• Tuberculosis and Respiratory Diseases
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• v.39 no.3
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• pp.228-235
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• 1992

Background: Although polymorphonuclear leukocytes (PMN) are important in protecting the airways and alveolar surfaces, there is evidence that they can also injure the lung while exercising their defensive role. However it has been unclear whether PMN-induced pneumocyte injury is mediated by their direct cytotoxic effect on target cells or by PMN-derived cytotoxic mediators. On the other hand histamine was known not only to act as an important chemical mediator participated in the pathogenesis of some atotic and allegic disorders, but also to have an inhibitory effect on normal PMN functions. Method: To study the mechanism by which PMN induce pneumocyte injury, we cocultured PMN from four healthy nonsmokers or their PMN-derived supernatants (PMN-SPN) with monolayers of $^{51}Cr$-labeled human A549 pneumocytes and compared PMN-and PMN-SPN-mediated pneumocyte injuries measured by $^{51}Cr$ release assay. We also compared the effects of histamine on each pneumocyte injury. Results: 1) PMN-SPN showed more injurious effect on A549 pneumocytes than that of PMN itself regardless histamine pretreatment of PMN. 2) Pneumocyte injury by PMN with histamine pretreatment was increased or decreased compared with that by PMN without histamine pretreatment, according to histamine concentrations, and PMN stimulating agents and their concentrations. 3) Pneumocyte injury by PMN-SPN with histamine pretreatment tended to be decreased compared with that by PMN-SPN without histamine pretreatment. Conclusion: Our results suggest that PMN-SPN may play more important role in mediating pneumocyte injury than PMN itself and that histamine may partially play a protective role on PMN-induced pneumocyte injury. Alternatively we conclude that the effects of histamine on PMN-induced pneumocyte injury may be affected by microenvironment in vivo.

• Tuberculosis and Respiratory Diseases
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• v.52 no.3
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• pp.219-229
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• 2002

Background : Sepsis-induced acute lung injury (ALI) is caused by many cellular and humoral mediators induced by an endotoxin. Histamine, which is widely distributed in the lungs and has been considered as an important mediator of sepsis. It increases P-selectin expression on the endothelial cell surfaces and induces IL-8 secretion. Therefore, an endotoxin-induced histamine may be related to neutrophil-mediated ALI by inducing the migration and activation of neutrophils in the lung tissue. However, the role of endogenous histamine in endotoxin ALI has not been clarified. The purpose of this study was to investigate how endotoxin-induced ALI is influenced by endogenous histamine and to identify the possible mechanism of action. Materials and Methods : The study consisted of 4 groups using Sprague-Dawley rats : 1) control group, where the rats were infused intratracheally by normal saline, 2) an endotoxin group, where lipopolysaccharide (LPS) was administered intratracheally 3) the $H_2$ receptor antagonist-treated group ($H_2$ group) and 4) the $H_1$ receptor antagonist-treated group ($H_1$ group), where $H_2$-receptor blocker (ranitidine) and $H_1$-receptor blocker(pyrilamine) were co-treated intravenously with the intratracheal administration of an endotoxin. The lung leak index using $I^{125}$-BSA, the total protein and LDH concentration in the lung lavage fluid, myeloperoxidase(MPO) activity in the lung tissue, the pathologic score and the total number of neutrophils, TNF-$\alpha$, IL-$1{\beta}$ and IL-10 in lung lavage (BAL) fluid were measured in each group as the indices of lung injury. Results : Compared to the control group, the endotoxin group exhibited significant increases in all lung injury indices. Significant reductions in the endotoxin-mediated increases in lung leak index (p<0.05) were observed in both the $H_1$ and $H_2$ groups. In addition the total protein (p<0.05) and LDH concentration (p<0.05) in the BAL fluid were also lower in the $H_2$ group compared to the endotoxin group. However, there was no change in the MPO activity in the lung tissue, the pathologic score and the total number of neutrophils in the BAL fluid in both the $H_2$ and $H_1$ groups compared to the endotoxin group. The increases in TNF-$\alpha$ IL-$1{\beta}$ and IL-10 concentrations in the BAL fluid observed in the endotoxin group were not reduced in the $H_2$ and $H_1$ groups. Conclusion : Antihistamine attenuated the enhanced alveolar-capillary permeability induced by the endotoxin via the $H_2$ receptor. However the attenuating mechanism may not be related to the pathogenesis of neutrophil dependent lung injury.

