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Biomedical subjects

W A Hodson

Publications and source records attributed to W A Hodson.

At least 37 records · Page 2Linked to original sources
PubMed1988

Histologic evolution of the reactions to hemorrhage in the premature human infant's brain. A combined ultrasound and autopsy study and a comparison with the reaction in adults.

With the development and routine use of real-time ultrasound scanning, it has been possible to collect 20 autopsy cases of infants in whom the ultrasound scan was first normal and then showed evidence of subependymal/intraventricular hemorrhage (SEH/IVH). Analysis of these cases with known postnatal origin of the hemorrhage permitted the development for the first time of a time scale to characterize the temporal evolution of the histopathologic reactions to hemorrhage in the premature human brain. This time scale was then used to define the histologic stage of the lesions in 27 other cases of infants who had a scan demonstrating SEH/IVH prior to death but who had not a previously normal scan. Only 2 cases were found to lie off the original scale, indicating a prenatal onset of the hemorrhage in about 5% of the total cases. Thus, postnatal events immediately preceding the onset of the hemorrhage are more likely to be implicated in the pathogenesis of SEH/IVH than prenatal or obstetric events. Comparison with similar reactions in the adult indicate that the early reactions by macrophages occur at about the same rate but the routine transfer of iron from macrophages to astrocytes and the much slower rate of absorption to form a cyst in the adult combine to form a complicated pattern that requires a different set of criteria for the intermediate and late stages in the adult.

Adult↗
PubMed1987

Sequence of inflammatory cell migration into lung during recovery from hyaline membrane disease in premature newborn monkeys.

The appearance of polymorphonuclear leukocytes (PMN) and macrophages (MAC) in lung during the development of hyaline membrane disease (HMD) may be important in lung injury and repair. These inflammatory cells may cause additional lung injury during recovery from HMD and contribute to the development of bronchopulmonary dysplasia (BPD). By morphometric methods, we compared the proportion of PMN and MAC in lung tissue of premature M. nemestrina monkeys with HMD to the proportion of these cells in the lungs of healthy control animals of a similar postnatal age and to fetuses of the same gestational age. Expressed as a fraction of all lung cells, healthy premature control monkeys have the same %PMN and %MAC in lung tissue as fetal animals. However, during the development of acute HMD, there is an increase in %PMN (p less than 0.05), but not in %MAC, compared to fetal animals. During recovery, there is a greater than 10-fold increase in %MAC (p less than 0.02), but no significant additional increase in %PMN compared to animals with acute HMD. We conclude that the sequence of inflammatory cell migration into the premature lung injured during HMD is first a polymorphonuclear one, followed by entry of macrophages. Control of this inflammatory response during recovery from HMD may play a role in the pathogenesis of BPD.

Animals↗
PubMed1986

A new agenda needed concerning "tragic choices".

Debate regarding the context of decision making on catastrophically ill infants has been focused on process and methodology. An expanded scope of inquiry is needed to increase our understanding of the dilemmas we face.

Attitude↗
PubMed1986

Surfactant quantity and composition during recovery from hyaline membrane disease.

The appearance of phosphatidylglycerol in the tracheal wash of infants with hyaline membrane disease (HMD) has been reported to be associated with clinical signs of recovery. We analyzed lung tissue and bronchoalveolar lavage surfactant in an animal model of HMD to determine whether phosphatidylglycerol or some other component is necessary for recovery. The amount and composition of phospholipid (PL) was determined in the premature Macaca nemestrina monkey (140 days' gestation) during an acute stage of HMD, and in two stages of recovery. These changes were compared to observations made in healthy premature controls (140 days), gestational age-matched fetuses (140 days), and fetuses of 150 days' gestation (term = 168 days). The amount of PL and its surfactant composition in lung homogenates of the right lower lobe and in lavage of the excised left lung was determined. Compared to 140-day fetuses, the healthy controls had a several-fold increase in lavage PL and disaturated phosphatidylcholine (DSPC) during the first few days of life (p less than 0.05). Prior to recovery, animals with HMD had no such increase in lavage PL or DSPC and demonstrated poor deflation stability. Recovery was associated with increased tissue and lavage PL (p less than 0.05) and increased fractions of phosphatidylinositol and DSPC (p less than 0.05), but not phosphatidylglycerol. The tissue compositional changes observed during recovery reflected maturational changes observed in the fetal animals studied at 10 days' greater gestational age.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Severe nonimmune fetal hydrops with fetal survival. A case report.

A case of severe idiopathic nonimmune fetal hydrops spontaneously resolved after delivery with only basic supportive therapy. This case emphasizes that natural occurrences occasionally are responsible for successes attributed to invasive intrauterine treatments.

Adult↗
PubMed1985

Changes in lung volume and deflation stability in hyaline membrane disease.

Total lung capacity (TLC), inspiratory capacity, functional residual capacity, and deflation stability of prematurely delivered Macaca nemestrina primates were measured serially during development of, and recovery from, hyaline membrane disease (HMD) to relate changes in lung volumes to changes in deflation stability. Gestational age-matched primates that did not develop HMD served as controls. TLC, measured by N2 washout, fell at 2-12 h of age (P less than 0.0001) in animals with HMD and remained lower than controls for at least 48 h (P less than 0.005). However, deflation stability, defined as the fraction of TLC remaining upon deflation to 10 cm H2O, improved from 2 to 12 h of age (P less than 0.001). Postmortem studies confirm the measurements of TLC and deflation stability and provide evidence that interstitial thickening and obstruction of air spaces with debris may be partially responsible for the observed changes in TLC in primates that develop HMD. It has been assumed that TLC is reduced in HMD because of atelectasis from elevated alveolar surface tension, but the sequential measurements in these animals suggest that other mechanisms also contribute.

