A significant decrease in the rate of threshold ROP in infants of <33 weeks gestation was observed after implementation of the new clinical O(2) management practice.

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Summary: A new model of transient cerebral ischemia in lO-day-old rats is described, Under microscopic guid ance, the right external and internal carotid arteries were electrically coagulated. A solid 0.47 mm diameter nylon thread was inserted into the right common carotid artery toward the ascending aorta up to 10-12 mm from the up per edge of the sternomastoid muscle (preischemic rats), A 60-min cerebral ischemia was induced by clamping the left external and internal carotid arteries (ischemic rats), followed by 3-h recirculation. 31p magnetic resonance (MRS) spectroscopic studies revealed that severe intra cellular acidosis occurred and A TP disappeared com pletely for at least the last 20 min of ischemia. Cerebral Hypoxic-ischemic encephalopathy (HIE) is one of the major and important causes of developmental disabilities such as mental retardation and cerebral palsy. It is the ultimate result of hypoxia and isch emia, which lead to metabolic deterioration. Al though, in most cases, hypoxia and ischemia occur simultaneously on asphyxia, ischemia may have a greater biochemical effect on the central nervous system (eNS). It is known that periventricular Ieu komalacia in the preterm infant is primarily due to an ischemic lesion (DeReuck et aI., 1972; Yoshioka et aI. , 1994). The pathogenesis of parasagittal cere bral injury, also called' 'watershed infarcts" , in full term infants is principally related to perfusion im pairment in the border zones between the end fields of the major cerebral arteries (Brierley, 1976 Abbreviations used: CBF, cerebral blood flow; CNS, central nervous system; HIE, hypoxic-ischemic encephalopathy; MABP, mean arterial blood pressure; MRS, magnetic resonance spectroscopy. 237blood flow (CBF), measured by the hydrogen clearance technique, decreased to � 11 % of the preischemic level in the frontal cortex soon after the induction of ischemia. On resuscitation, ATP recovered completely and the preis chemic intracellular pH level was restored within 180 min. CBF had recovered to �30% of the preischemic level at 5 min after resuscitation. The CBF recovery was not complete even at 180 min after resuscitation. With this model, the effects of pure ischemia without hypoxia on t h e neonatal brain and the process of recovery from transient ischemia can be studied. Key Words: Neonatal rat-Transient cerebral ischemia-31P-magnetic reso nance spectroscopy-Cerebral blood flow.Therefore, it is said that hypoxia alone does not lead to brain damage, but, rather, its combination with ischemia, or isolated cerebral ischemia, is a necessary prerequisite for tissue injury to occur (Vannucci, 1992).However, very little is known about the effects of pure ischemia without hypoxia on the perinatal brain since the only experimental method previ ously available for pure cerebral ischemia without hypoxia for the small laboratory animal involved decapitation. Thurston et al. (1969) found that ce rebral ATP in the mature mouse had almost com pletely disappeared at 4 min after decapitation, while that in the neonat...