Adhesives ; Burns ; Calcium Chloride ; Cicatrix ; Cicatrix, Hypertrophic ; Collagen ; Factor XIII ; Fibrin Tissue Adhesive ; Fibrin ; Fibrinogen ; Follow-Up Studies ; Gingiva ; Hemorrhage ; Humans ; Mouth ; Nose ; Polymers ; Skin Transplantation ; Skin ; Surgery, Oral ; Sutures ; Thrombin ; Tissue Donors ; Transplants ; Wound Healing

PURPOSE: In the treatrnent of respiratory distress syndrome, Infants are often exposed to hyperoxia. It can generate oxygen free radical, damage to lung and bronchi, and inactivate pulmonary surfactant(PS). Antioxidant therapy in animal and human models has been tried to overcome this detrimental effects. We hypothesized that the addition of oxygen free radical such as hydrogen peroxide(H) could compromise surface active properties(SAP) of PS and that further addition of antioxidant such as catalaseR(CAT, Sigma chemical, St. Louis) could recover SAP. METHODS: We prepared combinations of mixtures with SurfactenR(S-TA, Tokyo Tanabe, Japan), H202 and CAT. 1)0.625mgPL(phospholipids)/ml or 1.25mgPL/ml S - TA and H202 were mixed to the final concentrations of 0.1 and 1mM H respectively, and incubated at 37C for one hour. 2) 0.625mgPL/rnl S - TA, H202 and CAT 10U were mixed to the final concentrations of lmM H202, and incubated at 37 degree C for one hour. We used Pulsating Bubble Surfactometer (Electronetics, NY) measure in vitro minimum and maximum surface tensions(ST) and area-surface tension relationship. RESULTS: 1) For 0.625mgPL/ml S-TA and 1mM H mixture minimum. ST after 5 min of pulsation increased significantly(P=0.007) and the area-surface tension curve was deformed. But they were comparable to control levels for 1.25mgPL/ml S-TA. 2) When CAT was added to 0.625mgPL/ml S-TA and 1mM H mixture, the resultant minimum ST after 5 min of pulsation dropped to the control levels with recovery of hysteresis curve(P=0.0001). CONCLUSION: PS could be inactivated by addition of high concentrations of H but SAP can be recovered either by increasing PS concentration or by further addition of antioxidant CAT. Therefore, we suggest that in case of suspected surfactant inactivation an increase in surfactant concentration or administration of antioxidant must be considered.
Animals ; Bronchi ; Catalase* ; Cats ; Humans ; Hydrogen Peroxide* ; Hydrogen* ; Hyperoxia ; Infant ; Lung ; Oxygen

No abstract available.
Neutrophils*

PURPOSE: Antenatal steroid(ANS) therapy in premature infants is an effective therapeutic strategy in reducing the incidence of respiratory distress syndrome, intraventricular hemorrhage, necrotizing enterocolitis, and patent ductus arteriosus. For premature infants to gain improved survival, adequate weight loss during early postnatal days and maintenance of electrolyte balance is important, however, it is uncertain that ANS affect them. We hypothesized that ANS augment fluid and electrolyte balance and dinical outcome of very low birth weight(VLBW) who had received restricted fluid regimen. METHODS: Mechanically ventilated VLBW infants who survived over 30 days were selected. We reviewed medical records to compare weight loss, urine output, electrolyte concentration, blood pressure during five days of life and clinical outcome between premature infants who received ANS(n=15) and who were not(n=58). RESULTS: Gestational age, birth weight were similar between two groups. Volume of administered fluid, urine output, and initial weight loss during first five days of life were similar, however, weight loss on postnatal day five were lower in study group than control group(p=.039). Blood pressure, serum sodium concentration, serum potassium concentration, and urine specific gravity were similar between two groups. Incidence of respiratory distress syndrome was lower in study group(20%) than control group(48%)(p=.041), however, incidence of sepsis were greater in study group(33%) than control group(7%)(p=.029). CONDUSION: ANS did not affect fluid and electrolyte balance of very low birth weight(VLBW) infants who had received restricted fluid regimen. ANS decreased the incidence of respiratory distress syndrome in this population, however, increased the incidence of sepsis.
Birth Weight ; Blood Pressure ; Ductus Arteriosus, Patent ; Enterocolitis, Necrotizing ; Gestational Age ; Hemorrhage ; Humans ; Incidence ; Infant* ; Infant, Low Birth Weight* ; Infant, Newborn ; Infant, Premature ; Medical Records ; Parturition ; Potassium ; Sepsis ; Sodium ; Specific Gravity ; Water-Electrolyte Balance* ; Weight Loss

