We observed clinical features of 18 bronchopulmonary dysplasia (BPD) patients who were admitted to the neonatal intensive care unit in the Severance Hospital of Yonsel University College of Medicine from January 1. 1987 to June 30. 1991. Eight patients in whom ventilator settings were unchanged for more than 5 days because of lack of improvement in pulmonary function. The effects of dexamethasone in ventilator-dependent were included in the short-term dexamethasone therapy. 1) Eighteen BPD patients consisted of 15 premature infants (83%), 1 full-term infant, and 2 post-term infants, The mean gestational age of the patients were 30 weeks and the mean birth weight was 1,420gm. And there were 13 male and 5 female infants. 2) The underlying conditions which necessitated ventilatory support support were hyaline membrane disease in 13 patients (72%), apnea in 2 (11%), and meconium aspiration syndrome in 3. There patients with meconium aspiration syndrome were either full-term or post-term infants, of whom 2 had neonatal persistent pulmonary hypertension. 3) The mean age at the start of ventilator care was 8 hours and the mean PIP was 32 cm H2O. The mean duration of ventilator care of oxygen therapy and of high O2 requirement (FiO2>0.8) were 39 days, 75 days and 20 days, respectively. 4) Patent ductus arteriosus developed in 8 patients during mechanical ventilation, but they were all closed with the use of mefenamic acid, There were also 4 cases of pneumothorax, 2 cases of pulmonary parenchymal emphysema, and 1 case each of pneumomediastinum and pneumoperitoneum. 5) The mean gestational age of the dexamethasone-treated group was 30 weeks and the mean birth weight was 1,320gm, The mean age at which dexamethasone therapy was started was 39 days after birth, and in only 3.3 days 6 patients were successfully weaned from ventilator, In 5 cases the first trial of dexamethasone therapy was enough but the rest needed the 2nd trial for ventilator weaning. 6) In 6 BPD patient who were weaned from the ventilator after dexamethasone therapy, there were significant decreases in MAP (11.1 vs 8.0 cmH2O), and FiO2 (0.73 vs 0.61), but a significant increase in the urine output (2.56 vs 3.7ml/kg/hr) for the pretreatment (5 days prior to therapy) versus posttreatment period (first day of therapy). 7) The complications of dexamethasone treatment were transient hypertension and hyperglycemia in 3 patients, and systemic candidiasis and gastrointestinal bleeding in 2 patients who failed to be weaned after dexamethasone therapy. Our results suggest that the short-term dexamethasone therapy in bronchopulmonary dysplasia patients who are dependent on mechanical ventilation enables weaning in a short period of time. The inspiratory oxygen concentration and the mean airway pressure may be decreased and the urine output may be increased from the first day of medication, improves pulmonary function and decreases pulmonary interstitial edema.
Apnea ; Birth Weight ; Bronchopulmonary Dysplasia* ; Candidiasis ; Dexamethasone* ; Ductus Arteriosus, Patent ; Edema ; Emphysema ; Female ; Gestational Age ; Hemorrhage ; Humans ; Hyaline Membrane Disease ; Hyperglycemia ; Hypertension ; Hypertension, Pulmonary ; Infant ; Infant, Newborn ; Infant, Premature ; Intensive Care, Neonatal ; Male ; Meconium Aspiration Syndrome ; Mediastinal Emphysema ; Mefenamic Acid ; Oxygen ; Parturition ; Pneumoperitoneum ; Pneumothorax ; Respiration, Artificial ; Ventilator Weaning ; Ventilators, Mechanical ; Weaning

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

The incidence of cervical pregnancy and the number of combined intrauterine pregnancy and ectopic pregnancy seems to be increasing. So the possibility of heterotopic pregnancy should always be considered by every gynecologist, especially those who treat infertility problem. We experience a case of a heterotopic pregnancy coexisting of an intrauterine pregnancy and a cervical pregnancy after in-vitro fertilization and embryo transfer, and was successfully managed by transcervical evacuation and resulted in a normal intrauterine pregnancy. Here we present the case with review of literatures.
Embryo Transfer ; Female ; Fertilization ; Fertilization in Vitro* ; Incidence ; Infertility ; Pregnancy* ; Pregnancy, Ectopic ; Pregnancy, Heterotopic*

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

No abstract available.
Humans* ; Rotavirus*

No abstract available.
Pregnancy*

In addition to many of the widely accepted risk factors of bronchopulmonary dysplasia (BPD), such as prematurity, oxygen toxicity, barotrauma, and infection, the amount of fluid intake during the early phase of life has recently been reported to be an important factor, especially the amount of colloid. Forty-one premature infants who were admitted to the NICU of Severance Hospital, Yonsei University College of Medicine between Jan. 1990 and Jun. 1992 and treated for respiratory difficulty with mechanical ventilation and restrictive fluid therapy were included in the study. fourteen were diagnosed as BPD and the rest were grouped as Non-BPD. We confirmed prematurity, low birth weight, high oxygen concentration, high ventilator pressures and rates, perinatal asphyxia, acidosis, and low blood pressures as risk factors. However, with restrictive fluid therapy that we have used, there was no difference in the amount of total fluid, of crystalloid, or of colloid between BPD and Non-BPD groups, as were the urine output, serum electrolyte concentrations, and percent body weight change. The amount of colloid when used for the maintenance of adequate blood pressures and for the prevention and treatment of hypovolemia, oliguria, anemia of sepsis under the scheme of restrictive fluid therapy would not influence adversely in the development of BPD. Instead, the amount of colloid used may imply the severity of illness of the patient; that is, the more severe the condition of the patient the more the amount of colloid used.
Acidosis ; Anemia ; Asphyxia ; Barotrauma ; Body Weight Changes ; Bronchopulmonary Dysplasia* ; Colloids ; Fluid Therapy* ; Humans ; Hypovolemia ; Infant, Low Birth Weight ; Infant, Newborn ; Infant, Premature* ; Oliguria ; Oxygen ; Respiration, Artificial* ; Risk Factors* ; Sepsis ; Ventilators, Mechanical

