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Biomedical subjects

R E Myers

Publications and source records attributed to R E Myers.

16 recordsLinked to original sources
PubMed1979

Auditory evoked potentials and auditory behavior following prenatal and perinatal asphyxia in rhesus monkeys.

Two types of asphyxia were studied in monkeys, total asphyxia during mid-pregnancy (94--98 days gestation) and combined partial and total axphyxia at term (165 days gestation). Auditory evoked potentials and the acquisition of 2 auditory discrimination tasks were studied in asphyxiated animals as well as in group of controls. The brains of all asphyxiates were examined histologically. No auditory discrimination deficit was found in the asphyxiated animals; however, the auditory evoked potentials differentiated between control and asphyxiated animals, especially those with verified inferior colliculus damage.

Animals↗
PubMed1978

Asphyxia-induced disaggregation of cerebral polyribosomes in rhesus monkey fetuses.

The effects of 3 hours of controlled intrauterine asphyxia (acidotic hypoxia) on the sedimentation patterns of cerebral polyribosomes and on polyribosome supported in vitro protein synthesis were examined in 16 term monkey fetuses. Three outcomes resulted. Four fetuses showed no changes in polyribosome sedimentation profile or in sedimented polyribosome supported in vitro protein synthesis. Four showed changes in sedimentation profiles indicating partial breakdown of polyribosomes and significant decreases in polyribosome supported in vitro protein synthesis. Finally, 8 fetuses showed almost complete disaggregation of cerebral polyribosomes into 80-S monosomal units. This was associated with marked reduction in sedimented ribosomal mediated in vitro portein synthesis. Both the disaggregation of polyribosomes and the associated loss of in virto protein synthesis were related to the severity of the acidosis produced by asphyxia.

Animals↗
PubMed1978

The effects of isoproterenol on fetal oxygenation.

Infusion of isoproterenol (1 microgram/kg/min, i.v.) into the anesthetized pregnant rhesus monkey near term consistently reduced fetal oxygenation, despite diminishing myometrial activity. The decline in pO2 of fetal arterial blood (mean = 4.3 +/- 2.3 mmHg S.D.) was accompanied by an increase in pCO2 tension (mean = 4.6 +/- 2.7 mmHg) and a decline in pH (mean = 0.04 +/- 0.02 S.D.). There was an increase in heart rate and a widening of pulse pressure in the mother and also in the adequately oxygenated fetus providing evidence that the agent crosses the placenta. The poorly oxygenated fetuses developed bradycardia and hypotension. Administration of isoproterenol directly to the fetus elicited similar changes in the composition of blood, and in blood pressure and heart rate, to those observed after administration of the agent to the mother.

Animals↗
PubMed1977

Late decelerations and brain tolerance of the fetal monkey to intrapartum asphyxia.

Eight monkey fetuses near term were subjected to regulated asphyxia during labor by mechanically constricting the maternal abdominal aorta and diminishing blood flow to the uterus. A magnitude of asphyxia was produced and maintained for an initial three hours that was close to but not sufficient to elicit late decelerations. The asphyxia was then augmented during a fourth hour to cause late decelerations of magnitudes of 5 to 15 per cent of the initial heart rate. After termination of the fourth hour of asphyxia, the fetuses were delivered by hysterotomy and provided intensive care. During the three to nine months of survival after birth, all animals were neurologically intact; on necropsy the brains were free of pathologic changes both grossly and microscopically. These results support the thesis that fetal heart rate monitoring during labor exhibits a sensitivity sufficient to diagnose asphyxia of the fetus of clinical significance before it reaches a magnitude that may cause permanent neurological injury. The results are particularly pertinent to those clinical circumstances where the decreases in intervillous space blood flow brought about by uterine contractions are accentuated due to low maternal blood pressure.

Animals↗
PubMed1977

Nervous system effects of cardiac arrest in monkeys. Preservation of vision.

Thirteen juvenile monkeys were taught two visual discrimination tasks. After 12 to 24 hours of food deprivation, ten underwent 14-minute episodes of cardiac arrest. Three served as controls. Five of the ten arrested animals survived and were tested in the discrimination box. All continued to perform color and pattern discrimination tasks with one to eight days' delay. All appeared neurologically intact, while brain pathologic examination after 11 to 64 days' survival showed either intact brains or injury restricted to nuclear structures in the brain stem, cerebellar Purkinje cells, and hippocampus. Five animals died 4 to 36 hours after they were resuscitated. Two required prolonged cardiac massage and, despite return of adequate cardiovascular function, died early. A third animal dislodged its arterial catheter and exsanguinated. The remaining two animals, who received infusions of glucose just prior to arrest, developed widespread fasciculations and myoclonic seizures. They became decerebrate and opisthotonic and were killed after 10 and 36 hours. Their brains showed mild edema and widespread necrosis of cortex and basal ganglia. Thus, food-deprived monkeys tolerate 14 minutes of circulatory arrest well and show minimal neurologic and pathologic changes, while administration of glucose just before arrest markedly augments the severity of brain injury and alters its distribution.

