Immature rats subjected to a combination of unilateral common carotid artery ligation and hypoxia sustain brain damage confined largely to the ipsilateral cerebral hemisphere. To ascertain the extent and distribution of ischemic alterations in the brains of these small animals, we modified the Sakurada technique to measure regional cerebral blood flow using carbon-14 autoradiography. Seven-day-old rats underwent right common carotid artery ligation following which they were rendered hypoxic with 8% O 2 at 37° C. Before and during hypoxia, the rat pups received an injection of iodo[ l4 C]antipyrine for determination of regional cerebral blood flow. Blood flows to individual structures of the ipsilateral cerebral hemisphere were not influenced by arterial occlusion alone; flows to the contralateral hemisphere and to the brainstem and cerebellum actually increased by 25-50%. Hypoxla-ischemia was associated with decreases in regional cerebral blood flow of the ipsilateral hemisphere such that by 2 hours, flows to subcortical white matter, neocortex, striatum, and thalamus were 15,17,34, and 41% of control, respectively. The hierarchy of the blood flow reductions correlated closely with the distribution and extent of ischemic neuronal necrosis. However, unlike the pathologic pattern of this model, the degree of ischemia appeared homogeneous within each brain region. Blood flows to contralateral cerebral hemispheric structures were relatively unchanged from prehypoxic values, whereas flows to the brainstem and cerebellum nearly doubled and tripled, respectively. Thus, ischemia is the predominant factor that determines the topography of tissue injury to major regions of immature rat brain, whereas metabolic factors (intrinsic vulnerability) may influence the heterogeneous pattern of damage seen within individual structures. (Stroke 1988; 19:245-250) A critical question in perinatal medicine is whether hypoxia alone is capable of damaging the brain of a fetus or newborn infant or whether cerebral ischemia, with or without concurrent systemic hypoxia, is necessary for tissue injury to occur. Investigations in animals suggest that hypoxia alone does not damage the immature brain and that superimposed ischemia, produced either by arterial occlusion (stroke) or by systemic hypotension, is a necessary prerequisite for tissue destruction.l~* If this observation can be extended to human infants, then hypoxemia alone should be relatively innocuous so long as the cerebral arteries remain patent and systemic hypotension is avoided.We recently developed an experimental model of perinatal hypoxic-ischemic brain damage in developing rats.3 The technique involves the ligation of one common carotid artery followed by exposure of the rat to systemic hypoxia for 2 or more hours. We assumed that the single carotid artery occlusion provided the ischemia necessary to damage the immature brain, although cerebral perfusion was not assessed directly in the original investigation. In our present study, we measured regional cerebral blood flow ...

ABSTRACT. Unlike adult rats, glucose supplementation of immature rats does not lead to accentuated hypoxicischemic brain damage. To explore the reason for this agespecific paradox, we subjected 7-day postnatal rats to unilateral common carotid artery occlusion followed by a subcutaneous injection of either 0.1 ml 50% glucose or normal saline. They were then exposed to hypoxia with 8% oxygen, during which they received 2.5 wCi 2-[I4Cj-glucose or were quick-frozen for brain metabolite analysis. During hypoxia-ischemia, glucose transport into the ipsilateral cerebral hemisphere of the hyperglycemic rats was greater (+loo-150%) than in normoglycemic animals. However, glucose consumption was similar in the two groups. Glucose concentrations in brain were lower during hypoxia-ischemia in the normoglycemic animals, whereas lactate increased to similar levels in the two groups. The high-energy phosphate reserves, ATP and phosphocreatine, were depleted to a similar extent. Thus, hyperglycemia combined with hypoxia-ischemia, although associated with increased glucose transport into brain, does not lead to enhanced glucose utilization or lactate accumulation by brain over that of hypoxia-ischemia alone. (Pediatr Res 21: 524-529,1987) Abbreviation PCA, perchloric acidIt is unclear whether elevated blood glucose concentrations are protective or damaging to the human brain during perinatal hypoxia-ischemia. This is an important question, since glucose infusions ranging in concentrations from 5 to 25% are administered frequently to premature and distressed full-term newborn infants. Furthermore, blood glucose concentrations can be quite variable in newborn infants, with levels occasionally exceeding 500 mg/dl (1, 2). Based on data in experimental animals, many physicians believe that even modestly high blood glucose concentrations are beneficial to the newborn infant undergoing hypoxic stress (3). In this regard, Himwich et al. (4) found that immature rats pretreated with glucose and then rendered anoxic survive twice as long as untreated controls (see also Refs. 5-8). The mechanism of this glucose protection presumably relates to increased endogenous carbohydrate stores (glucose and glycogen) Received September 15, 1986; accepted December 24, 1986. All correspondence and reprint requests to Robert C. Vannucci, M.D., Department of Pediatrics, The Milton S. Hershey Medical Center, P.O. Box 850, Hershey, PA 17033.Supported by Grant 15738 from The National Institute of Child Health and Human Development and by a grant from the American Diabetes Association. 5 in brain and heart sufficient to maintain blood and tissue glucose levels for an extended interval during a hypoxic or anoxic insult (6, 7, 9, 10).Despite the heightened hypoxic resistance of glucose supplemented perinatal animals, recent experiments have shown that glucose can be damaging to the brain during hypoxia-ischemia. Myers and Yamaguchi (1 1) found that food-deprived juvenile monkeys recover relatively undamaged after a 10-to 14-min cardiorespiratory arrest, w...

Malignant ovarian germ cell tumors are rare tumors that mainly affect patients of reproductive age. The aim of this study was to investigate the reproductive outcomes and fertility preservation strategies in malignant ovarian germ cell tumors after fertility-sparing surgery. Data in literature support that fertility-sparing surgery is associated with an excellent oncological outcome not only in early stages malignant ovarian germ cell tumors but also in advanced stages. Moreover, the possibility of performing conservative treatment should be considered even in case of relapse or advanced disease, given the high chemosensitivity. Indeed, available data have shown that menstrual function is maintained after platinum-based regimens in over 85–95% of patients with malignant ovarian germ cell tumors and rate of premature menopause reported in literature ranges between 3% and 7.4%, while premature ovarian failure rates are between 3.4% and 5%. Moreover, reproductive outcomes are about 80% with no increase in the risk of teratogenicity compared to general population. Therefore, conservative surgery for malignant ovarian germ cell tumors currently may represent a therapeutic option in patients who wish to preserve fertility but must be available for extended follow-up and after subscribing to informed consent.