• Archives of Craniofacial Surgery
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• v.21 no.1
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• pp.27-34
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• 2020

Background: Free-flap reconstruction for recurrent head and neck cancer may be challenging depending on the previous treatments, those are, chemotherapy, radiotherapy, and surgery, including neck dissection or free tissue transfer. Specifically, the previous treatment could compromise the neck vessels, thereby making free-flap reconstruction more difficult. This study aimed to investigate the correlation between previous treatments and vascular compromise of the free flap. Methods: In this retrospective study, 124 free-flap reconstructions in 116 patients for recurrent head and neck cancer between 1993 and 2017 were investigated. The demographic characteristics, previous treatments, flap choices, infections, recipient vessels, and vascular crises were evaluated. Results: Of the 124 reconstruction cases, 10 had vascular crises. There were six revisions, totaling six flap failures. The success rate of free-flap reconstruction for recurrent cancer was 95.2%, which significantly differed from that for primary cancer (98.8%, p= 0.006). Moreover, in the recurrent cancer group, no correlation was found between previous treatments and vascular crises (p> 0.05). Increased rates of contralateral or uncommon anastomoses were found following neck dissection (p< 0.05). Conclusion: Previous neck dissection or radiotherapy could lead to scarring and tissue damage, which could in turn make microvascular reconstruction more challenging; however, the effect was not definite in this study. Approximately 60% of patients with previous neck dissection had compromised ipsilateral recipient vessels, which resulted in contralateral or uncommon anastomoses. In this study, free-flap reconstruction seems to be quite safe and preferable in patients with recurrent head and neck cancer based on the overall survival rate.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.5
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• pp.437-448
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• 2023

Diabetic ulcer is usually seen in people with uncontrolled blood sugar. Reportedly, many factors such as impaired glucose metabolism, and macrovascular and microvascular diseases caused angiogenesis disorders and delayed the healing of diabetic ulcers, thus affecting the body's metabolism, nutrition, and immune function. This study aimed to explore the effect of paeonol on skin wound healing in diabetic rats and the related mechanism. A rat model of diabetic ulcer was established. High glucose-treated mouse skin fibroblasts were co-cultured with M1 or M2-polarized macrophages treated with or without paeonol. H&E and Masson staining were used to reveal inflammatory cell infiltration and collagen deposition, respectively. Immunohistochemistry visualized the expression of Ki67, CD31, and vascular endothelial growth factor (VEGF). Western blot was used to detect interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-4, IL-10, CD31, VEGFA, and collagen I/III. The expression of iNOS and arginase 1 was revealed by immunofluorescence staining. Paeonol treatment augmented collagen deposition and the expression of Ki67, CD31, VEGF, and macrophage M2 polarization markers (IL-4 and IL-10) and reduced wound area, inflammatory cell infiltration, and macrophage M1 polarization markers (IL-1β and TNF-α) in the ulcerated area. In vitro, paeonol treatment promoted M2-polarization and repressed M1-polarization in macrophages, thereby improving the repair of cell damage induced by high glucose. Paeonol accelerates the healing of diabetic ulcers by promoting M2 macrophage polarization and inhibiting M1 macrophage polarization.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.21 no.2
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• pp.89-109
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• 1999

Vascular spasm which has been reported to occur in 25% of clinical cases continues to be a problem in microvascular surgery; When prolonged and not corrected, it can lead to low flow, thrombosis, and replant or free flap failure. Ischemia, intimal damage, acidosis and hypovolemia have been implicated as contributors to the vascular spasm. Although much work has been done on the etiology and prevention of vasospasm, a spasmolytic agent capable of firmly protecting against or reversing vasospasm has not been found. Therefore vascular freezing was introduced as a new safe method that immediately and permanently relieves the vasospasm and can be applied to microsurgical transfers. Cryosurgery can be defined as the deliberate destruction of diseased tissue or relief the vascular spasm in microvascular surgery by freezing in a controlled manner. 96 Sprague Dawley rats each weighing within 250g were used and divided into 2 group, experimental 1 and 2 group. In the experimental 1 group, right epigastric vessels (artery and vein) were freezed with a cryoprobe using $N_2O$ gas for 1 min. In the experimental 2 group, after freezing for 1 min, thawing for 30 secs and repeat freezing for 30 secs. Left side was chosen as control group in both group. We sacrified the experimental animals by 1 day, 3 days, 1 week, 2 weeks, 4 weeks & 5 months and observed the sequential change that occur during regeneration of epigastric vessels using a histologic, histomorphometric, immunohistochemical and SEM study after the vascular freezing. The results were as follows1. In epigastric arteries, internal diameters had statistically significant enlargement in 1 day, 3 days of Exp-1 group and 1 day, 3 days, 1 week & 2 weeks of Exp-2 group. Wall thickness had statistically significant thinning in 2 weeks of Exp-2 group. 2. In epigastric veins, internal diameters had enlargement of statistical significance in 1 day of Exp-1 and Exp-2 group. 3. The positive PCNA reactions in smooth muscle appeared in 1 week and increased until 2 weeks, decreased in 4 weeks. There was no statistical significance between Exp-1 and Exp-2 group. 4. The positive ${\alpha}$-SMA reaction in smooth muscles showed weak responses until 1 week and slowly increased in 2 weeks and showed almost control level in 4 weeks. 5. The positive S-100 reactions in the perivascular nerve bundles showed markedly decrease in 1 day, 3 days and increased after 1 week and showed almost control level in 4 weeks. Exp-1 group had stronger response than Exp-2 group. 6. In SEM, we observed defoliation of endothelial cell and flattening of vessel wall. Exp-2 group is more destroyed and healing was slower than Exp-1 group. To sum up, relief of vasospasm (vasodilatation) by freezing with cryoprobe was originated from the damage of smooth muscle layer and perivascular nerve bundle and the enlargement of internal diameter in vessels was similar to expeimental groups, but Exp-2 group had slower healing course and therefore vessel freezing in microsurgery can be clinically used, but repeat freezing time needs to be studied further.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.25 no.4
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• pp.281-294
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• 1999

