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Laura R. Ment, William B. Stewart, and Charles C. Duncan

✓ Local cerebral glucose utilization has been measured by means of carbon-14 (14C)-autoradiography with 2-deoxyglucose in the newborn beagle puppy model of intraventricular hemorrhage. Our studies demonstrate gray matter/white matter differentiation of uptake of 14C-2-deoxyglucose in the control pups, as would be expected from adult animal studies. However, there is a marked homogeneity of 14C-2-deoxyglucose uptake in all brain regions in the puppies with intraventricular hemorrhage, possibly indicating a loss of the known coupling between cerebral blood flow and metabolism in this neuropathological condition.

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Laura R. Ment, Charles C. Duncan, and Robert Geehr

✓ The authors report 18 infants with benign enlargement of the subarachnoid spaces seen at their institution during a 1-year time interval. This condition is characterized by the computerized tomography findings of dilatation of the subarachnoid spaces, normal or slightly enlarged ventricular size, and prominence of the basilar cisterns. Most cases were found in children referred for the evaluation of abnormally increasing head circumference measurements. Although it was not possible to document the development, and, in several cases, improvement of this process, in these patients enlargement of the subarachnoid spaces was a benign diagnosis, not associated with serious neurological dysfunction.

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Beagle puppy model of intraventricular hemorrhage

Effect of superoxide dismutase on cerebral blood flow and prostaglandins

Laura R. Ment, William B. Stewart, and Charles C. Duncan

✓ Intraventricular hemorrhage (IVH) represents a major problem for preterm neonates and is thought to occur secondary to alterations in cerebral blood flow (CBF) to damaged germinal matrix tissues. Many investigators believe that both local CBF and changes in capillary morphology and permeability may be partially controlled by prostaglandins. To evaluate this hypothesis, the authors have studied the effects of superoxide dismutase (SOD), a known free-radical scavenger, on newborn beagle pups that were randomly assigned by computer to four groups consisting of either SOD- or saline-pretreated animals that underwent either insult by hemorrhagic hypotension/volume reexpansion or no insult. Prostaglandin levels were determined prior to and 60 minutes following the administration of the solutions, and carbon-14 iodoantipyrine autoradiography was performed for determination of CBF.

It was demonstrated that, although SOD significantly decreased the incidence of IVH in this model (p < 0.05), it caused no alterations in baseline CBF or prostaglandin levels. In addition, SOD did not prevent either the systemic blood pressure changes or the alterations in CBF found in response to a hemorrhagic hypotensive insult. The authors propose that neonatal IVH results from a combination of factors, one of which is prostaglandin-mediated alterations in CBF to a damaged capillary matrix.

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Beagle puppy model of perinatal cerebral insults

Cerebral blood flow changes and intraventricular hemorrhage evoked by hypoxemia

Laura R. Ment, William B. Stewart, Charles C. Duncan, and Bruce R. Pitt

✓ Asphyxia, with its attendant hypoxemia, is by far the most common cause of neonatal cerebral infarction, and frequently results in lesions of the parieto-occipital white matter in addition to other neuropathological changes. This study examines the effects of hypoxemia on regional cerebral blood flow (CBF) in the newborn beagle pup. The animals were anesthetized, underwent a tracheotomy, and were paralyzed. Pups were randomly divided into two groups: one group was subjected to hypoxemia produced by altering the oxygen concentration in the inspired air, and the other received no insult. In the hypoxemic pups, the pO2 was 13.1 ± 2.1 mm Hg (mean ± standard deviation). Autoradiographic determinations of CBF were performed by the carbon-14-iodoantipyrine technique 15 minutes after randomization. Significant increases in CBF were found throughout the brains of the hypoxemic pups. The CBF was increased to cortical and central gray regions and to frontal and temporal white matter but was unchanged in the parietal white matter, one of the classic sites of radiological and neuropathological injury in neonates with perinatal asphyxia. An unexpected finding was the increased incidence of germinal matrix and/or intraventricular hemorrhages in the hypoxemic pups.

