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Biomedical subjects

R C Vannucci

Publications and source records attributed to R C Vannucci.

16 recordsLinked to original sources
PubMed1979

Frontal ventricular dimensions of the brain in infants and children.

Four hundred computerized tomographic scans of the brain in infants and children from birth to 15 years of age were reviewed. Of these, 142 were judged to exhibit normal ventricular dimensions as determined by the biventricular (V/H) index, the length of a line drawn between the heads of the caudate nuclei (V) relative to the width of the cerebral hemispheres (H) at the same level. When all scans were analyzed collectively, the V/H index followed a Gaussian distribution (mean, .11 +/- .03) [SD]; range, .00 to .20). The index did not increase with advancing age within the pediatric population (0 to 15 years), as it does in adults.

Adolescent↗
PubMed1978

Cerebral carbohydrate metabolism during hypoglycemia and anoxia in newborn rats.

The cerebral metabolic responses to perinatal hypoglycemia and anoxia were studied in newborn rats given regular insulin (30 units per kilogram of body weight). Animals were observed for up to 2 hours with no apparent ill effects in spite of blood glucose concentrations of 0.75 mmol per liter. When exposed to 100% nitrogen at 37 degrees C, hypoglycemic animals survived only one-tenth as long as littermate controls with normal blood glucose levels (4.7 mmol/L). Pretreatment of hypoglycemic rats with glucose (10 mmol/kg) 10 and 30 minutes prior to nitrogen exposure nearly completely reversed the anoxic vulnerability. Hypoglycemia led to progressive reductions in cerebral glycogen and glucose; however, only glucose reverted to normal levels 20 minutes after systemic glucose administration. The glycolytic intermediates glucose 6-phosphate and lactate were also lower during hypoglycemia. Brain glucose levels below 0.1 mmol per kilogram were associated with a disrupted cerebral energy state, reflected by declines in phosphocreatine (33%) and adenosine triphosphate (ATP) (10%). Cerebral energy utilization (metabolic rate) was minimally reduced (-7.2%) by hypoglycemia and returned to the control value (2.36 mmol approximately P/kg/min) with glucose treatment. The cerebral energy reserves ATP, adenosine diphosphate, and phosphocreatine declined more rapidly and to a lower level in hypoglycemic rats subjected to 2 1/2 minutes of anoxia than in normoglycemic animals rendered similarly hypoxic. The findings suggest that decreased anoxic resistance of hypoglycemic newborn rats is not primarily a function of reduced brain glycogen or altered cerebral metabolic rate. The presence of endogenous cerebral glucose stores combined with continued circulating glucose (cerebrovascular perfusion) appear to be critical factors for maintaining perinatal hypoxic survival.

Adenosine Diphosphate↗
PubMed1978

Cerebral blood flow and oxygen consumption in the newborn dog.

Cerebral blood flow (CBF), CBF responses to changes in arterial CO2 tension, and cerebral metabolic rate for oxygen (CMRO2) were measured in newborn dogs, by means of a modification of the Kety and Schmidt technique employing 133Xe. Mongrel dogs of 1-7 days of age were paralyzed and passively ventilated with 70% N2O and 30% O2. CBF was derived by analysis of paired serial 20-microliter samples of arterial and of cerebral venous blood from the superior sagittal sinus. At an arterial PCO2 of 36.9 +/- 3.7 Torr and a mean arterial blood pressure of 62 +/- 10 Torr, CBF was 23 +/- 8 ml/min per 100 g. The arteriovenous oxygen content difference averaged 5.6 vol%, and CMRO2 was 1.13 +/- 0.30 ml O2/min per 100 g. CBF increased or decreased by 0.58 ml/min/100 g per Torr change in PCO2. Our results suggest that in the newborn, basal CBF and CBF responses to CO2 are considerably lower than in the adult and parallel the lower metabolic needs of the newborn brain.

Animals↗
PubMed1978

Cerebral oxidative metabolism during intrauterine growth retardation.