BACKGROUND: Spinally administered neostigmine, but not morphine, has been well known to reverse the mechanical allodynia in human and animal studies. The efficacy of morphine in neuropathic pain state is somewhat controversial. Using an isobolographic analysis, we examine the spinal interaction between neostigmine and morphine in a rat model of neuropathic pain. METHODS: Male Sprague Dawley rats were prepared with tight ligation of left lumbar 5th and 6th spinal nerves and chronic lumbar intrathecal catheter. Intrathecal dose response curves were established for the antiallodynic effect of neostigmine (0.3, 1.0, 3.0, and 10 microgram) and morphine (0.3, 1.0, 3.0, and 10 microgram) alone to obtain the ED50 for each agent. ED50 fractions (1/2, 1/4, 1/8, and 1/16) of drug combination of neostigmine-morphine were administered. Allodynic thresholds for left hindpaw withdrawal to von Frey hairs application were assessed and converted to %MPE. The ED50 of neostigmine-morphine combinations was established and isobolographic analysis of the drug interaction was carried out. RESULTS: Intrathecal neostigmine and morphine alone produced dose-dependent reductions of tactile allodynia. ED50 values are 0.43 microgram (0.21~0.86 microgram) for neostigmine and 0.39 microgram (0.07~2.01 microgram) for morphine. The log dose responses were plotted from the peak effect of %MPE in each group of neostigmine and morphine. The experimental ED50 1.34E-2 microgram (2.1E-4-0.85 microgram) for neostigmine and morphine combination was found to be significantly below the theoretical additive ED50 value 0.41 microgram (P<0.05). CONCLUSION: The results suggest that intrathecal neostigmine and morphine alone produce a dose dependent antagonism on touch evoked allodynia and intrathecal neostigmine is synergistic at the spinal level when combined with intrathecal morphine in a rat model of neuropathy.
Animals ; Catheters ; Drug Interactions ; Hair ; Humans ; Hyperalgesia ; Ligation ; Male ; Models, Animal ; Morphine* ; Neostigmine* ; Neuralgia* ; Rats, Sprague-Dawley ; Spinal Nerves

Objective: We evaluated the protective effect of dexamethasone (DX) administration on brain damage produced in a perinatal model of cerebral hypoxia-ischemia in the rat. Since hyperglycemia has been shown to reduce hypoxic-ischemic brain injury (HI) in immature tar, we investigated the role of glucocorticoid-induced hyperglycemia in the neuroprotective mechanism of DX. Methods: Hypoxic-ischemic brain injury in 7-day-old rats was induced by right common carotid artery occlusion and 2 hours of 8% oxygen. Pups received 3 doses of DX (0.5mg/kg/d intraperitoneally) 48 hours, 24 hours and immediately before HI (Dx1)(n=12), a single dose of DX 24 hours(DX2)(n=16), 3 hours (DX3)(N=10)or immediately before HI (DX4)(n=14), a single dose of DX immediately after HI (DX5) (n=9), 3 doses of DX immediately, 24 hours and 48 hours after HI (DX6) (n=14) and a single dose of DX 24 hours before HI with insulin (0.5U/kg, subcutaneously, 1.5 hours before HI)(IN)(n=8). Control pups (n=15) received a single dose of normal saline 24 hours before HI. Blood glucose was estimated before hypoxia, 1 hour and 2 hours after hypoxia using glucometer in DX 1~4. IN and control rats. Pups were killed at 14 days of age for determination of mortality during HI, gross cerebral infarction and right cerebral hemisphere atrophy. We measured the diameter of each cerebral hemisphere and cortical thickness from a coronal section at the dorsal hippocampus level, and expressed the % atrophy from the change in the right vs left hemisphere diameter. Results: The mortality that occurred during and after HI was similar in all groups. The incidence of gross cerebral infarction was 0.0%, 0.0%, 75.0%, 83.3%, 87.5%, and 90.0% in DX 1~6, respectively, 0.0%in IN, and 100.0% in control group. There was a significant difference (p<0.001)in the incidence of gross cerebral infarction of DX1, DX2, IN vs control group. The mean % atrophy was 5.4 +/- 2.2, 4.9 +/- 1.8, 21.7 +/- 8.1, 29.7 +/- 5.0, 37.4 +/- 5.5, 33.4 +/- 9.3 in DX 1~6, respectively, 1.5 +/- 1.1 in IN, and 29.1 +/- 3.4 (mean+/-SEM) in control group. There was a significant difference in % atrophy of DX1, DX2, IN vs control group. Before hypoxia, there was no significant difference in blood glucose between saline, all DX, and DX with insulin treated groups. But after hypoxia, pups in DX1 and Dx2 were more hyperglycemic compared to DX 3~4, IN, or saline treated groups. Conclusions: Dexamethasone administration in the neonatal period protects the brain during the subsequent periods of hypoxia-ischemia in rats and glucocorticoid-induced hyperglycemia does not explain the neuroprotective effects dexamethasone.
Animals ; Anoxia ; Atrophy ; Blood Glucose ; Brain Injuries ; Brain* ; Carotid Artery, Common ; Cerebral Infarction ; Cerebrum ; Dexamethasone* ; Hippocampus ; Hyperglycemia* ; Hypoxia-Ischemia, Brain ; Incidence ; Insulin ; Mortality ; Neuroprotective Agents ; Oxygen ; Rats*

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