Immediate and Late Ventilatory Response to High and Low O2 in Preterm Infants and Adult Subjects

Sankaran, Koravangattu; Wiebe, Henry W.; Seshia, Mary; Boychuk, Rodney B; Cates, Don; Rigatto, Henrique

doi:10.1203/00006450-197908000-00001

Cited by 47 publications

(24 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…AP = a pressure change (cmHzO) as recorded from the ICP monitor during an occlusion). In addition, inspiratory and expiratory air flow was monitored by using a nose piece and screen flow meter (22,24). An infrared CO2 analyzer (model LB2; Beckman, Schiller Park, IL) was used to monitor alveolar CO2 (Pacon).…”

Section: Summary Materials and Methodsmentioning

confidence: 99%

Estimated Cerebral Blood Flow in Term Infants with Hypoxic-Ischemic Encephalopathy

1981

View full text Add to dashboard Cite

Summary MATERIALS AND METHODSEstimated cerebral blood flow (eCBF) was measured sequenSeven asphyxiated infants showing evidence of HIE and seven tially in seven term infants with evidence of hypoxic-ischemic normal-term infants were studied. ,411 infants in the control group encephalopathy (HIE) and compared with that of normal-term were selected from the normal newborn nurseries of the Royal infants. The eCBF was determined by a noninvasive method Alexandra Hospital and were found to be completely normal upon involving brief bilateral jugular venous occlusion with simultaneous general physical and detailed neurological examinations (21). All measurement of occipitofrontal circumference. There was a sig-infants in the asphyxia group were cared for in the Newborn nificant decrease in eCBF on day 2 (30 f 4 ml/min/100 g brain Intensive Care Nursery of the same hospital. Infants with evidence weight) and on day 4 (36 + 5 mJ/min/100 g brain weight) compared of infection, congential heart disease, congenital abnormalities of with control values (56 2 4 ml/min/100 g brain weight; 54 2 4 mJ/ the nervous system, or respiratory distress unrelated to asphyxia min/100 g brain weight) (P < 0.01). The alveolar CO2 was signifi-were not included in this study. Only those infants who fulfilled cantly lower on days 2 and 4 in the HIE group (P < 0.001), and the following criteria during an initial 24 hr period of observation these values increased to control values by day 6. There was no in the Newborn Intensive Care Nursery were selected: significant correlation between estimated cerebral blood flow and 1. Gestation >37 wk, both by maternal dates and clinical alveolar C 0 2 in infants with HIE. We conclude that term infants assessment, with a birth weight appropriate for gestational with evidence of hypoxic-ischemic encephalopathy demonstrate age. lowered eCBF in the first 4 days of life.2. A history suggestive of fetal disCress including meconium staining, fetal heart rate abnormalities, severe antepartum hemorrhage, or a complicated delivery including breech Speculation extraction, difficult forceps extraction, failed forceps, and/ Some of the treatment schedules used for infants with hypoxicor cesarean section for prolonged labor or fetal distress. ischemic encephalopathy may, in fact, alter brain blood flow.3. Immediate neonatal asphyxia as evidenced by the need for Therefore, consideration of low cerebral blood flow in these infants immediate intubation and resuscitation or Apgar scores of becomes very important when such therapy is contemplated.3 or less at 1 min or 5 or less at 5 min. 4. Neurologic dysfunction as evidenced by seizures, marked abnormalities of behavioral state, posture, tone, motility, Perinatal asphyxia or hypoxic-ischemic encephalopathy (HIE) and reflexes (3,25). Some infants had other system abnoris a significant cause of neonatal mortality and morbidity (1, 2, 6, malities related to asphyxia, i.e., renal, hepatic, and meta-15, 30). The majority of infants who demonstrate neurologic and bolic dysfuncti...

show abstract

Section: Summary Materials and Methodsmentioning

confidence: 99%

Estimated Cerebral Blood Flow in Term Infants with Hypoxic-Ischemic Encephalopathy

1981

View full text Add to dashboard Cite

show abstract

“…The ventilatory responses to acute hypoxia of animals and humans change dramatically from fetal to adult life: in fetal animals, exposure to hypoxia is inhibitory to breathing movements (1), whereas in the adult, hypoxia causes a sustained increase in ventilation (2). Neonatal animals produce an intermediate biphasic response, with ventilation increasing and then falling again during sustained hypoxia (3).…”

mentioning

confidence: 99%

O2-sensitive K+ currents in carotid body chemoreceptor cells from normoxic and chronically hypoxic rats and their roles in hypoxic chemotransduction.