Cerebral oxidative metabolism during intrauterine growth retardation was investigated utilizing a pregnant-rat model. Dams were subjected to unilateral uterine artery ligation on the 17th day of gestation. At term, they were sacrificed by decapitation and the fetuses delivered by cesarean section. Body and brain weights of fetuses from ligated uterine segments were smaller than those of offspring from nonligated horns of the experimental rats or those from sham-operated dams. Blood glucose at birth was reduced by 25% in growth-retarded fetuses. Cerebral oxidative metabolites, including glycogen, glucose, lactate, ATP, and phosphocreatine, were not different from control levels. These findings suggest that neither tissue hypoxia nor deficient glucose delivery to brain can account for the stunted cerebral growth observed in fetuses following uterine artery ligation.

Adenosine Triphosphate↗
PubMed1977

Intraspinal metastatic disease in childhood cancer.

This paper describes the clinical manifestations and diagnostic studies in 26 children with intraspinal metastases of solid malignant neoplasms. The site of the metastatic lesion was verified in all cases by lumbar and/or cisternal myelography. Therapy consisted of Cobalt50 irradiation in 20 patients, of whom 11 (55%) manifested neurologic improvement. Recovery of ambulatory function was most favorable in lesiosn that involved the conus medullaris and cauda equina and spared the cervical and thoracic spinal cord. Early recognition and initiation of treatment before severe neurologic dysfunction developed was necessary to prevent severe, permanent disability.

Adrenal Cortex Hormones↗
PubMed1977

Oxidative metabolism in fetal rat brain during maternal halothane anesthesia.

The present study examines the effects of maternally administered halothane on fetal brain metabolism as determined by direct tissue analysis. Term pregnant rats were paralyzed, ventilated, and administered halothane in concentrations of 0.4, 1, or 2%. For comparison of fetal response to anesthetic agents, other maternal rats were administered pentobarbital (50 or 200 mg/kg). Dams receiving 0.4% halothane or 50 mg/kg pentobarbital remained normotensive, whereas 2% halothane or 200 mg/kg pentobarbital led to a 65% reduction in maternal blood pressure and a 3-fold increase in blood lactate. Fetal blood lactate tended to parallel the maternal lactacidemia. Fetuses of dams anesthetized with 0.4% halothane or 50 mg/kg pentobarbital exhibited concentrations of cerebral metabolities comparable to those of control animals. A 2% halothane level was associated with metabolic disturbances in fetal brain, indicative of cerebral hypoxia. Pentobarbital 200 mg/kg, although producing maternal hypotension and lactacidemia to a degree similar to 2% halothane, preserved a more optimal fetal cerebral energy state as reflected in a lower lactate/pyruvate ratio and normal ATP. The metabolic influence of pentobarbital may serve to protect the hypoxic fetus from neurological damage, an effect apparently not shared by maternally administered halothane.

Adenosine Triphosphate↗
PubMed1976

Carbohydrate metabolism in fetal and neonatal rat brain during anoxia and recovery.

Systemic and cerebral metabolic responses to acute anoxia were studied in term-fetal and neonatal rats in order to account for the greater anoxic tolerance of fetuses. Measurements of blood acid-base balance were correlated with changes in the concentrations of adenine nucleotides, creatine, phosphocreatine, and glycogen in brain, and of glucose, pyruvate, and lactate in brain, blood, and cerebrospinal fluid during 1) exposure (20-40 min) to 100% nitrogen at 37 degrees C, and 2) subsequent recovery in air. Blood PCO2 was higher initially in fetuses and increased more rapidly during anoxia in fetuses than in neonates, exceeding 150 mmHg after 20 min. Brain glycogen, phosphocreatine, and total adenine nucleotides declined more slowly in fetuses than in neonates during anoxia, whereas brain glucose levels declined at similar rates in the two groups. From the changes in these preformed and potential energy stores, it was estimated that total cerebral energy consumption during anoxia was significantly lower in fetuses. The data suggest that the more severe hypercapnia superimposed on anoxia in fetuses decreased cerebral metabolic demands, and thus prolonged survival. An incidental finding was that L-lactate readily enters the immature brain from the blood during anoxia, and in the early recovery phase may constitute the preferred substrate for cerebral oxidative metabolism, sparing glucose.

Adenosine Triphosphate↗