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Biomedical subjects

C E Hunt

Publications and source records attributed to C E Hunt.

At least 55 records · Page 3Linked to original sources
PubMed1989

Prenatal cocaine exposure is associated with respiratory pattern abnormalities.

As retrospectively determined, the rate of sudden infant death syndrome in 66 infants prenatally exposed to cocaine was 15%, compared with only 4% among infants exposed to opiates. This prospective evaluation of cardiorespiratory pattern in 32 cocaine-exposed and 18 methadone-exposed infants was therefore performed to further evaluate the effects of intrauterine exposure. The two groups were similar in maternal age, race, and cigarette, alcohol, and marijuana use and in gestational age, sex, and birth weight. Apnea density and episodes of periodic breathing exceeded the 95th percentile for normal infants in 12 (38%) of 32 of cocaine-exposed infants vs only 1 (6%) of 18 opiate-exposed infants. Five cocaine-exposed but no opiate-exposed infants had apnea of infancy, and all 5 of these infants had an abnormal cardiorespiratory pattern. In all 13 infants with an abnormal cardiorespiratory pattern, theophylline treatment resulted in normalization of the respiratory pattern and was associated with absence of any (further) clinical events. In summary, infants prenatally exposed to cocaine have a higher incidence of cardiorespiratory pattern abnormalities than do infants with methadone or no prenatal drug exposure.

Apnea↗
PubMed1989

Loss of oxygen tolerance in newborn rabbits: relationship to changes in eicosanoid and antioxidant levels.

Relative tolerance of newborn animals to hyperoxia has been reported. This study investigated the age limitation of oxygen tolerance and mechanisms for its loss. Developmental changes in lungs of normoxic New Zealand rabbits were studied on days 1, 3, 4, 5, and 10 of life. These were contrasted with newborn and 7-day-old rabbits exposed to greater than 95% O2 for 65 hours. Normoxic rabbits demonstrated a decrement in bronchoalveolar lavage (BAL) 6keto-PGF1a, thromboxane B2, and lower lung catalase, total glutathione, and superoxide dismutase with maturation. Newborns were more tolerant to oxygen than 7-day-old rabbits. Oxygen exposure beginning on day 1 did not result in identifiable lung damage. Exposure beginning on day 7 resulted in microscopic evidence of injury and significant increases in BAL white cells, neutrophils and protein, and a trend toward higher BAL LTB4 compared to normoxic age-matched controls. Antioxidants were higher in the hyperoxic 7 day-olds, but remained lower than values in hyperoxic newborns. These results suggest that loss of oxygen tolerance in maturing rabbits is related to a developmental decrement in antioxidants and prostacyclin.

Animals↗
PubMed1989

Role of eicosanoids in relative oxygen tolerance of newborn rabbits.

Prolonged exposure to hyperoxia can result in significant lung injury, although newborn animals are more oxygen-tolerant than adults. Mechanisms affording tolerance to the newborn are incompletely understood. This study examined the hypothesis that eicosanoids play a significant role in newborn oxygen tolerance. One litter of term newborn albino rabbits and 15 adult rabbits were exposed to 65 hours of greater than 95% O2. An additional litter of newborns served as a normoxic control. Normoxic newborn rabbits had very high quantities of 6-keto-PGF1a and low TXB2 in bronchoalveolar lavage (BAL) fluid. Sixty-five hours of oxygen exposure in newborn rabbits produced no evidence of lung injury on light microscopy, 97% of BAL white cells were alveolar macrophages and BAL protein was low. An equal period of oxygen exposure produced significant lung injury in adult rabbits. BAL fluid from oxygen-injured adults contained a 17-fold greater percentage of PMN and 16-fold higher protein than oxygen-exposed newborns. Hyperoxic adults had significantly lower 6-keto-PGF1a, and significantly higher LTB4 and LTC4 in BAL compared to hyperoxic newborns. This study confirms the hypothesis of relative oxygen tolerance in newborn rabbits compared to adults, and suggests that this tolerance may have been afforded by higher pulmonary levels of the protective prostacyclin metabolite.

