Renal artery injury is a rare complication in blunt trauma, but can cause devascularization of the kidney, leading to renal failure. It requires early diagnosis and management. The treatment of renal artery injury still remains controversial, but recent studies have reported the successful treatment outcome with endovascular stent placement. Nevertheless, there is no standard treatment strategy in cases of pediatric patients. We report a case of a 16-year-old girl with right renal artery occlusion associated with a grade IV liver laceration. She was treated with only balloon angioplasty, and the kidney showed marked improvement of parenchymal perfusion with normalized renal function. Treatment with only balloon angioplasty can be a treatment option in pediatric patients with renal artery injury.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.13 no.1
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• pp.16-29
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• 1991

The occurrence of thrombotic occlusion & endothelial injuries at the site of anastomosis have been considered as major problems in microvascular surgery. The purpose of this study was to ascertain whether a end-in-end(sleeve, telescope) anastomosis compared favorably with end-to-end anastomosis in healing procedures on the endothelium and to study the possibility of clinical application in end-in-end method. The microvascular anastomoses have been performed with end-in-end method in the femoral arteries of 20 rats group, also with end-to-end method on the same arteries of another 20 rats group, and then the four anastomosed vessels in subdivided groups on each group were taken after period of 1, 3, 7, 14, 21 days following by anastomoses for scanning electron microscope observation. The results were as following: 1. The patency rate was 90% in the end-in-end group and 85%in the end-to-end group and late thrombus occurred at 7, 14 days on both groups, which suggested -consistent monitoring of patency was required for two weeks at least. 2. Platelet aggregates at the site of anastomosis began to organize on post-operation 3 days and in the end-in-end group, the initially decreased lumen of inserted vessel was gradually increasing on 7 days due to atrophy of the medial layers. 3. Re-endothelialization was completed between 7 and 14 days in end-in-end group, whereas between 14 and 21 days in end-to-end group.

• Journal of Chest Surgery
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• v.11 no.4
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• pp.469-475
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• 1978

• Journal of Chest Surgery
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• v.22 no.2
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• pp.290-296
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• 1989

• Journal of Chest Surgery
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• v.41 no.6
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• pp.772-776
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• 2008

The indications and applications of arthroscopic surgery for the knee joint have increased with the development in surgical techniques and the improvement of arthroscopic equipment. The use of arthroscopic surgery has led to a significant decrease in morbidity for the patient with intra-articular abnormalities, in terms of both the diagnosis and the surgical treatments. Even though arthroscopy is a minimally invasive technique with relatively low morbidity, it is not without risk of complications, of which neurovascular complications are among the most serious and devastating. Here we report on 2 cases of popliteal artery injury during arthroscopic knee surgery and its specific diagnosis and treatment.

• Journal of Chest Surgery
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• v.30 no.11
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• pp.1128-1131
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• 1997

Injuries to versa cave continue to be associated with a high mortality. Essentials to successful treatment are immediate recognition of the injury and prompt control of the hemorrhage. We have experienced one case of inferior versa java perforation by a chest rainage tube in the patient with post-operative chronic empyema thoracic. The patient was 38-year old male who was taken RLL lobectomy after 6 cycle of chemotherapy due to small cell carcinoma in the RLL & suffered from post-operative chronic empyema thoracis at D hospital. He moved to our hospital for further evaluation with accidental removal of chest drainge tube. We inserted closed drainage tube and dark blood gushed out abruptly just after insertion of the drainage tube. CTscan, MRI, and angiogram were performed and showed the perforation of IVC just below RA. The IVC was repaired using simple interrupted 4-0 Prolene suture through right posterolateral thoracotomy. The patient recovered without event and doing well until now.

• Journal of the Institute of Electronics and Information Engineers
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• v.53 no.9
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• pp.137-142
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• 2016

When injecting intravenously of CT inspection, the effusion of the contrast meium can induce the tissue damage with the blood vessel outside. We detect extravasation which is generated in the course where we inject the contrast medium into the blood vessel. And we use the bolus tracking system for the detection of that. By using MPR and VR images, moreover we detected the extravasation in order to prevent the tissue damage. In order to detect the effusion of the contrast medium, we used 16-MDCT and 64-MDCT. Three dimensional images about the outflow of the blood vessel can provide the treatment information which is important in the patient treatment. Moreover we applied the image processing technique in order to improve sharpness between contrast media and organization. And sharpness and contrast was improved.

• Journal of Convergence for Information Technology
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• v.12 no.4
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• pp.119-125
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• 2022

In the study, we endeavored to investigate the effect of phenylephrine, isoprenaline and prazosin on the tissue-specific vascular contractility and to determine the mechanism involved. There were few reports addressing the question whether thin or thick filament modulation is included in phenylephrine, isoprenaline and prazosin-induced regulation. We hypothesized that isoprenaline and prazosin play a role in tissue-dependent regulation of vascular contractility. Denuded arterial muscles of Sprague-Dawley male rats were suspended in organ baths and isometric tensions were transduced and recorded using isometric transducers and an automatic data acquisition system. Interestingly, sustained continuous contraction of thoracic and abdominal aorta. Furthermore, isoprenaline and prazosin together with phenylephrine inhibited transiently and persistently vasoconstriction of thoracic and abdominal aorta suggesting that additional mechanisms (e.g. decreased receptor density, chemical interaction, postreceptor signaling or distribution of agonists) might be included in the modulation of vascular contractility.