Animals↗
PubMed1977

Effects upon the fetus of oxygen administration to the mother. A study in monkey.

Catheters were placed into assorted arteries and veins of 8 anaesthetized pregnant monkeys and their fetuses. Oxygen-sensitive electrodes were also inserted subcutaneously into 3 of the 8 fetuses. Periodic samples of maternal and fetal blood were analyzed for PO2, PCO2 and pH. Oxygen administration to the mothers reliably increased the PO2 of blood taken from the fetal carotid artery and less constantly augmented the PO2 of blood withdrawn from the femoral artery and vein. During 5-6 hours of study the oxygen tension of fetal blood samples of all animals progressively declined. However, the most marked declines in PO2 values at all fetal sites were regularly observed at those times as--or after--the mothers emerged from anaesthesia. At these times also the magnitudes of the increases in fetal blood PO2 brought about by administering oxygen to the mothers diminished markedly and in parallel at all sample sites. The closely similar magnitudes of these various reductions at all fetal sample sties indicate that the basic mechanisms leading to decreased oxygen delivery lie outside the fetuses and are most likely due to decreased maternal blood flow to the uterus because of increased maternal sympathetic stimulation. These reductions in oxygen delivery to the fetus are all regularly reversed by reanasthetizing the mothers. The studies carried out with oxygen-sensitive electrodes demonstrate that administering oxygen to the mothers regularly increases oxygen tension of fetal tissues but after a 50 sec delay.

Animals↗
PubMed1975

Response of the primate fetus to intra-amniotic saline injection.

The amniotic fluid was replaced with 20 per cent sodium chloride solution during the second half of gestation in 12 pregnant rhesus monkeys. This produced a congealing of the fetal blood in the small umbilical vessels which overlie in the placental chorionic plate. Death of severe asphyxia followed within 20 to 50 minutes in the younger fetuses due to a prompt cessation of umbilical blood flow. During this time, the rise in serum sodium of the fetus was moderate and could not be implicated as the cause of fetal death. In older fetuses, the asphyxia produced by the saline injection was transient and less severe, occasionally permitting survival. The caliber of the affected fetal umbilical blood vessels and their blood flow rates are presented as the principal determinants of the rapidity of development and the severity of the asphyxia produced by saline instillation.

Abortion, Induced↗
PubMed1975

Fetal asphyxia due to umbilical cord compression. Metabolic and brain pathologic consequences.

Term monkey fetus 1620 sustained 50 min of rapidly developing severe asphyxia which began immediately after its in utero version. The arterial blood pO2 decreased from a normal value of 34 to 11-12 mm Hg while the blood pH fell from 7.35 to 6.70. During this asphyxia, hemoglobin-oxygen saturations below 5% were recorded. The complete collapse of the umbilical circulation several minutes prior to the reoxygenation of the fetus added an episode of total asphyxia. With reoxygenation following delivery, fetal cardiovascular performance improved rapidly though over an hour was required for recovery from the severe acidosis. The animal prospered but was found moribund on the 13th postnatal day due to dehydration. Brain examination after euthanasia revealed severe paracentral cortical and basal ganglia damage. Damage also appeared symmetrically in nuclei in the lower brain stem and in thalamus. These three zones of injury are attributed to the partial, the partial combined with the total, and the total asphyxia, respectively. The present case makes clear that compression of the umbilical cord may cause damage of a variety of types depending on the severity and duration of the asphyxia induced. It also demonstrates the possibility of recovery from a systemic acidosis where the pH values have fallen to levels below 6.70 for up to an hour.

Animals↗
PubMed1975

Central nervous system findings in the newborn monkey following severe in utero partial asphyxia.

Seizures, brain swelling, and cortical necrosis have been observed in the newborn rhesus monkey following a 2 to 4-hour period of intrauterine partial asphyxia produced by halothane-induced maternal hypotension. These clinical and neuropathologic findings are similar to those seen in human newborn infants who have experienced an episode of intrauterine asphyxia from such a cause as premature placental separation. The present study strongly indicates that fetal partial asphyxia, from any cause, in the absence of fetal circulatory collapse or fetal head compression, may be the primary event that sets in motion a vicious cycle of brain swelling and impaired cerebral blood flow, leading finally to cerebral necrosis.

Animals↗
PubMed1975

Four patterns of perinatal brain damage and their conditions of occurrence in primates.