Animals↗
PubMed1989

Oleic acid lung injury increases plasma prostaglandin levels.

To determine whether lung injury causes increased plasma prostaglandin (PG) levels, 35 rabbits received oleic acid and 35 served as controls. Half of each group also received 4 ml/kg of Intralipid over one hour and at least five in each subgroup received indomethacin 7.5 mg/kg. Arterial and venous plasma concentrations of PGE2, 6-keto-PGF1 alpha, and PGF2 alpha-M were measured. Venous PGE2 was significantly higher in the oleic acid-injured than in the normal lung group, 1560 +/- 270 (Mean +/- SEM) versus 880 +/- 140 pg/ml (p less than .05). Plasma levels were reduced by 50% with indomethacin, but PGE2 levels remained significantly higher than in the normal lung group, 850 +/- 180 versus 480 +/- 60 for arterial (p less than .05) and 820 +/- 140 versus 480 +/- 80 for venous (p less than .05), respectively. PGF2 alpha-M levels were significantly higher in the lung injury group, 240 +/- 50 versus 50 +/- 40 pg/ml for arterial (p less than .05) and 220 +/- 50 versus 95 +/- 40 for venous (p less than .05), respectively. These lung injury-related increases in PGE2 and PGF2 alpha-M appear related both to increased pulmonary production and to decreased pulmonary clearance. With Intralipid infusion, however, arterial PGE2 increased by 500 +/- 260 pg/ml compared to baseline (p less than .05) with no change in venous PGE2, indicating in this instance that the increase in arterial PGE2 levels is related to increased pulmonary production.

Animals↗
PubMed1989

Assessing validity of infant monitor alarms with event recording.

We evaluated the performance of an event recorder system in a large, consecutive series of referred monitored patients to determine the relative incidence of true apnea and true bradycardia, false alarms, and alarms for movement or a loose lead. In addition, we developed an event classification system based on the reason for the event being recorded. The recorder stored transthoracic impedance and electrocardiogram signals on a floppy disk before, during, and after each monitor alarm. These events on 302 disks from 83 patients were analyzed and classified as true, false, or movement-loose lead. Of 14,131 events, only 8% were caused by apnea or bradycardia (true events). Of true events, 70% were triggered by apnea and 30% by bradycardia. These true events occurred in 48% of the patients. False alarms constituted 23%, and movement-loose lead 69%, of all events. Even when movement-loose lead events were excluded, nearly three of four events were found to be false. Event recording proved helpful clinically, allowing discontinuation of the monitor in 49% of patients, modification of monitor alarm settings, or reassurance and counseling for parents.

Apnea↗
PubMed1989

Prostaglandin E1 infusion fails to prevent hyperoxic lung injury in adult rabbits.

Arachidonic acid (AA) metabolites may be important mediators in the hyperoxic lung injury process. We have previously demonstrated, in an adult model of hyperoxic lung injury, that bronchoalveolar lavage (BAL) fluid levels of AA metabolites of the cyclooxygenase pathway increase before evidence of overt injury. Nonselective inhibition with indomethacin or dexamethasone failed to ameliorate the injury process, possibly because production of prostaglandin I2 (PGI2) was suppressed. In this study, we attempted to ameliorate hyperoxic lung injury using an infusion of prostaglandin E1 (PGE1), since PGE1 has some of the potentially protective effects of PGI2. Thirty-two adult rabbits were exposed to greater than 95% oxygen; eight served as controls and 24 received PGE1 infusion (five, nine, and ten received 0.1, 0.06, and 0.03 micrograms/kg.min, respectively). At the end of the 65-h exposure period, BAL of the left lung was performed; the right was saved for light microscopy. PGE1 infusion at the 0.06 and 0.03-micrograms/kg.min doses resulted in significantly fewer polymorphonuclear leukocytes (PMN) in BAL fluid (p less than .05). However, PGE1 infusion did not significantly ameliorate the lung injury process. In summary, although PGE1 infusion inhibited the influx of PMN into the lung, treatment did not result in any significant amelioration of the hyperoxic lung injury process.