Vasospasm causes microvascular surgery to fail as a main factor in the loss of transferred flap dye to the diminution of blood flow in reconstruction surgery. Although there has been extensive research to resolve the vasospasm problem, no one has reached an ideal solution to date. However, cryotherapy, which is often used for destruction of tumor lesions, is being presented as a new way of releasing vasospasm. After making a histomorphometric measurement on vasodialation during the course of 1, 3 and 7 days, 2 and 4 weeks, and 5 months periods and observing the change of blood vessel in a histologic, immunohistochemical, and scanning electronic microscopic approach, the results were as follows : 1. Vascular inner diameters of the experimental 1 and 3 days groups were measured $476.3{\pm}28.20{\mu}m$, $497.15{\pm}48.79{\mu}m$ respectively showing statistically meaningful vasodilation(P<0.05), which continued by the experiment 4 weeks group. However, in the experimental 5 months group, the vascular inner diameter appeared similar to the control groups. Even though the thickness of smooth muscular layers come out to be thinner in all the experimental groups compared to the control group, it was difficult to find any statistical meaningfulness. In addition, the vascular external diameters of every experimental groups were shown to be longer than the control group. 2. In light microscopic view, severe injury was evident on the smooth muscular layer cell from the experimental 1 day group, started recovering partially from the experimental 7 days group, and was mostly restored in the experimental 4 weeks group and layer of adventitial stripping were nearly recoverd 2 weeks group. 3. The PCNA positive cells of smooth muscular layer were observed from the experimental 7 days group and had a tendency to increase by the experimental 2 weeks group. In the experimental 4 weeks and 5 months group, the number of PCNA possitive cells observed was comparable to the control group. 4. ${\alpha}$-SMA level of smooth muscular layer cells, having been significantly lower than the control group in the severly damaged experimental 1 day group. It was seen to be increased in the experimental 7 days group and turned out to show similar ${\alpha}$-SMA level in 4 weeks to the control group. 5. In the view of SEM, the endothelial cells were destructed and falling off, and also present the appearance of flattening in the experiment 1 day group. The endothelial layer cells started partially recovering from the 7 days group after the freezing injury. On 4 weeks and 5 months, the endothelial cells were fully coverd the damaged area, also it's appearance is similar to control group. In conclusion, the vascular freezing after the removal of adventitia caused damages to smooth muscular layer cells, and brought about vasodilation, which continued by the 4th week. The smooth muscular layer cells started partially reviving from the 7rd day after the damage by vascular freezing, and recovered their similar figure to the control group's 4 weeks later. This was considered the result of cells which surround the damaged blood vessel being influxed into the smooth muscular layers. Therefore, this local freezing injury on the blood vessel was thought to be applied clinically to relieve severe vasospasm which cannot be treated by vasodilation drug, a microvascular surgery.