BACKGROUND: Purinergic and cholinergic agonists elicit negative-inotropic and chronotropic effects, anticip-ating their protective action from the damage of overloaded myocardium. However, the actions of the agents during the ischemic insults are not yet clearly informed. The aim of this study was to investigate the role of the purinergic and cholinergic agonists on the simulated ischemic myocardium of the rat atrial fiber preparations. METHOD: Various action potential parameters (maximum diastolic potential MDP;action potential amplitude APA;velocity of phase 0 depolarization dV/dtmax;action potential duration APD90) were measured and compared in electrically paced, normal (NPSS) and modified physiological salt solution (MPSS) superfused rat atrial fibers in vitro, using conventional 3M-KCl microelectrode technique. Ischemia-simulated modified physiologic solutions were prepared by changing the solution's composition. RESULTS: Hypoxic-and/or hyperkalemic-MPSS decreased all the action potential (AP) variables. However, no significant changes of the AP variables were developed by the acidic-or glucose-free MPSS. Adenosine (Ado) and cyclopentyladenosine (CPA) only decreased the APD90 in a dose-dependent manner. Acetylcholine (Ach) and carbachol (Cch) hyperpolarized the MDP, increased the dV/dtmax with certain doses, and decreased the APD90 dose-depen-dently. The potency for APD90-decrease was greater in order, CPA>Cch>Ach>Ado. Ado and CPA did not affect the hypoxic, hypokalemic MPSS-induced dV/dtmax-decrease. On the other hand, Ach and Cch sig-nificantly inhibited the dV/dtmax-decrease by the hypoxic hypokalemic-MPSS. Ado, CPA, Ach and Cch sig-nificantly augmented the hypoxic, hypokalemic MPSS-induced APD90-decrease. The inhibition by the Ach and Cch on the MPSS-induced dV/dtmax-decrease was not affected by DPCPX, but atropine significantly attenuated the inhibition by the cholinergic agonists. DPCPX inhibited the augmentation by the Ado and CPA on the MPSS induced APD90-decrease, and atropine inhibited the effect of the cholinergic agonists. CONCLUSION: Both purinergic and cholinergic agonists not only shorten the AP duration by themselves but also enhance the AP-shortening effect elicited by the ischemia, and therefore, it is inferred that both agonists prevent further tissue damage from the ischemic insults.
Acetylcholine ; Action Potentials ; Adenosine ; Animals ; Atropine ; Carbachol ; Cholinergic Agonists* ; Hand ; Ischemia ; Microelectrodes ; Myocardium* ; Rats*

As the newly reconstructed nipple tends to be flattened, especially if submitted to pressure, prudent dressings using various protective devices as a physical support against pressure on a new nipple is important. We used a breathing bag connecting tube as a protective device in nipple reconstruction. A breathing bag connecting tube recycled was cut and trimmed at 1cm above the height of the reconstructed nipple. Before stitch out, the newly reconstructed nipple with a local flap was dressed and protected in this way for 10 days after surgery. After stitch out, patients learnt how to manage the new nipple at home. The sole means of nipple dressing was affixing the breathing bag connecting tube with adhesive tape. Two patients had worn the tube for two months with the best compliance. Owing to the soft composition of the tube material, it is possible for a surgeon to have an easy cutting and trimming of the tube at appropriate heights as well as for a patient to show better compliance yielding better results. The cost factor is another advantage.
Adhesives ; Bandages ; Compliance ; Fibrinogen ; Humans ; Nipples* ; Protective Devices ; Respiration*

BACKGROUND: To investigate the role of alpha-adrenergic receptors in the development of delayed afterdepolarization, the effect of alpha-adrenoceptor stimulation and blockade on ouabain induced delayed afterdepolarization(DDAD) was examined in rabbit heart Purkinje fibers. METHODS: Purkinje fibers, taken from adult rabbit(1.8 - 2.0kg) heart anesthetized with penobarbital, were mounted in a Luicite chamber and superfused with Tyrode's solution. The transmembrane potentials were measured by the conventional microelectrode technique while the fibers were being stimulated with rectangular pulses of 50% above threshold voltage. The delayed afterdepolarizations were induced by overdrive excitation in the presence of ouabain. RESULTS: Delayed afterdepolarizations were not observed during superfusion of the control Tyrode's solution containing propranolol(5x10(-7)M). However, the addition of ouabain in the presence of propranolol elicited DADs which were dose-, time- and drive cycle length- dependent. Phenylephrine(PE ; 10(-7)M), and alpha-adrenoceptor agonist, potentiated the ouabain-induced DAD during the initial superfusion(for 10 or 20 min) of the test Tyrode's solution. However, it was followed by attenuating-effects after a superfusion time of 50 to 60 min. Both effects showed ouabain dose-dependence. Ouabain(2x10(-7)M), in the presence of propranolol, depolarized the maximum diastolic potential and shortened the action potential duration, and the addition of PE(10(-7)M) did not affect the characteristics of action potential except a decrease in velocity of phase 0 depolarization. Prazosin, an alpha1-adrenoceptor antagonist, inhibited the PE's enhancing effects of ouabaininduced DDAD at 20 min superfusion, but did not affect the attenuating-effects of PE at 60 min superfusion. On the other hand, yohimbine, an alpha2-adrenoceptor antagonist, did not affect the PE's DAD potentiating-effects at 20 min superfusion, but inhibited the attenunating-effects of PE at 60 min superfusion. CONCLUSION: It is inferred that alpha-adrenergic stimulation induce delayed afterdepolarization and triggered activity in the rabbits, being responsible for the arrhythmia development, and the effects are mainly due to the action of alpha1-subtpe adrenoceptor stimulation.
Action Potentials ; Adult ; Arrhythmias, Cardiac ; Hand ; Heart ; Humans ; Membrane Potentials ; Microelectrodes ; Ouabain ; Prazosin ; Propranolol ; Purkinje Fibers ; Rabbits ; Receptors, Adrenergic, alpha* ; Yohimbine