Alprostadil↗
PubMed1989

Diaphragm pacing in infants and children. A life-table analysis of implanted components.

Since 1976, we have implanted bilateral phrenic nerve electrodes for diaphragm pacing in 33 infants and children. This population includes 23 patients with congenital central hypoventilation syndrome (CHS), two with late onset CHS and hypothalamic dysfunction, three with hypoventilation associated with Chiari II malformation and myelomeningocele, and five with quadriplegia. Our experience, totalling 192 system-years and 96 patient-years of pacing, has enabled us to document the nature and frequency of problems related to the implanted components of the Avery Laboratories (S-232-1) pacemaker system when used in a pediatric population. By life table analysis, the mean time to need for replacement of any implanted component was 56.3 months. A total of 26 failures requiring component replacement occurred and were classified into four types: (1) receiver failure (15 cases), (2) electrode wire or wire insulation breakage (six cases), (3) infection requiring diaphragm pacer system removal (three cases), and (4) mechanical nerve injury (two cases). We conclude that the present diaphragm pacing system is effective but not without risk of biomedical component failure. The present system might be substantially improved by (1) a modified receiver design with a hermetic seal to prevent fluid penetration, (2) stronger, better insulated electrode wires, and (3) modifications of surgical technique and electrode type to prevent phrenic nerve damage.

Actuarial Analysis↗
PubMed1989

Impaired arousal from sleep: relationship to sudden infant death syndrome.

There is a relationship between deficient sleep arousal response to asphyxia, the presence of symptomatic apnea, and the risk for recurrent episodes of life-threatening sleep apnea. This documented abnormality in arousal responsiveness, which could result in the inability to respond to apnea-induced asphyxia, is the only respiratory control deficit that could result in sudden death. Inability to arouse from sleep in response to asphyxia may also be the underlying abnormality explaining numerous other behavioral deficits reported in infant groups with symptomatic apnea or otherwise thought to be at increased risk for sudden infant death syndrome (SIDS), including awake behavioral differences in temperament. An arousal response deficit to asphyxia may thus be a critically important and fundamental pathophysiological component of the essential defect necessary for the occurrence of sudden death during sleep. As with any other observed abnormality, however, it has not yet been possible to design an asphyxic arousal response test with sufficient accuracy and sensitivity to identify prospectively those infants otherwise destined to die of SIDS. Although an impairment in arousal responsiveness may be necessary for SIDS to occur such a deficit may not be sufficient to cause SIDS unless or until another factor(s) occurs that can cause sleep-related asphyxia. Although impaired respiratory control appears to be the likely precipitating cause of sleep-related asphyxia, it is also possible that factors unrelated to respiratory control are important in causing asphyxia; superimposed on an underlying arousal deficit, these could result in SIDS.(ABSTRACT TRUNCATED AT 250 WORDS)

Arousal↗
PubMed1988

Respiratory pattern at hospital discharge in asymptomatic preterm infants.

Pneumogram (PG) recordings were performed in 87 very low birthweight (VLBW) asymptomatic infants just prior to hospital discharge to determine the relationships between: 1) a prior history of apnea of prematurity (AOP) and cardiorespiratory pattern; and 2) cardiorespiratory pattern at hospital discharge and postconceptional age. Apnea density (A6/D%) and longest apnea were significantly greater in those with (n = 66), versus without (n = 21) a prior history of AOP (P less than 0.05 and P less than 0.01, respectively). Although PG values for the 21 VLBW infants without a prior history of AOP did not differ significantly from those of full-term infants, for the 66 VLBW infants with a prior AOP history A6/D% (P less than 0.01), episodes of periodic breathing (P less than 0.05) and longest apnea (P less than 0.001) were significantly greater compared with full-term infants. Postconceptional age was significantly less in the VLBW infants with A6/D% values above, compared with those within the 95th percentile for normal infants (median age, 36 and 37.5 weeks; P = 0.01). Therefore, respiratory pattern abnormalities in asymptomatic VLBW infants ready for hospital discharge are related to a prior history of AOP and may be significantly higher than in full-term infants at the postconceptional ages at which hospital discharge now tends to occur.

