ABSTRACT
PURPOSE: Perinatal asphyxia is an important cause of neonatal mortality and subsequent lifelong neurodevelopmental handicaps. Although many treatment strategies have been tested, there is currently no clinically effective treatment to prevent or reduce the harmful effects of hypoxia and ischemia in humans. In the clinical setting, maternal hyperthermia induces adverse effects on the neonatal brain, but recent studies have shown that hyperthermic pretreatment (PT) plays some role in hypoxic-ischemic (HI) injuries of the developing brain. The present study investigated the effect of hyperthermic PT on HI brain injuries in newborn rats. METHODS: HI was produced in 7-day-old neonatal rats by unilateral common carotid artery ligation, followed by hypoxia with 8% oxygen at 38degrees C for 2 hours. Twenty-four hours before HI, one-half of the pups were exposed to a 40degrees C environment for 2 hours. The severity of the brain injury was assessed 7 days after the HI. RESULTS: Hyperthermic PT reduced the gross and histopathologic findings of brain injury from 64.7 to 31.2% (P<0.05). There were no differences in location and severity of injury between the pretreated and control brains. CONCLUSION: These findings indicate that hyperthermic PT provides neuroprotective benefits on HI in the developing brain. Also, these findings suggest maternal hyperthermia may have protective effect on perinatal HI brain injuries.
Subject(s)
Animals , Humans , Infant , Infant, Newborn , Rats , Hypoxia , Asphyxia , Brain , Brain Injuries , Carotid Artery, Common , Fever , Infant Mortality , Ischemia , Ligation , OxygenABSTRACT
PURPOSE: This study was undertaken to determine whether any features of apoptosis would occur in the established model of cerebral hypoxia-ischemia in neonatal rats. It was also undertaken to evaluate the effect of post-insult hyperoxia on hypoxic ischemic cerebral injury. METHODS: Seven-day-old neonatal rats underwent unilateral carotid artery dissection followed by 2 hours of hypoxia. To this end rat pups, allocated into 2 groups, were resuscitated with high concentration O2(>FiO2 95%) or room air for a 1-hour period. All of them were killed at 3 days after the above procedures. Their brains were perfusion fixed and removed to examine tissue damage by light microscope and apoptosis by terminal deoxynucleotidyl transferase mediated dUTP- biotin nick end labeling(TUNEL) reactivity. RESULTS: The result demonstrates that hypoxia-ischemia model induces tissue damage and TUNEL. Post-insult exposure to high reactivity concentration O2 does not aggravate hypoxic-ischemic cerebral injury 3 days after the insult but increases TUNEL reactivity in injured tissue. CONCLUSIONS: These findings suggest that many cells die by apoptosis following hypoxia-ischemia in neonatal brain and resuscitation with high concentration O2 seems to provide an adverse effect over a brain injury by induction of apoptosis.
Subject(s)
Animals , Rats , Hypoxia , Apoptosis , Biotin , Brain Injuries , Brain , Carotid Arteries , DNA Nucleotidylexotransferase , Hyperoxia , Hypoxia-Ischemia, Brain , In Situ Nick-End Labeling , Ischemia , Models, Animal , Oxygen , Perfusion , ResuscitationABSTRACT
Urinary ascites in newborns is a rare event that usually is associated with posterior urethral valves and other obstructing anomalies of the genitourinary tract. A case of neonatal urinary ascites without genitourinary tract abnormalities is reported. This premature male neonate was treated by artificial ventilation due to respiratory distress syndrome. The umbilical artery catheter was placed without difficulties and functioned well until removal. Periumbilical leak of urine was not observed. He showed abdominal distension and oliguria on second postnatal day. He was found to have ascites, hyponatremia and elevation of BUN content disproportionate to the mild elevated serum creatinine value. Radiological examination revealed normal genitourinary tract except intraperitoneal extravasation of contrast material from the bladder. Conservative management resulted in complete resolution of the lesion in this patient.
Subject(s)
Humans , Infant, Newborn , Male , Ascites , Catheters , Creatinine , Drainage , Hyponatremia , Oliguria , Umbilical Arteries , Urinary Bladder , VentilationABSTRACT
PURPOSE: The morphogenic mechanism of tetralogy of Fallot is known to be an antero-superior deviation and hypertrophy of the subpulmonary infundibulum. We performed this study to measure the subpulmonary infundibulum in patients with tetralogy of Fallot and compare those with normal control. METHODS: Echocardiographic data and medical reports of 12 patients, with classical tetralogy of Fa11ot who were diagnosed echocardiographically from Dec. 1996 to Jan. 1999 in Kyungpook National University Hospital, were retrospectively reviewed. A control group consisted of 11 children who underwent a complete echocardiographic examination for a heart murmur and were found to be structually norrnal. Measurements of the subpulmonary infundibulum were performed in systolic still frames with the subxiphoid short axis view. RESULTS: Compared with the normal control children, the following indexed infundibular dimensions in patients with tetralogy of Fallot were significantly smaller' volume, length, cross-sectional area, diameters of pulmonary valve annulus, main, left and right pulmonary arteries, PA index and McGoon ratio. The following measurements were increased in tetralogy patients ' the angle between infundibular septum and ventricular septum, and infundibular free wall thickness. CONCLUSION: We confirmed both antero-superior deviation of infundibular septum and infundibular hypoplasia as morphologic abnormalities in tetralogy of Fallot. We also revealed relatively equal contributions of shortening of infundibular length, and increased infundibular septal and free wall thickness to infundibular hypoplasia.