• Archives of Plastic Surgery
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• v.37 no.2
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• pp.122-128
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• 2010

Purpose: Many descriptions of the digital arterial anatomy including skin territory of the finger have been published. Relatively few studies on venous architecture of the finger have been performed in this area, in part, attributable to the technical difficulties encountered in dissecting small vessels. The purpose of this study is to present the precise microsurgical anatomy of the vein related to the digital artery and venae comitantes of the components. Methods: Arterial and venous anatomy of their relation to the fingers were examined in 38 specimens of two fresh cadavers and 36 clinical cases. All specimens were evaluated grossly, surgical microscopically, or / and light microscopically to observe the three & two-dimensional structure of the artery and joining vein, evidence of the venae comitantes, and venous valve. Results: No longitudinal venae comitantes along the digital artery were found in any specimens. The size of the venae comitantes of each digital artery was much smaller than other vein, but always existed any level of digital artery. One or two venae comitantes in the digital artery ran spiral, oblique, helical, fibrillar, or irregular branched shape. The authors also found the vein of the finger, that had bicuspid valves, but not in venae comitantes. Conclusion: Recently, venous outflow problem rather than arterial circulation is the most common cause tissue failure after microvascular surgery in the hand. Sometimes, if it is not recognized early, there is an increased risk of tissue damage and loss. The authors concluded that this study presents a useful knowledge for the characterization of the venous structure and evidence for venae comitantes like a venule in the digital artery at varying levels of the finger.

• The Journal of the Korea Contents Association
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• v.10 no.9
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• pp.259-266
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• 2010

The study focuses on the value of Micro CT, a high resolution X-ray imaging device, by using it on rats to observe the overall portal vein image of the liver and the microvasculature of each lobes, visualize the 4 segmental lobes and acquire 3D image of the microvasculature through the reconstruction of sectional image data. Less of the damage to liver of the 5 mice, the device was able to separate the liver into 4 segmental lobes and displayed the 4 portal vein microvasculature in 2D. By using the 3D MIP technique, observation of the whole portal vein system microvasculature in 3D image was made possible along with each of the portal vein segment's branches until the 6th branch. Measured the size of 6branch, the average was measured at 1branch : $0.51mm{\pm}0.08$, 2 branch : $0.32mm{\pm}0.12$, 3 branch : $0.23mm{\pm}0.11$, 4 branch : $0.19mm{\pm}0.08$, 5 branch : $0.13mm{\pm}0.06$, 6 branch : $70.5{\mu}m{\pm}14.1$. The 3D image and the images of the microvasculatures in the result of study proved that the Micro-CT can be considered many useful device in obtaining high resolution images.

• Clinical and Experimental Pediatrics
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• v.53 no.3
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• pp.428-431
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• 2010

Thrombotic thrombocytopenic purpura (TTP) is a thrombotic microangiopathy characterized by endothelial cell damage, resulting in microangiopathic hemolytic anemia, thrombocytopenia, and various degrees of neurological and renal impairment caused by microvascular thrombi. It is rare in children and frequently follows a fatal course. TTP is divided into 2 types: one is inherited and associated with ADAMTS-13 gene mutations and the other is acquired and associated with anti-ADAMTS-13 autoantibodies. The measurement of ADAMTS-13 activity in plasma, identification of ADAMTS-13 circulating inhibitor, anti-ADAMTS-13 IgG, and ADAMTS-13 gene sequencing are crucial to the diagnosis of TTP. Plasma exchanges are the first-line treatment for acquired TTP, combined with steroids and immunosuppressive drugs. Here, we describe the case of an adolescent patient with TTP, confirmed by decreased level of ADAMTS-13 activity and an increased level of ADAMTS-13 inhibitor, who was successfully treated by plasma exchanges.

• Journal of Chest Surgery
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• v.31 no.8
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• pp.739-748
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• 1998

Background: It has been well documented that transient occlusion of the coronary artery causes myocardial ischemia and finally cell death when ischemia is sustained for more than 20 minutes. Extensive studies have revealed that ischemic myocardium cannot recover without reperfusion by adequate restoration of blood flow, however, reperfusion can cause long-lasting cardiac dysfunction and aggravation of structural damage. The author therefore attempted to examine the effect of postischemic reperfusion on myocardial ultrastructure and to determine the rationales for recanalization therapy to salvage ischemic myocardium. Materials and methods: Young Holstein-Friesian cows(130∼140 Kg body weight; n=40) of both sexes, maintained with nutritionally balanced diet and under constant conditions, were used. The left anterior descending coronary artery(LAD) was occluded by ligation with 4-0 silk snare for 20 minutes and recanalized by release of the ligation under continuous intravenous drip anesthesia with sodium pentobarbital(0.15 mg/Kg/min). Drill biopsies of the risk area (antero-lateral wall) were performed at just on reperfusion(5 minutes), 1-, 2-, 3-, 6-, 12-hours after recanalization, and at 1-hour assist(only with mechanical respiration and fluid replacement) after 12-hour recanalization. The materials were subdivided into subepicardial and subendocardial tissues. Tissue samples were examined with a transmission electron microscope (Philips EM 300) at the accelerating voltage of 60 KeV. Results: After a 20-minute ligation of the LAD, myocytes showed slight to moderate degree of ultrastructural changes including subsarcolemmal bleb formation, loss of nuclear matrix, clumping of chromatin and margination, mitochondrial destruction, and contracture of sarcomeres. However, microvascular structures were relatively well preserved. After 1-hour reperfusion, nuclear and mitochondrial matrices reappeared and intravascular plugging by polymorphonuclear leukocytes or platelets was observed. However, nucleoli and intramitochondrial granules reappeared within 3 hours of reperfusion and a large number of myocytes were recovered progressively within 6 hours of reperfusion. Recovery was apparent in the subepicardial myocytes and there were no distinct changes in the ultrastructure except narrowed lumen of the microvessels in the later period of reperfusion. Conclusions: It is likely that the ischemic myocardium could not be salvaged without adequate restoration of coronary flow and that the microvasculature is more resistant to reversible period of ischemia than subendocardium and subepicardium. Therefore, thrombolysis and/or angioplasty may be a rational method of therapy for coronarogenic myocardial ischemia. However, it may take a relatively longer period of time to recover from ischemic insult and reperfusion injury should be considered.