Apnea↗
PubMed1988

Apnea-onset definition significantly affects pneumogram results.

Pneumogram (PG) scoring methods have not been standardized. To determine the extent to which varying definitions for apnea-onset and apnea-termination will result in clinically significant differences in calculated apnea density (A6/D%) and periodic breathing, we analyzed 40 randomly selected PGs. All PGs were initially scored using end-expiration (EE) to mark the beginning of each apnea. As the second definition, peak inspiration (PI) was used to identify the onset of each apnea. All apneas greater than or equal to 6 s in duration and all episodes of periodic breathing were identified. The differences between results obtained by each definition were compared by paired t-test. The differences between the EE and PI definitions were statistically significant (p less than 0.01) for A6/D%, periodic breathing, longest apnea, and number of apneas greater than 11 s, with the PI definition consistently resulting in higher values. In summary, calculated PG results are significantly different, both clinically and statistically, depending on the scoring definition utilized for apnea-onset. Although each definition will yield results that are internally consistent, it is crucial that the normative standards used for comparison be derived utilizing the same scoring definition.

Cardiography, Impedance↗
PubMed1988

Fundamental considerations in pacing of the diaphragm for chronic ventilatory insufficiency: a multi-center study.

Records were reviewed of 477 patients who had diaphragm pacemakers implanted for treatment of chronic hypoventilation. Three groups were established for comparison. (1) Center group: 165 patients operated on in six medical centers participating in a cooperative study; (2) Noncenter group, sufficient data available: 203 patients operated on by surgeons with experience limited to a few cases; (3) Nonstudy group, minimal data available: 109 patients operated on as in group 2; vital statistics only were contributed. The protocol for data gathering was comprised of 154 major variables. Basic data on age, sex, diagnosis and etiology were analyzed for homogenicity of data among the groups. A comprehensive analysis of the pacing methods, complication and results from the Center group yielded information on the early experience with diaphragm pacing important to its future application.

Diaphragm↗
PubMed1988

Diaphragm pacing in infants and children.

Since 1976 we have implanted bilateral diaphragm pacers in 34 infants and children: 26 with central hypoventilation syndrome (CHS), three with myelomeningocele, and five with quadriplegia. Compared to adults, several modifications have been necessary to achieve effective ventilation in infants and younger children. In all instances, a tracheostomy has been necessary due to impaired neuromuscular control of upper airway patency during pacing. Bilateral pacing has been necessary to achieve adequate ventilation; in the CHS children with normal awake ventilation, bilateral pacing during sleep eliminates the need for positive pressure ventilation. For the remaining children, adequate awake ventilation is achieved with bilateral pacing, thus permitting substantially greater mobility and limiting use of the ventilator to sleep time. Our longest survivor has now been paced for 10.7 years, and in no instance has phrenic nerve damage occurred secondary to electrical stimulation. Our current pacing regime is characterized by moderate respiratory rates (21 breaths/min), long interpulse intervals (95 ms), and short inspiratory times (0.6 sec), resulting in 50%-75% fewer stimuli/min compared to our previous regime. For all infants and children requiring 24-hour ventilatory assistance, our recent successes in maintaining ventilation using significantly fewer stimuli suggest that long-term continuous pacing is a realistic future goal.

Child↗
PubMed1988

Effects of almitrine on respiration in unanesthetized newborn rabbits.

