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Biomedical subjects

J Goddard-Finegold

Publications and source records attributed to J Goddard-Finegold.

24 records · Page 2Linked to original sources

Reduction in incidence of periventricular, intraventricular hemorrhages in hypertensive newborn beagles pretreated with phenobarbital.

Periventricular and intraventricular intracerebral hemorrhages occur frequently in premature newborns and are markers for, or contribute significantly to, neurologic morbidity in survivors. Hemorrhages are hypothesized to result from rapid fluctuations in cerebral perfusion pressure and/or cerebral blood flow. Phenobarbital sodium has been given to premature infants in anticonvulsant dosages in attempts to prevent hemorrhages, but its efficacy in clinical studies has been disputed. In this study, in the 24 to 72-hour-old newborn beagle, an animal model for periventricular and intraventricular intracerebral hemorrhage, phenobarbital sodium was administered to obtain anticonvulsant serum levels prior to phenylephrine-induced hypertensive insult. None of the animals was hypoxic or hypercarbic. Resulting hypertensive systemic mean arterial BPs were 99 +/- 8 mm Hg in the 15 control pups and 93 +/- 15 mm Hg in the 15 phenobarbital sodium-treated pups (not statistically significantly different). The duration of the hypertension was the same in both groups. Phenobarbital caused a significant decrease in mean arterial BP in the treated group just after its administration (P less than .05). Six of the 15 control pups (40%) and one of the 15 treated pups (7%) demonstrated macroscopic and microscopic periventricular and intraventricular hemorrhage (P less than .05, chi 2, Yates correction). Thus, in nonasphyxiated newborn beagles, phenobarbital sodium significantly reduced the incidence of hemorrhage after hypertensive insult.

Animals↗

Cerebral blood flow and experimental intraventricular hemorrhage.

We evaluated the effects of acute hypovolemic hypotension followed by rapid, corrective blood infusion upon sequential regional cerebral blood flows (rCBF) in nine anesthetized 24-48-h-old beagle pups using the radioactive microsphere technique. After 5 min of hemorrhagic hypotension, during which time systemic arterial blood pressures were reduced 35-45%, cerebral blood flow to all regions increased by 31-42% over steady-state values. After blood reinfusion, rCBF increased by 39-88% over control values. Highest blood flows during hypovolemia were in the medulla and pons; slightly lower values were in the cerebellum, midbrain, cortex, and thalamus; and the lowest flows were in the white matter. These flows paralleled the hierarchy of flows to these regions in the steady state. Increases in blood flow during hemorrhagic hypotension were statistically significant when compared with the control values in the medulla (P less than 0.01), pons (P less than 0.01), midbrain (P less than 0.01), cerebellum (P less than 0.01), and cortex (P less than 0.01). One minute after reinfusion of the withdrawn blood volume, blood flows further increased by substantial margins in the medulla and pons; by moderate degree in the thalamus, midbrain, and cerebellum; and mildly in the cortex and white matter. Reinfusion state flow increases were significant when compared with control values in the medulla (P less than 0.01), pons (P less than 0.01), midbrain (P less than 0.01), cerebellum (P less than 0.01), cortex (P less than 0.05), and white matter (P less than 0.01). After flow values were corrected to compensate for variations in PCO2, the increases remained significant during both hypovolemia and reperfusion for medullary, thalamic, cortical, and white matter flows. Three of the nine puppies had macroscopic intraventricular hemorrhages at autopsy.

Animals↗

Prediction of brain blood flow using pulsed Doppler ultrasonography in newborn lambs.

The purpose of this study was to evaluate the ability of pulsed Doppler ultrasonography to predict brain blood flow by comparing measurements made in basal cerebral arteries using a pulsed Doppler system with measurements of brain blood flow using radioactive microspheres in lambs. We measured the instantaneous maximum velocity during peak systole and end diastole and the mean velocity over the pulse cycle in basal cerebral arteries, calculated Pourcelot's index of resistance and Gosling's pulsatility index, and used regression analysis to compare the pulsed Doppler measurements with brain blood flow measured with radioactive microspheres. Pulsed Doppler measurements of the peak systolic, end diastolic, and mean flow velocity in basal cerebral arteries were directly related to brain blood flow. In contrast, no linear relationship was detected between the resistance or pulsatility indices and brain blood flow measured by microspheres (p greater than 0.14). Prediction of brain blood flow for individual subjects lacks the quantitative precision necessary for use as a clinical tool. However, the direct relationship between brain blood flow and the peak systolic, end diastolic, and mean flow velocities in basal cerebral arteries supports the use of these measurements in clinical research for the qualitative assessment of change in brain blood flow.

Animals↗

Cerebrovascular regulation and neonatal brain injury.

Neuropathology occurring as a result of hemodynamic injury occurs in up to 25% of preterm newborns of less than 1,500 gm birth weight and in a much smaller, but nonetheless meaningful, proportion of more mature infants. Abnormalities in cerebrovascular regulation have been proposed as major contributing factors to both ischemic and hemorrhagic injuries in the newborn brain. In this review we explore several factors that play a role in cerebrovascular regulation in the immature brain and relate them to what is known about vascular regulation in the mature brain and to the types of pathology that occur in the newborn brain. One goal in this "decade of the brain" should be to increase our basic and clinical knowledge about the cerebrovasculature of the newborn in order to enhance our ability to predict and prevent perinatal brain injury.

Asphyxia Neonatorum↗