• Restorative Dentistry and Endodontics
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• v.22 no.1
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• pp.1-33
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• 1997

The objective of this study was to analyze the in vitro and in vivo corrosion products of low and high copper amalgams. The four different types of amalgam alloy used in this study were Fine cut, Caulk spherical, Dispersalloy, and Tytin. After each amalgam alloy and Hg were triturated according to the directions of the manufacturer by means of the mechanical amalgamator(Amalgam mixer. Shinhung Co. Korea), the triturated mass was inserted into a cylindrical metal mold which was 12mm in diameter and 10mm in height. The mass was condensed by 150Kg/cm compressive force. The specimen was removed from the mold and aged at room temperature for about seven days. The standard surface preparation was routinely carried out by emery paper polishing under running water. In vitro amalgam specimens were potentiostatically polarized ten times in a normal saline solution at $37^{\circ}C$(potentiostat : HA-301. Hukuto Denko Corp. Japan). Each specimen was subjected to anodic polarization scan within the potential range -1700mV to+400mV(SCE). After corrosion tests, anodic polarization curves and corrosion potentials were obtained. The amount of component elements dissolved from amalgams into solution was measured three times by ICP AES(Inductive Coupled Plasma Atomic Emission Spectrometry: Plasma 40. Perkim Elmer Co. U.S.A.). The four different types of amalgam were filled in occlusal and buccal class I cavities of four human 3rd molars. After about five years the restorations were carefully removed after tooth extraction to preserve the structural details including the deteriorated margins. The occlusal surface, amalgam-tooth interface and the fractured surface of in vivo amalgam corrosion products were analyzed. In vivo and in vitro amalgam specimens were examined and analyzed metallographically by SEM(Scanning Electron Microscope: JSM 840. Jeol Co. Japan) and EDAX(Energy Dispersive Micro X-ray Analyser: JSM 840. Jeol Co. Japan). 1. The following results are obtained from in vitro corrosion tests. 1) Corrosion potentials of all amalgams became more noble after ten times passing through the in vitro corrosion test compared to first time. 2) After times through the test, released Cu concentration in saline solution was almost equal but highest in Fine cut. Ag and Hg ion concentration was highest in Caulk spherical and Sn was highest in Dispersalloy. 3) Analyses of surface corrosion products in vitro reveal the following results. a)The corroded surface of Caulk spherical has Na-Sn-Cl containing clusters of $5{\mu}m$ needle-like crystals and oval shapes of Sn-Cl phase, polyhedral Sn oxide phase. b)In Fine cut, there appeared to be a large Sn containing phase, surrounded by many Cu-Sn phases of $1{\mu}m$ granular shapes. c)Dispersalloy was covered by a thick reticular layer which contained Zn-Cl phase. d)In Tytin, a very thin, corroded layer had formed with irregularly growing Sn-Cl phases that looked like a stack of plates. 2. The following results are obtained by an analysis of in vivo amalgam corrosion products. 1) Occlusal surfaces of all amalgams were covered by thick amorphous layers containing Ca-P elements which were abraded by occlusal force. 2) In tooth-amalgam interface, Ca-P containing products were examined in all amalgams but were most clearly seen in low copper amalgams. 3) Sn oxide appeared as a polyhedral shape in internal space in Caulk spherical and Fine cut. 4) Apical pyramidal shaped Sn oxide and curved plate-like Sn-Cl phases resulted in Dispersalloy. 5) In Tytin, Sn oxide and Sn hydroxide were not seen but polyhedral Ag-Hg phase crystal appeared in internal space which assumed a ${\beta}_l$ phase.