The findings described in the present study are summarized in Table 1. It may be noted that anoxia or total asphyxia, whether in the newborn animal or in the (see article) adult, leads to patterns of injury in the brainstem. Hemispheral structures outside the thalamus seem to be entirely spared in those animals which survive. In contrast to this, situations leading to hypoxia associated with severe acidosis, usually of a mixed respiratory and metabolic type, cause brain edema; and when the edema is limited in its distribution, the damage is restricted to specific cortical loci. When the cerebral edema becomes more generalized owing to spread of the process, more and more extensive regions of the hemispheres are damaged until the entire cerebrum may become necrotic. On the other hand, clinical circumstances which lead to hypoxia but without acidosis of any great magnitude--usually due to the indolence of the process or to an associated hyperventilation of the mother--produce lesions which may be restricted to the white matter. These processes may be characterized by perivenular white matter hemorrhage and/or focal areas of periventricular leucomalacia. Finally, those clinical circumstances which lead to combined episodes of hypoxia plus anoxia with acidosis favor a predominance of lesions that affect the basal ganglia.

Animals↗
PubMedDate not supplied

Production of fetal asphyxia by maternal psychological stress.

Several lines of evidence indicate that maternal psychological stress leads to adverse pregnancy outcome in rhesus monkey. Chronic anxiety causes an increased stillbirth rate, fetal growth retardation, and altered placental morphology. On another time scale, lightening of maternal anesthesia during surgery produces an impaired fetal oxygenation while re-institution of anesthesia ameliorates the fetal asphyxia. The present study, for the first time, demonstrates a relationship between specific episodes of meternal psychological stress and exacerbation of fetal asphyxia in utero. Eight term pregnant rhesus monkeys were anesthetized with sodium pentobarbital. Catheters were placed both into the maternal and the fetal femoral arteries for the continuous recording of blood pressure and heart rate and for the intermittent campling of maternal and fetal blood. An open-ended catheter recorded intrauterine pressures. Following a complete repair, the anesthesia of the mothers was allowed to lighten. As the mothers awakened, the fetuses invariably showed the developemnt of fetal asphyxia. A fetal acidosis developed and the fetal oxygenation and repair of acidosis. Studies while the mothers were fully awake showed the repeated and regular development of episodes of heightened fetal asphyxia produced by episodes of stressful stimulation of the mothers. Episodes of maternal psychological stress led to changes in both fetal vital signs and blood chemical findings. These alterations in fetal state regularly followed the onset of the episodes of psychological stress by 50 seconds. These changes also usually remitted 50 seconds following the termination of the periods of stress. These results demonstrated a direct and unequivocal relationship between meternal psychological stress and fetal asphyxia. It is assumed the maternal stress produces impairments in the circulation to the uterus through an increased sympathetic nervous system activity and a shunting of the maternal blood-flow from the abdominal viscera to other organs as occurs in the fight-orflight reaction.

Animals↗
PubMedDate not supplied

Neurologic and cardiovascular effects of hypotension in the monkey.

Thirty monkeys were exposed to controlled systemic hypotension of different magnitudes and duration to determine factors leading to brain injury or cardiovascular failure. Fourteen monkeys developed brain injury. Of these, 6 survived indifinitely and 8 were sacrificed or died within 12-62 hours due to neurologic deterioration accompanied by respiratory failure. Sixteen animals did not develop brain injury, but 9 of these died within 24 hours from documented cardiovascular failure with the remaining 7 survived indefinitely. A highly reproducible threshold for the development of brain injury was found at a mean arterial blood pressure (MABP) of 25 mm Hg. Maintenance MABP was less than or equal to 25 mm Hg in 13 of 14 lesioned monkeys and greater than 25 mm Hg in 15 of 16 non-lesioned monkeys. Maintenance MABP averaged 20.1 +/- 1.1 mm /g in lesioned and 32.1 +/- 1.7 mm Hg in non-lesioned animals (p less than 0.001). Among the non-lesioned animals, death from delayed cardiovascular failure ensued when MABP was maintained between 27 and 35 mm Hg for 90 min or longer. Animals exposed to this range of hypotension for less than 90 min or to MABP exceeding 35 mm Hg for as long as 3 h survived intact. EEG changes occurring during hypotension most accurately predicted neurologic outcome. The threshold MABP required to produce cerebral electric silence was 21-22 mm Hg. Monkeys developing marked brain injury had greater than 25 minutes of EEG flattening, while slightly injured animals had it for 5-15 minutes and those without injury for less than 5 min. Changes in acid-base state, common carotid artery blood flow, and cerebral uptake of glucose and oxygen during hypotension also correlated with neurologic and cardiovascular outcome. Hypoxemia and hypercarbia were not contributory factors in the production of brain injury in this study.

Animals↗