We previously demonstrated that almitrine, a peripheral chemoreceptor stimulant, increased tidal volume (VT), expired minute ventilation (VE), and respiratory frequency (f) and decreased inspiratory (TI) and expiratory time (TE) in sleeping adult cats. We now hypothesized that almitrine would induce an increase in ventilation in a young animal model. Respiration was studied by the barometric method in 11 unanesthetized New Zealand White rabbit pups between 3 and 6 days of age. Recordings were made in 0.21 FIO2 at base line and after cumulative intraperitoneal infusions of almitrine (2.5, 5.0, and 7.5 mg/kg). The chamber pressure deflection (proportional to VT after appropriate calculation) was computer sampled at 200 Hz. At least 100 breaths for each dose in each animal were analyzed. We found that a 7.5-mg/kg intraperitoneal dose of almitrine increased f to 135 +/- 9% (SE) of base line and decreased TE and TI to 72 +/- 8% and 79 +/- 8% of base line, respectively. Changes in VE, VT/TI, and VT were not significant. Recognizing that apnea is associated with inadequate ventilation and a prolonged TE (failure of the "inspiratory on-switch"), these results, particularly the increase in f and decrease in TE, suggest that almitrine might be useful in treating apnea in preterm infants.

Almitrine↗
PubMed1988

Magnetic resonance imaging and computerized tomography in central hypoventilation.

Central hypoventilation syndrome (CHS) is a disorder of respiratory control. It may be an idiopathic primary disease or it may be the secondary consequence of an infectious process or Chiari II malformation. Clinical data suggest that the primary defect involves the brainstem respiratory centers. To date, pathologic evaluation has linked primary CHS with decreased density of neurons and myelinated nerve fibers in the medulla and brainstem gliosis, and absence of the external arcuate nucleus. Magnetic resonance imaging (MRI) is now considered the most reliable imaging technique for evaluating the brainstem. In the hope of finding gross structural abnormalities that might correlate with the clinical and pathologic features of CHS, we used MRI and computerized tomography (CT) to evaluate the brain, brainstem, and spinal cord of 17 infants and children with central hypoventilation (11 primary, 6 secondary). Each of the 11 children with primary CHS demonstrated a normal brainstem and spinal cord by MRI. However, 9 of 11 infants had mild ventricular dilatation and modest prominence of the sulci interpreted as either mild atrophy or mild extraventricular obstructive hydrocephalus. Results of studies in the one child with postinfectious disease were normal. The 5 infants with Chiari II malformation demonstrated characteristic brainstem changes. MRI results modified clinical care, resulting in symptomatic improvement after hindbrain decompression by cervical laminectomy in 1 infant and surgical drainage of syringobulbia in 1 child. In summary, in primary CHS, the MRI and CT provided evidence for a more diffuse CNS process rather than a specific brainstem lesion. Such a lesion may be too small or too subtle to resolve with MRI or CT. In secondary central hypoventilation, MRI modified surgical management in 2 cases, resulting in symptomatic improvement of hypoventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Arnold-Chiari Malformation↗
PubMed1988

Failure of non-selective inhibition of arachidonic acid metabolism to ameliorate hyperoxic lung injury.

We have previously reported that bronchoalveolar lavage fluid cyclo-oxygenase products of arachidonic acid (AA) metabolism increase prior to the development of significant hyperoxic lung injury. To further assess the role of AA metabolites in the development of hyperoxic lung injury, we have utilized this same model of hyperoxic lung injury and administered either indomethacin (an inhibitor of the cyclo-oxygenase pathway of AA metabolism) or dexamethasone (inhibitor of AA release). A total of 46 adult rabbits were exposed to greater than 95% oxygen for 65 hours. Fourteen animals were given either 2 or 3 mg/kg/day indomethacin, 7 served as controls: 18 animals were given either 0.5 or 1.0 mg/kg/day of dexamethasone, 7 served as controls. The surviving animals were sacrificed after 65 hours of hyperoxia and bronchoalveolar lavage of the left lung was done; the right lung was examined by light microscopy. Treatment with indomethacin or dexamethasone failed to ameliorate the hyperoxic lung injury process. However, in both the indomethacin and dexamethasone treatment groups, significant suppression of 6-keto-PGF1 alpha, a PGI2 metabolite, was observed. Some suppression of TXB2 production was observed, but there was no evidence of any decrease in leukotriene production. We postulate that failure to ameliorate hyperoxic lung injury with either indomethacin or dexamethasone therapy was related to significant suppression of PGI2, a potentially protective AA metabolite, and/or to failure to significantly decrease production of potential pathogenic participants, such as TXA2 or LTB4.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Sudden infant death syndrome: 1987 perspective.