• Tuberculosis and Respiratory Diseases
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• v.54 no.1
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• pp.91-103
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• 2003

Background : Histamine is widely distributed in the lung. It increases capillary permeability and the P-selectin expression on vascular endothelial cell surfaces. We studied the role of endogenous histamine on the pathogenesis of endotoxin-induced acute lung injury (ALI) in rats. Methods: We instilled either normal saline (control group) or lipopolysaccharide (3 mg/Kg, LPS group) to tracheas of Sprague-Dawley rats. H1-receptor blocker (mepyramine, 10 mg/Kg, H1RB group), H2-receptor blocker (ranitidine, 10 mg/Kg, H2RB group), and H3-receptor blocker (thioperamide, 2 mg/Kg, H3RB group) were administered through vein or peritoneum along with intratracheal LPS administration. Statistical significance was accepted at p<0.05. Results : LPS increases the histamine level in BAL fluid significantly at 2 h after the treatment compared with control group. LPS significantly increases protein concentration, PMN cell count in bronchoalveolar lavage (BAL) fluid, and myeloperoxidase (MPO) activity in the lung tissue at 6 h compared to control group. PMN cell count in BAL fluid and MPO activity in lung tissue were significantly lower in H2RB-group compared to LPS-group. However, protein concentration in BAL fluid showed no significant differences between the LPS alone and LPS with histamine receptor blockade. Conclusions : Endogenous histamine might be involved in the recruitment of PMNs in LPS-induced ALI via H2 receptor. However, its role in ALI would not be significant in this model.

• Journal of Veterinary Clinics
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• v.20 no.1
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• pp.12-21
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• 2003

In this study, we evaluated effects of three anastomotic techniques of small intestine on adhesions in the dog. Twenty six healthy mixed dogs were randomly assigned to three groups. Group I(n = 8) was sutured with a simple continuous suture, group II(n = 7) was sutured with a simple interrupted approximating suture and group III(n = 11) was sutured with a single layer continuous Connell suture. On completion of any intestinal anastomosis, a pedicle of greater omentum was wrapped around the suture line in all experimental dogs. One percent sodium carboxymeth-ylcellulose (5ml/kg) was administrated into the abdomen by feeding tube prior to closing the last part of peritoneum in all dogs. Postoperative adhesions were evaluated at 14th day after operation. The adhesions consisted primarily in two dogs in group I, three dogs in group II and group III. There were adhesions between intestinal serosal surfaces in eight dogs in all groups, but there were no intestinal serosa-visceral peritoneum adhesion and intestinal serosa-mesentery adhesion. Mean adhesion scores were less than score 2 in all groups. Between anastomotic site and omental graft, there were 13.13$\pm$4.97 mm (mean$\pm$S.D.) adhesion formation in group I and 17.29$\pm$4.68 mm in group II and 14.64$\pm$3.80mm in group III. A simple continuous suture resulted in the least adhesion formation and a simple interrupted approximating suture resulted in the greatest adhesion formation among the groups. However, there were no significant differences among three suture techniques in the severity of adhesions. Intestinal intussusception only encountered in one dog during the 14 days, the dog operated and survived. Daily monitoring of temperature, activity, appetite, defecation and micturition were done. All of those vital signs were within normal values and there were no obvious differences among the groups. In conclusion, even though there were no significant differences among three groups, a simple continous suture pattern is recommended to prevent adhesions when operating intestinal anastomosis in dogs.

• Restorative Dentistry and Endodontics
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• v.24 no.4
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• pp.560-569
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• 1999

