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The author hypothesizes that individuals who suffer brain hypoxia prenatally, perinatally, or immediately postnatally constitute a population at risk for minimal brain dysfunction and for schizophrenia in adulthood. This hypothesis has implications for early intervention with children who have MBD and their families and for multidisciplinary management of these cases throughout childhood.
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Heavily myelinated cultures of newborn mouse cerebellum were exposed to hypoxia and studied by electron microscopy. The cultures were placed in an incubating medium deprived of oxygen (95 to 97 per cent deprivation) for 7 to 60 minutes and fixed immediately for electron microscopy. The amount of oxygen present in the medium and time course of hypoxia were constantly monitored and recorded by an oxygen probe of polarographic oxygen sensor type and a recorder. In contrast to previous in vivo studies, this in vitro model of hypoxic cell injury has provided accurate information concerning the relationship between degree of hypoxia and cell lesion. Hypoxia affected neurons which showed "swelling" and disorganization of cristae in mitochondria and reduced cytoplasmic matrix density due to the dispersion of polysomes. A small population of neurons with an increased cytoplasmic density and "swollen" mitochondria was also noted. Clearing and degeneration of presynaptic terminals and postsynaptic dendrites were observed. After a longer period of hypoxia most neurons showed an extensive degenerative change consisting of rarefaction of cytoplasm and loss of cytoplasmic organelles. In contrast to neuronal changes, no structural alteration was observed in astrocytes and oligodendrocytes.
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A functional classification of hypoxia of the brain has been presented and some of its significant aspects have been discussed. Mechanisms of protection from hypoxia of the brain were reviewed under the headings of prevention, hyperventilation, hypothermia and protection by barbiturates. In prevention of hypoxia of the brain, avoidance of factors producing a fall in cerebral perfusing pressure was emphasized. Hyperventilation is not advised unless one can readily measure regional cerebral blood flow. In the operating room, normocarbia or slight hypocarbia is recommended. Animal studies indicate a protective role of barbiturates in ischaemic hypoxia of the brain. However, it should be emphasized that, at present, hypothermia is the only established means of protection against hypoxia of the brain in man, when it is induced prior to the hypoxic insult. The evidence for protection by barbiturates has been found only in experimental animals. If one can extrapolate the results of studies in animals to man, then potential benefits would be expected in clinical stroke, cardiac arrest, in operations on the carotid artery and in head injury.
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The effects of hypoxia and superimposed hypercapnia or hypertension during hypoxia on brain tissue water content, pH, and electric activity were studied in Sprague-Dawley and stroke-prone spontaneously hypertensive rats. Auditory brainstem responses and sensory evoked potentials were recorded during the experiment as the indices for cerebral oxygen metabolism. The brains were removed immediately, 1 day, and 2 days after hypoxic insult for gravimetric study. The brain water content increased in all groups on the 1st and 2nd days after hypoxia. The percentage change from the control water content increased only on the 1st day in hypoxic rats. In contrast, it increased on both the 1st and 2nd days after hypoxia in hypercapnic or hypertensive rats. The evoked potentials of hypoxic and hypercapnic-hypoxic rats showed that peak latencies were prolonged significantly during hypoxia and recovered 1 and 2 days after hypoxia. The brain tissue pH decreased during hypoxia and recovered after hypoxia. This study suggests that brain edema develops within 2 days of hypoxic insult and that superimposed hypercapnia or hypertension promotes the brain edema.
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The influence of acute and prolonged (with resuscitation) hypoxia, upon some glycolytic substrates and high energy phosphate compounds in the rat brain, was studies. Acute hypoxia decreased the content of glucose and glucose-6-phosphate as well as of high energy phosphate compounds. Stimultaneously, an increase of lactic level was recorded. Some adaptation features could be observed, when 30-minute hypoxia with resuscitation was studied. Brain content of high energy compounds returned to the normal value, while that of glucose increased twice over control. However, the level of lactic acid was still increased.
Intraoperative and postoperative neurologic complications in cardiosurgical patients refer to grave cerebral affections which aggravate markedly the operative issue and prognosis for patients' life. In 525 operations on the heart and major vessels neurologic complications were noted in 47 patients. In 21 of them death was directly caused by these complications. The character of cerebral lesions (brain hypoxia, acute disorders in the cerebral circulation) and their frequency were conditioned by the kind of operative interventions and characteristic features of the cardiovascular pathology. Routine prophylactic measures and their results are described.
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4, 14 and 28 days old rats were exposed to hypoxic environment of 6% O2-94% N2 for 30 min. Tyrosine hydroxylase and tryptophan hydroxylase activity was studied in different brain regions (hemispheres, striatum, midbrain and brainstem in vivo by measuring the accumulation of dihydroxyphenylalanine (Dopa) and 5-hydroxytryptophan (5-HTP) respectively, after inhibition of aromatic L-amino acid decarobyxlase with NSD 1015. Tyrosine and tryptophan levels in the different brain regions were measured simultaneously. The tyrosine and tryptophan levels in the various brain parts were generally not influenced during exposure to hypoxia. Tyrosine hydroxylase activity decreased in most areas in the 4 and 14 days old rats, and all brain areas studied in the 28 days old rats. Tryptophan hydroxylase activity decreased markedly in all brain areas at all ages studied. It is concluded that the enzymes tyrosine hydroxylase as well as tryptophan hydroxylase seem to be equally affected during hypoxia in the different brain regions studied.
Cerebral hypoxia and embolism evoke the release of prostaglandin (PG)-like substances, predominantly of E type, into cerebral venous blood. This has been shown by bioassay used for monitoring the level of PG-like substances in sagittal sinus blood (ssb) in dogs. Hypoxia was induced by inhalation of 8% O2 in N2, embolism by an injection of air into internal carotid artery. This led to an increase in the level of PG-like substances in ssb, with no detectable change in the concentration of PGs in peripheral venous blood, indicating that PGs detected in ssb originate from cerebral venous outflow. The output amounted 6 ng/ml (in PGE2 equivalents). Hydrocortisone (HC) in a dose of 30 mg/kg suppressed the release of PG-like substances induced by either hypoxia or embolism. These results were confirmed by radioimmunoassay of PGs in ssb. Plasma levels of PGs E and F2 alpha were elevated following cerebral embolism as compared to initial values and greatly suppressed by HC administration. Suppression of PG formation by HC in this experimental system seems to be related to the membrane--stabilizing action of this hormone. This is of interest in view of the usefulness of steroid therapy in cerebrovascular pathology.
To study the determinants of carbon monoxide (CO) induced hyperpnea simultaneous measurements were made of carboxyhemoglobin level in arterial blood (HbCO), ventilation (VE), cerebral blood flow (CBF), O2 delivery to the brain (CBF X O2 content of arterial blood), O2 consumption of the brain (CMRO2), and O2 tension in cerebral venous blood (PVO2) during inhalation of 1% CO in 40% O2 by six unanesthetized goats. HbCO increased to 65% in 10 min; VE remained constant until a HbCO level of approximately 50% was reached and then increased abruptly; CBF increased progressively; O2 delivery to the brain and CMRO2 decreased somewhat with CO inhalation; these decreases reached statistical significance at a HbCO level of 30-40% whereupon the rate of decline with respect to HbCO level increased substantially; and PVO2 decreased progressively from an average of from 31 to 14.6 Torr and averaged 19.2 Torr when hyperpnea was manifest. When considered in the light of previous studies which indicate that CO-induced hyperpnea is not caused by stimulation of the carotid bodies, these data suggest that this phenomenon is related to brain hypoxia. Calculations of brain tissue O2 tension with the Krogh equation support this contention.