• Journal of Chest Surgery
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• v.39 no.12 s.269
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• pp.879-890
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• 2006

Background: The dysfunction of multiple organs is found to be caused by reactive oxygen species as a major modulator of microvascular injury after hemorrhagic shock. Hemorrhagic shock, one of many causes inducing acute lung injury, is associated with increase in alveolocapillary permeability and characterized by edema, neutrophil infiltration, and hemorrhage in the interstitial and alveolar space. Aggressive and rapid fluid resuscitation potentially might increased the risk of pulmonary dysfunction by the interstitial edema. Therefore, in order to improve the pulmonary dysfunction induced by hemorrhagic shock, the present study was attempted to investigate how to reduce the inflammatory responses and edema in lung. Material and Method: Male Sprague-Dawley rats, weight 300 to 350 gm were anesthetized with ketamine(7 mg/kg) intramuscular Hemorrhagic Shock(HS) was induced by withdrawal of 3 mL/100 g over 10 min. through right jugular vein. Mean arterial pressure was then maintained at $35{\sim}40$ mmHg by further blood withdrawal. At 60 min. after HS, the shed blood and Ringer's solution or 5% albumin was infused to restore mean carotid arterial pressure over 80 mmHg. Rats were divided into three groups according to rectal temperature level($37^{\circ}C$[normothermia] vs $33^{\circ}C$[mild hypothermia]) and resuscitation fluid(lactate Ringer's solution vs 5% albumin solution). Group I consisted of rats with the normothermia and lactate Ringer's solution infusion. Group II consisted of rats with the systemic hypothermia and lactate Ringer's solution infusion. Group III consisted of rats with the systemic hypothermia and 5% albumin solution infusion. Hemodynamic parameters(heart rate, mean carotid arterial pressure), metabolism, and pulmonary tissue damage were observed for 4 hours. Result: In all experimental groups including 6 rats in group I, totally 26 rats were alive in 3rd stage. However, bleeding volume of group I in first stage was $3.2{\pm}0.5$ mL/100 g less than those of group II($3.9{\pm}0.8$ mL/100 g) and group III($4.1{\pm}0.7$ mL/100 g). Fluid volume infused in 2nd stage was $28.6{\pm}6.0$ mL(group I), $20.6{\pm}4.0$ mL(group II) and $14.7{\pm}2.7$ mL(group III), retrospectively in which there was statistically a significance between all groups(p<0.05). Plasma potassium level was markedly elevated in comparison with other groups(II and III), whereas glucose level was obviously reduced in 2nd stage of group I. Level of interleukine-8 in group I was obviously higher than that of group II or III(p<0.05). They were $1.834{\pm}437$ pg/mL(group I), $1,006{\pm}532$ pg/mL(group II), and $764{\pm}302$ pg/mL(group III), retrospectively. In histologic score, the score of group III($1.6{\pm}0.6$) was significantly lower than that of group I($2.8{\pm}1.2$)(p<0.05). Conclusion: In pressure-controlled hemorrhagic shock model, it is suggested that hypothermia might inhibit the direct damage of ischemic tissue through reduction of basic metabolic rate in shock state compared to normothermia. It seems that hypothermia should be benefit to recovery pulmonary function by reducing replaced fluid volume, inhibiting anti-inflammatory agent(IL-8) and leukocyte infiltration in state of ischemia-reperfusion injury. However, if is considered that other changes in pulmonary damage and inflammatory responses might induce by not only kinds of fluid solutions but also hypothermia, and that the detailed evaluation should be study.