The pathophysiology of SIDS remains unknown. Although a multifactorial cause appears plausible on the basis of available data, new data are needed to determine which components of this multifactorial hypothesis are most important and whether other factors need to be added. We need to better understand control of breathing in the newborn infant and the manner in which maturation of cardiorespiratory control progresses during infancy. The unique period of vulnerability for SIDS, in which risk is less in the neonate than at 2 to 6 months of age, remains unexplained. Is there a worsening in some aspect of cardiorespiratory control in infants destined to die of SIDS? An improved understanding of the increased risk in black infants, preterm infants, and infants with intrauterine drug exposure, although only a small percentage of all SIDS deaths, should contribute substantially to our understanding. Appropriately designed and well-controlled prospective studies are needed in asymptomatic infants at risk, to determine the true contemporary nonintervention rate of SIDS and the extent to which any assessment or intervention lowers this rate. Prospective pneumogram screening studies have demonstrated significant group differences in respiratory patterns in normal infants compared with later SIDS victims, but have failed to achieve sufficient sensitivity and specificity to be useful for populationwide prospective screening. To assess aspects of brainstem cardiorespiratory control in addition to those assessed by a conventional pneumogram, future studies will need to be based on an expanded or modified technology. On the basis of both physiologic considerations and available technology, addition of an oxygen saturation channel offers the most promise for providing a more comprehensive assessment of cardiorespiratory control. If there is an underlying deficiency in asphyxic arousal responsiveness, for example, with or without other respiratory control deficits, continuous monitoring of oxygen saturation as part of a second-generation pneumogram system currently has the greatest promise for providing a modified pneumogram assessment of greater clinical use. The use of continuous oxygen saturation as a home monitoring technique should also be investigated. Power spectrum analysis of cardiorespiratory variability also appears to have potential advantages over conventional pneumogram analyses, and needs to be evaluated in prospective studies. The following statements summarize our current knowledge regarding SIDS, apnea, pneumograms, and home monitors: The cause(s) of SIDS remains unknown.(ABSTRACT TRUNCATED AT 400 WORDS)

Apnea↗
PubMed1987

Comparison of respiratory inductive plethysmography and thoracic impedance for apnea monitoring.

Thoracic impedance apnea monitors may fail to detect obstructive apnea, may falsely alarm when the infant is breathing, and may confuse cardiac artifact with respiratory impedance. Therefore, we compared the performance of a respiratory inductive plethysmograph and a thoracic impedance monitor with a reliable measure of airflow, either nasal CO2 or pneumotachograph, during 29 studies in 28 patients referred for sleep laboratory evaluation. Sleep time averaged 72 +/- 37 (SD) minutes. The inductance plethysmography and the impedance monitor detected 99.6% +/- 0.6% and 98.3% +/- 3.0% of breaths, respectively. However, in two studies, the impedance monitor detected many extra breaths, once because of cardiac-induced impedance changes and once because of partial airway obstruction-induced impedance changes. In 11 studies, cardiac artifact was sometimes misinterpreted as a breath by the impedance monitor. The impedance monitor, but not the inductance plethysmograph, missed breaths following sighs in 16 of 29 studies. Both monitors detected all 60 episodes of central apnea. The inductance plethysmography detected 35 of 38 episodes of obstructive apnea, but the impedance monitor identified only two such events. Apnea was detected falsely four times by the inductance plethysmograph and 14 times by the impedance monitor. These results suggests that a respiratory inductive plethysmograph would have significant advantages over impedance monitoring, including the ability to detect obstructive apnea, and freedom from cardiac artifact.

Apnea↗