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Posthemorrhagic hydrocephalus

Low incidence in very low birth weight neonates with intraventricular hemorrhage

Laura R. Ment, Charles C. Duncan, David T. Scott, and Richard A. Ehrenkranz

✓ In addition to seizures and long-term neurodevelopmental handicaps, infants with intraventricular hemorrhage (IVH) are at risk for posthemorrhagic hydrocephalus (PHH), and the incidence of this problem in preterm infants with known IVH has been reported to vary from 25% to 74%. Over a 46-month period, 438 neonates of 1250-gm birth weight or less were admitted to this Newborn Special Care Unit, and 269 survived the first 36 postnatal hours. Of these, 265 patients underwent computerized tomography and/or cranial ultrasound scanning for evaluation of germinal matrix and/or intraventricular hemorrhage (GMH/IVH): 133 infants were found to have experienced GMH/IVH, and 27 of these died within the 1st postnatal week. Of the 95 survivors with GMH/IVH, 43 were known to have GMH only; the other 52 experienced IVH and were therefore at risk for PHH. Patients with GMH/IVH underwent repeat investigations for the development of ventriculomegaly and possible PHH. Only five patients with IVH developed PHH, defined as ventriculomegaly, elevated intracranial pressure, and increasing occipitofrontal head circumference. Serial cranial ultrasound studies of 95 other consecutively admitted patients in this birth-weight range revealed an equal incidence (45%) of low intracranial pressure ventriculomegaly in both the hemorrhage and non-hemorrhage groups, but none of them required shunting for hydrocephalus. One infant with congenital aqueductal stenosis was also identified.

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Laura R. Ment, William B. Stewart, Charles C. Duncan, and Richard Lambrecht

✓ Intraventricular hemorrhage (IVH) is a major neurological problem of the preterm infant and originates in the germinal matrix tissues of the developing brain. The newborn beagle pup has been demonstrated to provide an excellent model for this neonatal neuropathological condition. By the production of hemorrhagic hypotension followed by relative volume reexpansion, such hemorrhages can be produced in this animal. Carbon-14(14C)-iodoantipyrine was used for measuring the cerebral blood flow in this experimental model and demonstrated that, although the germinal matrix is a relatively low-flow area in the newborn beagle pup, the selective flow to this region increases significantly in animals with IVH.

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Beagle puppy model of perinatal cerebral infarction

Acute changes in cerebral blood flow and metabolism during hemorrhagic hypotension

Laura R. Ment, William B. Stewart, Charles C. Duncan, Bruce R. Pitt, Aldo Rescigno, and Judy Cole

✓ Asphyxia, with its attendant hypotension, is by far the most common cause of neonatal cerebral infarction and frequently results in lesions of the parieto-occipital white matter. This study examines the effects of hypotension on regional cerebral blood flow (CBF), local cerebral glucose utilization (LCGU), and serum prostaglandin levels in newborn beagle pups. The animals (24 to 96 hours old) were anesthetized, tracheotomized, and paralyzed. Pups were randomly divided into two groups: one was subjected to hemorrhagic hypotension and the other received no insult. Hypotension was induced by slow venous hemorrhage to maintain a mean arterial blood pressure of 20 to 30 mm Hg. Autoradiographic determinations of LCGU using carbon-14 (14C)-2-deoxyglucose were performed 45 minutes after randomization to groups. Autoradiographic determinations of CBF were performed using 14C-iodoantipyrine on a second group of pups 15 minutes after randomization. Prostaglandins were measured immediately before and 15 minutes after insult or control manipulation. There were no significant differences in the values for thromboxane B2 or 6-keto-prostaglandin F1α, the stable breakdown products of thromboxane A2, and prostacyclin. Prostaglandin E2 levels significantly increased in response to hemorrhagic hypotensive insult. In addition, although regional CBF was maintained in cortical and central gray matter structures during hypotension, CBF to the periventricular temporal and parietal white matter zones significantly decreased, and LCGU was increased in these same regions during hypotensive insult. The uncoupling of CBF and metabolism in these periventricular white matter regions may be responsible for the neuropathological sequelae of perinatal asphyxia.