Purpose: This study attempted to study the intra-articular changes due to intramedullary nailing through the suprapatellar approach by evaluating the joint cartilage damage and presence of foreign bodies through a comparison of the pre- and post-operative status evaluated by knee arthroscopy. Materials and Methods: This retrospective study analyzed fifteen patients who underwent intramedullary nailing through the suprapatellar approach for proximal tibial shaft fracture from January 2017 to March 2020. The condition of the joint cartilage and the presence of foreign substances in the patellofemoral joint were evaluated. The cartilage status of the patellofemoral joint was evaluated using the International Cartilage Repair Society (ICRS) grading system. Data from the ICRS grading and the visual analogue scale (VAS) scores of the femoral and patellar cartilage were compared to each independent variable surveyed. Results: All the intra-articular structures before nailing were normal. In all cases after nailing, articular cartilage damage of the patellofemoral joint and intra-articular debris were observed. The average VAS score was 0.6 (0-1) before surgery and 2.27 (0-4) after surgery. There were no statistically significant differences except for the correlation in the diameter of the tibia nail and femoral ICRS grade (p=0.001) and the damage to the cartilage was greater in the femoral cartilage than that to the patella (p=0.001). Conclusion Intra-articular damage appears to be unavoidable in suprapatellar nailing. Further research is needed on the long-term effects of intra-articular damage and on methods to reduce this damage.

No abstract available.
Coronary Artery Disease* ; Coronary Vessels* ; Risk Factors*

BACKGROUND: To evaluate the role of free fatty acids on the ischemic myocardium, influences of various free fatty acids upon transmembrane action potential and ATP-sensitive K+(KATP) channel activity were examined in the ventricular myocardium and single cardiac myocytes. METHODS: KATP channel activities were measured in the enzymatically (collagenase) isolated single rat ventricular cardiac myocytes by the method of the excised inside-out and the cell-attached patch clamp, and transmembrane action potentials were recorded using the conventional 3M-KCl microelectode techniques in the rat ventricular myocardium. RESULTS: Free fatty acids [FFAs; arachidonic acid (AA), linoleic acid (LA) and lysophosphatidylcholine (LPC)] reduced the KATP channel activity in a dose-dependent manner in the inside-out patch, and 50%-inhibition concentrations (IC50) were 88 +/- 11.2, 49 +/- 12.5, and 188 +/- 17.4 M respectively. Both frequency of channel opening and the mean open-burst duration were markedly decreased, but the amplitude of single channel currents were not changed by the FFAs. AA (50 micrometer) and LPC (50 micrometer) did not affect the dinitrophenol (DNP, 50 micrometer)-induced KATP channel activity, whereas LA (50 micrometer) had a tendency to reduce the activity. The channel inhibition effects by 10 micrometer AA in the inside-out patch were significantly augmented by diclofenac (10 micrometer), but was not changed by nordihydroguaiaretic acid. FFAs never stimulated KATP channel activity, even in the inside-out patch where KATP channel activity reduced in the presence of internal ATP (100 micrometer). Time for 90% repolarization (APD90) significantly increased during superfusion of the FFAs, to 22 (50 micrometer AA), 24 (50 micrometer LA), and 18 (50 micrometer LPC) % from those of the contol at the time of 10 min superfusion, but the other action potential characteristics were not changed by the FFAs. AA (10 micrometer) attenuated cromakalim (10 micrometer)-induced APD90 shortening effects. CONCLUSION: It was inferred that FFAs inhibit the KATP channel activity directly by themselves and/or indirectly by their metabolites in the rat ventricular cardiomyocytes, and therefore, duration of action potential lengthens to be a burden over the ischemic myocardium accounting for the injury of myocardium at the late stage of ischemia.
Action Potentials* ; Adenosine Triphosphate ; Animals ; Arachidonic Acid ; Cromakalim ; Diclofenac ; Fatty Acids, Nonesterified* ; Ischemia ; Linoleic Acid ; Lysophosphatidylcholines ; Masoprocol ; Myocardium* ; Myocytes, Cardiac ; Potassium Channels* ; Potassium* ; Rats*