• Journal of Life Science
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• v.18 no.11
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• pp.1513-1520
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• 2008

The 4-Hydroxynonenal (HNE) affects vascular dysfunctions probably through the interruption of the cellular redox balance. To better understand vascular abnormalities resulting from the accumulation of HNE, we delineated mechanism by which mitochondrial apoptosis occurs in the YPEN-1 endothelial cells. HNE treatment led to the loss of mitochondrial membrane potential (${\delta}{\Psi}_m$), resulting in the release of cytochrome c. Data showed decreased Bcl-2 and increased Bax protein levels in HNE-treated cells. NAC, a reactive oxygen species (ROS) scavenger, and penicillamine, the peroxynitrite scavenger, blocked HNE-mediated ROS generation, thereby thwarting the cytochrome c release and apoptosis. The treatment of the cells with zVAD-fmk, a broad range caspase inhibitor did not suppress HNE-induced apoptosis, suggesting that the apoptosis might be the possibility of caspase-independent process. Our findings delineate the underlying mechanism of the HNE induced endothelial apoptosis by triggering depolarization of mitochondria membrane potential that can lead to the deterioration of vasculature homeostasis and subsequent vascular dysfunction with aging.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1265-1276
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• 1998

Background : Nitric oxide(NO) is an endogenously produced free radical that plays an important role in regulating vascular tone, inhibition of platelet aggregation and white blood cell adhesion to endothelial cells, and host defense against infection. The highly reactive nature of NO with oxygen radicals suggests that it may either promote or reduce oxidant-induced cell injury in several biological pathways. Oxidant injury and interactions between pulmonary vascular endothelium and leukocytes are important in the pathogenesis of acute lung injury, including acute respiratory distress syndrome(ARDS). In ARDS, therapeutic administration of NO is a clinical condition providing exogenous NO in oxidant-induced endothelial injury. The role of exogenous NO from NO donor or the suppression of endogenous NO production was evaluated in oxidant-induced endothelial injury. Method : The oxidant injury in cultured rat lung microvascular endothelial cells(RLMVC) was induced by hydrogen peroxide generated from glucose oxidase(GO). Cell injury was evaluated by $^{51}$chromium($^{51}Cr$) release technique. NO donor, such as S-nitroso-N-acetylpenicillamine(SNAP) or sodium nitroprusside(SNP), was added to the endothelial cells as a source of exogenous NO. Endogenous production of NO was suppressed with N-monomethyl-L-arginine(L-NMMA) which is an NO synthase inhibitor. L-NMMA was also used in increased endogenous NO production induced by combined stimulation with interferon-$\gamma$(INF-$\gamma$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), and lipopolysaccharide(LPS). NO generation from NO donor or from the endothelial cells was evaluated by measuring nitrite concentration. Result : $^{51}Cr$ release was $8.7{\pm}0.5%$ in GO 5 mU/ml, $14.4{\pm}2.9%$ in GO 10 mU/ml, $32.3{\pm}2.9%$ in GO 15 mU/ml, $55.5{\pm}0.3%$ in GO 20 mU/ml and $67.8{\pm}0.9%$ in GO 30 mU/ml ; it was significantly increased in GO 15 mU/ml or higher concentrations when compared with $9.6{\pm}0.7%$ in control(p < 0.05; n=6). L-NMMA(0.5 mM) did not affect the $^{51}Cr$ release by GO. Nitrite concentration was increased to $3.9{\pm}0.3\;{\mu}M$ in culture media of RLMVC treated with INF-$\gamma$ (500 U/ml), TNF-$\alpha$(150 U/ml) and LPS($1\;{\mu}g/ml$) for 24 hours ; it was significantly suppressed by the addition of L-NMMA. The presence of L-NMMA did not affect $^{51}Cr$ release induced by GO in RLMVC pretreated with INF-$\gamma$, TNF-$\alpha$ and LPS. The increase of $^{51}Cr$ release with GO(20 mU/ml) was prevented completely by adding 100 ${\mu}M$ SNAP. But the add of SNP, potassium ferrocyanate or potassium ferricyanate did not protect the oxidant injury. Nitrite accumulation was $23{\pm}1.0\;{\mu}M$ from 100 ${\mu}M$ SNAP at 4 hours in phenol red free Hanks' balanced salt solution. But nitrite was not detectable from SNP upto 1 mM The presence of SNAP did not affect the time dependent generation of hydrogen peroxide by GO in phenol red free Hanks' balanced salt solution. Conclusion : Hydrogen peroxide generated by GO causes oxidant injury in RLMVC. Exogenous NO from NO donor prevents oxidant injury, and the protective effect may be related to the ability to release NO. These results suggest that the exogenous NO may be protective on oxidant injury to the endothelium.