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Beagle puppy model of perinatal cerebral infarction

Regional cerebral prostaglandin changes during acute hypoxemia

Laura R. Ment, William B. Stewart, Charles C. Duncan, Bruce R. Pitt, and Judith S. Cole

✓ Perinatal cerebral infarction, or stroke, is a not uncommon finding in newborns who survive after intensive care. Asphyxia, with its component parts hypoxemia and hypotension, represents the most common cause of perinatal cerebral infarction and may result in neuropathological changes in the periventricular white matter. Previous studies have demonstrated regional alterations in cerebral blood flow (CBF) in response to hypoxemic insult. This work examines the effects of hypoxemia on regional cerebral prostaglandin levels in the developing brain, since some observers believe that local CBF is controlled in part by prostaglandins. In this study, newborn beagle pups were anesthetized, subjected to tracheotomy and artificially ventilated to maintain normoxemia and normocarbia. Mean arterial blood pressure (MABP) was continuously monitored by means of an indwelling catheter and transducer, and craniectomies were performed. When the pups were physiologically stabilized, they were randomly assigned to receive acute hypoxemic insult (pO2 14.0 ± 1.55 mm Hg, mean ± standard deviation) accomplished by altering the oxygen concentration in the inspired air) or to receive no insult (mean pO2 84.3 ± 13.0 mm Hg). Fifteen minutes following stable hypoxemic or normoxic conditions, all pups underwent in vivo freezing of the intracranial contents under anesthesia followed by rapid sacrifice.

No significant differences were noted between the MABP, pH, or pCO2 values for the control and hypoxemic pups during the experimental period. Regional cerebral prostaglandin data demonstrated a significant increase in prostaglandin (PG)E2 in the gray matter of hypoxemic pups when compared to the normoxic controls (p < 0.02). No significant differences were noted for 6-keto-PGE, the stable metabolite of prostacyclin, or thromboxane (TX)B2, the stable metabolite of TXA2, in the gray matter. In addition, although 6-keto-PGE was significantly lower in the periventricular white matter of the hypoxemic pups (p < 0.05), there were no changes in the white matter in either PGE2 or TXA2. This regional differential synthesis of PGE2 in response to hypoxemic insult may explain the relative failure of CBF to the periventricular white matter and thus the neuropathological alterations attributed to it.

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Beagle puppy model of perinatal cerebral infarction

Acute changes in regional cerebral prostaglandins during hemorrhagic hypotension

Laura R. Ment, William B. Stewart, Charles C. Duncan, Judy Cole, and Bruce R. Pitt

✓ Perinatal cerebral infarction is a not uncommon finding in newborn babies surviving intensive care. Asphyxia, with its attendant hypotension, is the most common cause of this problem and may result in neuropathological changes in the periventricular white matter. Previous studies have demonstrated uncoupling of cerebral blood flow and metabolism in the periventricular white matter regions of newborn beagle pups exposed to hemorrhagic hypotension. This work examines the effects of hypotension on serum and regional cerebral prostaglandin levels in the newborn beagle pup. The animals were anesthetized, tracheostomized, and paralyzed. Pups were randomly assigned to two groups: one was subjected to hemorrhagic hypotension and the other received no insult. Hypotension was induced by slow venous hemorrhage calculated to maintain a mean arterial blood pressure at 20 to 30 mm Hg. Serum prostaglandin determinations were made immediately before and 15 minutes after random assignment to hypotension or control groups. In addition, regional cerebral prostaglandin determinations were performed 15 minutes after randomization. Analysis of the serum prostaglandin data revealed that there were no significant differences in the values for thromboxane B2 or 6-keto-prostaglandin (PG) F, which are the stable breakdown products of thromboxane A2 and prostacyclin, respectively. Prostaglandin E2 levels increased in response to hemorrhagic hypotension insult. Regional cerebral prostaglandin determinations demonstrated decreases in thromboxane B2 and 6-keto-PGF in both gray and white matter. Although gray matter PGE2 was increased in pups exposed to hemorrhagic hypotension, this increase was not found in the periventricular white matter of injured pups. This regional difference in PGE2 synthesis in response to insult may explain the periventricular white matter neuropathological changes attributed to it.