Abstract: To the Editor.— Using mice, workers at DuPont, 1 Allen and Hanburys Ltd, 2 and Riker Laboratories, 3 and, most recently, Egle and associates, 4 were unable to demonstrate cardiotoxicity of aerosol propellants. They did not do the same experiments described by Taylor and Harris, 5 which revealed that the fluorocarbons, or freons, used to propel aerosols are toxic to the heart. Errors by these authors and Silverglade 6 need correction. We did not apply complete asphyxia in our experimental mouse model. The essence of our technique' is to apply a degree of asphyxia that otherwise untreated mice will tolerate for four minutes without developing bradyarrhythmias. Without propellants, the degree of partial, or mild, asphyxia that we apply causes tachycardia at both 25 seconds and four minutes of asphyxia, not bradycardia. In contrast, after the mice inhale three breaths of propellant, application of exactly the same partial asphyxic challenge now

Abstract: An infant monkey exhibited the clinical evidences of severe brain injury following birth. It was blind, partially deaf and showed severe motor disabilities. Postmortem brain examination at 1½ years of

Abstract: Five-day-old rats subjected to prolonged asphyxia at body temperature (37 °) developed brain oedema as measured by increase in brain water and an increase in brain Na+/K+ ratio.

Abstract: Publisher Summary This chapter observes the behavioral, physiological and structural maturation and aging in monkeys, asphyxiated at birth. Asphyxiated animals consistently required significantly less adaptation to new testing situations than normal animals. Asphyxiated animals were noticeably less disturbed by extraneous distractions than were members of the normal group. The surviving monkeys were severely handicapped at birth. Some showed athetosis, convulsions, scissors-gait, spasticity, nystagmus and slow and uncoordinated progression. To evaluate the physiological and behavioral effects of damage to the brain at the time of birth, brain damage was induced in 23 monkey fetuses by the same method as the previous group. The asphyxiated infants had difficulty with the regular formula given to the controls. It is essential to regard the brain damage produced by birth asphyxia as a new concept in neurology, distinct from other central nervous system disorders such as epilepsy, stroke, parkinsonism and the degenerative diseases. It should be kept in mind that the brain damage of birth asphyxia occurs before critical stages of development are completed and must have a different impact on the behavior of the subject.

Abstract: Extract: During postnatal brain development in the rat there is a progressive decrease in the Na+/K+ ratio, which correlated with increasing activity of Na+-K+-activated ATPase. Undernutrition during intrauterine and early postnatal development (4–6 days) did not alter the Na+/K+ ratio, although there was a deficit in brain weight. However, undernutrition during the suckling period retarded the progressive fall in Na+/K+ ratio and rise in ATPase activity. The altered Na+/K+ ratio in these animals did not appear to be caused by change in brain carbohydrate metabolism. Developing rats undernourished until 4–6 days resembled the intrauterine growth-retarded human baby as regards deficits in body weight, relative sparing of the brain compared with other organs, and depleted carbohydrate reserves. The undernourished 4–6-day-old rat tolerated asphyxia as well as the well nourished rat of the same age. After asphyxia, the Na+/K+ ratio reverted to unity and there was an increase in brain water. Liver carbohydrate reserves did not appear to be a limiting factor that determined the point of death. Speculation: The normal gradients of Na+ and K+ between the cell and its environment in developing rat brain may be altered by asphyxia or undernutrition as a result of a defect in the Na+ pump mechanism. Such a defect may be caused by asphyxia at a time in rat brain development equivalent to that of the human brain in the perinatal period, i.e., in the first stages of the brain growth spurt. Undernutrition, however, may retard development of the Na+ pump only when its time of application includes the period of most rapid brain growth and maturation.

Abstract: Preventive im administration of ATP (adenosinetriphosphate) in newborn rats produces a significant increase in the depressed endogenous ATP level and a significant correction of the disturbed acid-base balance The dependence on the dose, the difference between ATP and Vasodilan®1 and between preventive and therapeutic effect are confirmed

Abstract: — The concentration of ascorbic acid in whole rat brain during the first week of postnatal life was up to 100 per cent higher than in adult animals. A progressive fall in concentration occurred between 4 and 30 days of age. Corresponding changes did not occur in liver and adrenal gland, two other organs rich in ascorbic acid. Rats subjected to growth retardation during the fetal and suckling periods had, at 25 days of age, levels of ascorbic acid in the cerebellum and brainstem significantly higher than those of control animals. A period of prolonged asphyxia in 5-day-old rats resulted in a significant 4 per cent reduction in whole brain ascorbic acid concentration.