Wyatt

Wright²,

Bee³

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

127

View full text Add to dashboard Cite

Carotid body-mediated ventilatory increases in response to acute hypoxia are attenuated in animals reared in an hypoxic environment. Normally, 02-sensitive K+ channels in neurosecretory type I carotid body cells are intimately involved in excitation of the intact organ by hypoxia. We have therefore studied K+ channels and their sensitivity to acute hypoxia The ventilatory responses to acute hypoxia of animals and humans change dramatically from fetal to adult life: in fetal animals, exposure to hypoxia is inhibitory to breathing movements (1), whereas in the adult, hypoxia causes a sustained increase in ventilation (2). Neonatal animals produce an intermediate biphasic response, with ventilation increasing and then falling again during sustained hypoxia (3). This transient increase, along with the sustained increase seen in adults, is a result of stimulation of peripheral chemoreceptors, primarily the carotid body (4, 5). Ventilatory responses to acute hypoxia of neonatal animals born and raised in hypoxic environments are blunted or absent (6), and a similar lack of ventilatory response to hypoxia has also been noted in adult animals exposed to hypoxia chronically (7) and in high-altitude residents (8). It is conceivable that common mechanisms underlie the lack of ventilatory response to hypoxia of chronically hypoxic neonatal animals and high-altitude residents.The carotid bodies of chronically hypoxic animals or humans show dramatic morphological changes following prolonged hypoxia: most notably, type I carotid body cellsThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact. undergo hyperplasia and hypertrophy (9, 10). Type I cells are widely accepted as the chemosensory element of the carotid body, and various stimuli including hypoxia stimulate Ca2+-dependent release of neurotransmitters from these cells in a manner that correlates with increased discharge of afferent chemosensory fibers (5, 11). In recent years, several groups have used patchclamp techniques to investigate ion channels in type I cells, and there are several reports describing 02-sensitive K+ channels in these cells (12)(13)(14)(15)(16). These findings have given rise to a proposed mechanism for hypoxic chemotransduction in which inhibition of K+ channels by hypoxia leads to depolarization and increased excitability of type I cells sufficient to activate voltage-gated Ca2+ channels. This leads to Ca2+ influx and triggering of neurosecretion, an essential step in the chemotransductive pathway (5). Here we have compared ionic channels and their modulation by acute hypoxia in type I cells isolated from neonatal rats born and raised in normoxia and hypoxia in order to investigate whether the lack of chemoreceptor-mediated increases in ventilation seen in animals reared under chronically hypoxic conditions can be attributed to altered electrophysiological properties of type I cells. ...

show abstract

“…In adults, the elimination of peripheral drive is thought to be manifest by a reduction in the variability and slope of the ventilatory response (Lloyd et al 1958;Fencl, 1976). Since indirect evidence suggests that hyperoxia reduces peripheral drive in the newborn (Cross & Warner, 1951;Brady, Cotton & Tooley, 1964;Sankaran, Wiebe, Seshia, Boychuk, Cates & Rigatto, 1979), we speculated that changes in the variability and slope of the ventilatory response might also be effected by manipulating the t02 during rebreathing tests in newborn babies. In terms of the TcPo2 levels maintained during normoxic and hyperoxic tests, this objective was achieved: mean TcPo2 levels during normoxic tests did not differ significantly from the eupnoeic levels which we measured, or which have been reported elsewhere (Martin, Okken & Rubin, 1979), but did increase significantly during hyperoxic rebreathing (the TcPo2 is an indirect, although fairly accurate measure of Pa°2 at least under normoxic conditions: Le Soeuf, Morgan, Soutter, Reynolds & Parker, 1978;Wimberley, Frederiksen, Witt-Hansen, Melberg, Friis-Hansen, 1985).…”

Section: Measurementsmentioning

confidence: 99%

The reproducibility of the response of the human newborn to CO2 measured by rebreathing and steady‐state methods.

Cohen

Henderson‐Smart

1994

The Journal of Physiology

View full text Add to dashboard Cite

1. The ventilatory response (VR) of the full-term newborn to CO2 was studied during quiet sleep using rebreathing and steady-state methods. 2. Rebreathing responses were obtained under normoxic (fractional inspired oxygen concentration, F1 02 = 0-21) and hyperoxic (Fi ,2 = 0 4) conditions. Ten infants were tested three to five times using each of the two rebreathing protocols and the results averaged. 3. Overall, there was no significant difference between either the mean variability (coefficient of variation) or slope of the VR measured under normoxic and hyperoxic conditions. 4. Four infants were studied using a steady-state technique. There was marked test-to-test variability in VRs measured by this method. 5. The results appear to indicate that the variability of the VR of the newborn to CO2 is not a result of chemoreflex changes in ventilation elicited in response to fluctuations in arterial P02.It is believed that during non-rapid eye movement (non-REM) sleep, the generation of a normal breathing rhythm is largely dependent upon the brain receiving a constant flow of afferent information of metabolic or autonomic origin, for example, from chemoreceptors and pulmonary mechanoreceptors (Sullivan, 1980

show abstract

Immediate and Late Ventilatory Response to High and Low O2 in Preterm Infants and Adult Subjects

Cited by 47 publications

References 13 publications

Estimated Cerebral Blood Flow in Term Infants with Hypoxic-Ischemic Encephalopathy

Estimated Cerebral Blood Flow in Term Infants with Hypoxic-Ischemic Encephalopathy

O2-sensitive K+ currents in carotid body chemoreceptor cells from normoxic and chronically hypoxic rats and their roles in hypoxic chemotransduction.

The reproducibility of the response of the human newborn to CO2 measured by rebreathing and steady‐state methods.

Contact Info

Product

Resources

About