Blood supply rather than nerve supply implies pulp vitality. To evaluate pulp vitality clinically, electric pulp test and thermal test which are based on sensory nerve response have been used in addition to many auxiliary data such as past dental history, visual inspection, radiographic examination, percussion, palpation and transillumination test. However, reactivity of the nerves to the stimulation is not synonymous with normalcy. Therefore measurement of pulpal blood flow using a laser Doppler flowmeter became a new trial to test the pulp vitality. The purpose of the present study was to evaluate normal pulpal blood flow level of maxillary teeth in adult to provide a guideline in determining the vitality of dental pulp. Pulpal blood flow was measured in maxillary central and lateral incisors, canines, first and second premolars and first molars of seventy nine adults of 22 - 30 years old using a laser Doppler flowmeter (PeriFlux 4001, Perimed Co., Stockholm, Sweden, 780 nm infrared laser, 1mW). For directly-made splints, silicone rubber impressions were taken directly from the mouth. For indirectly-made splints, alginate impressions were taken from the mouth and stone cast were made. After making depressions on the buccal surfaces of the cast teeth to indicate the hole positions, second impressions with vinyl polysyloxane putty were taken from the cast. Holes for the laser probes were made at the putty impressions 4mm above the gingival level. Laser probe (PF416 dental probe, 1.5mm) was inserted in the prepared hole and the splint was set in the mouth. After 10 minutes of patient relaxing, pulpal blood flow was recorded for 5 minutes on each tooth. The recorded flow was saved in the computer and calculated with a software 'Perisoft' version 5.1. Pulpal blood flow was also recorded in six teeth of five individuals with no response to electric pulp test and cold test, with periapical radiolucency, or with history of root canal treatment to compare with nonvital teeth. The difference between the mean flow values of each group of teeth were analyzed using one-way ANOVA and Duncan's Multiple Range test. The results were as follows: 1. The average pulpal blood flow values of all the tested teeth of each location were between 9 - 16 Perfusion Unit. Pulpal blood flow value was highest in maxillary lateral incisors, followed by first premolars, second premolars, canines, central incisors, and then first molars (p<0.01). 2. In six anterior teeth, indirectly-made splint group showed higher pulpal blood flow values than directly-made splint group (p<0.01). In posterior teeth, however, there was no significant flow value difference between directly-made splint group and indirectly-made splint one (p>0.05). 3. Teeth with vital pulps showed higher signal values than teeth with nonvital pulps (p<0.01), and the flow photographs showed heartbeat-synchronous fluctuations and vasomotions, while those were absent in non vital tooth.

• Tuberculosis and Respiratory Diseases
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• v.43 no.2
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• pp.210-220
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• 1996

Background : Neutrophils or monocytes separated in vitro by the adherence to plastic surface are known to be activated by surface adherence itself and subsequent experimental data might be altered by surface adherence. In the process of surface adherence, adhesion molecules have a clear role in intracellular signal pathway of cellular activation. Human alveolar macrophages(HAM) are frequently purified by the adherence procedure after bronchoalveolar lavage. But the experimental data of many reports about alveolar macrophages have ignored the possibility of adhesion-induced cellular activation. Method : Bronchoalveolar lavage was performed in the person whose lung of either side was confirmed to be normal by chest CT. With the measurement of hydrogen peroxide release from adherent HAM to plastic surface and non-adherent HAM with or without additional stimulation of phorbol myristate acetate(PMA) or N-formyl-methionyl-leucyl-phenylalanine (fMLP), we observed the effect of the adherence to plastic surface. We also evaluated the effect of various biological surfaces on adhesion-induced activation of HAM. Then, to define the intracellular pathway of signal transduction, pretreatment with cycloheximide, pertussis toxin and anti-CD11/CD18 monoclonal antibody was done and we measured hydrogen peroxide in the culture supernatant of HAM. Results : 1) The adherence itself to plastic surface directly stimulated hydrogen peroxide release from human alveolar macrophages and chemical stimuli such as phorbol myristate acetate(PMA) or N-formyl-methionyl-leucyl-phenylalanine(fMLP) colud not increase hydrogen peroxide release in these adherent macrophages which is already activated. 2) PMA activated human alveolar macrophages irrespective of the state of adhesion. However, fMLP stimulated the release of hydrogen peroxide from the adherent macrophages, but not from the non-adherent macrophages. 3) HAM adherent to A549 cell(type II alveolar epithelium-like human cell line) monolayer released more hydrogen peroxide in response to both PMA and fMLP. This adherence-dependent effect of fMLP was blocked by pretreatment of macrophages with cycloheximide, pertussis toxin and anti-CD18 monoclonal antibody, Conclusion : These results suggest that the stimulatory effect of PMA and fMLP can not be found in adherent macrophage because of the activation of human alveolar macrophage by the adherence to plastic surface and the cells adhered to biologic surface such as alveolar epithelial cells are appropriately responsive to these stimuli. It is also likely that the effect of fMLP on the adherent macrophage requires new protein synthesis via G protein pathway and is dependent on the adhesion between alveolar macrophages and alveolar epithelial cells by virtue of CD11/CD18 adhesion molecules.