Animals↗
PubMed1984

Effects of prolonged high-frequency oscillatory ventilation in premature primates with experimental hyaline membrane disease.

The effects of 24 h of high-frequency oscillatory ventilation (HFOV) applied to premature primates with hyaline membrane disease (HMD) were assessed by serial gas exchange and in vivo lung distensibility measurements, and by postmortem lung phospholipid analysis. Results in 7 animals with HMD treated with HFOV were compared with those in 6 animals with HMD treated with conventional mechanical ventilation. No differences in arterial to inspired PO2 ratios, total lung capacity, airway lavage, or lung homogenate phospholipid or disaturated phosphatidylcholine were found between the 2 groups. Arterial PCO2 was lower in the HMD-HFOV group at 6 and at 12 h. There was no difference in lung dry to wet weight ratios; the ratio in both groups of HMD animals was less than that for premature primates without HMD. We conclude that HFOV is useful in maintaining adequate CO2 elimination but does not improve arterial oxygenation or alter the natural history of experimental HMD.

Animals↗
PubMed1983

Antenatal glucocorticoid administration: effects on oxygen-hemoglobin affinity and hemoglobin levels in experimental hyaline membrane disease.

Dexamethasone or saline was administered in a randomized fashion to pregnant Macaca nemestrina for 3 days prior to preterm abdominal delivery. The steroid-treated animals demonstrated a greater hemoglobin concentration and a greater mean corpuscular hemoglobin concentration in cord blood. There was no difference between the groups in mean P50 in cord blood. The infants of steroid-treated animals had less frequent and less severe hyaline membrane disease. We conclude that antenatal steroid administration ameliorates postnatal respiratory distress without inducing changes in P50 and with only a small change induced in cord blood hemoglobin.

Animals↗
PubMed1983

Effect of high-frequency oscillation on gas exchange and pulmonary phospholipids in experimental hyaline membrane disease.

Arterial PO2 and PCO2 obtained with 2 modes of mechanical ventilation were compared in 5 premature monkeys with hyaline membrane disease (HMD) during the first 7 h of life. High-frequency oscillation (HFO) (10 Hertz) was compared with conventional positive-pressure ventilation (CMV) by matching the mean airway pressure generated by the 2 systems. Each animal served as its own control; HFO sustained an improved PaCO2 (39 +/- 8 versus 25 +/- 7 mmHg). An insignificant improvement in arterial PO2 was noted. The improved CO2 exchange occurred with a lower peak airway pressure (35 +/- 4 versus 23 +/- 11 cm H2O). Comparison of the postmortem pressure-volume curves and lung and lavage phospholipid concentrations from the animals treated with HFO in the current study to a matched set of animals treated exclusively with CMV in a previous study failed to reveal any differences. We conclude that HFO is effective in eliminating CO2 in experimental HMD without apparently altering lung biochemical or mechanical properties in a manner different from that found with CMV.

Animals↗
PubMed1983

Comparative effects of inhaled volcanic ash and quartz in rats.

To investigate the relative toxicities of inhaled volcanic ash and quartz, we exposed matched groups of rats to either respirable volcanic ash (100 mg/m3), quartz (100 mg/m3), or clean air only for 6 h daily for 10 days. Thereafter, we examined animals sequentially for as long as 9 months, and measured changes in lung histopathologic aspects, air-space cells and lipids, and lung density. Neutron activation studies demonstrated that 3.3% of the inhaled daily dose of volcanic ash was detectable in the lung parenchyma. Volcanic ash was less toxic to the lung than quartz. Immediately after exposure, the lungs of animals treated with volcanic ash had ultrastructural evidence of damage to type I pneumocytes and early alveolar edema formation. By contrast, quartz-treated animals had an intense acute injury, with intraalveolar accumulation of lipid, protein, macrophages, and granulocytes. Six months after exposure, animals treated with volcanic ash had moderate interstitial thickening and fibrosis, whereas the quartz-treated animals had severe pulmonary fibrosis. Quartz, but not volcanic ash, caused a marked increase in lavage granulocytes, protein, and phospholipids. Lung density increased in quartz-exposed, but not in volcanic-ash-exposed animals. These data indicate that volcanic ash is less harmful to the lung parenchyma than is quartz. Persons exposed to volcanic ash for short periods are at much less risk of subsequent lung damage than are those who are exposed to similar amounts of quartz in the workplace.

Absorptiometry, Photon↗
PubMed1982

Experimental hyaline membrane disease in the premature monkey: effects of antenatal dexamethasone.

A blind, randomized trial of antenatal glucocorticoid treatment was conducted using the premature monkey (Macaca nemestrina) model of hyaline membrane disease (HMD). Twelve dams received dexamethasone (2 mg/dose) 72, 48, and 24 h before abdominal delivery at 135 +/- 1 days of gestation. Twelve control animals received saline. Infants of dexamethasone-treated dams had significantly lower incidence and severity of HMD than did infants of control animals (50 versus 92%, p less than 0.05). Improvement with treatment was markedly greater for males than for females. Differences in volume-pressure behavior of the excised lungs included greater distensibility in the infants from dexamethasone-treated dams (20.6 +/- 7.1 ml/g dry lung versus 14.7 +/- 6.1, p less than 0.05) and enhanced deflation stability with treatment. Accelerated production of surface active material (SAM) phospholipids in infants from dexamethasone-treated dams was indicated by increases in total lung phospholipid (84.5 +/- 8.1 mg/g dry lung versus 75.1 +/- 9.9, p less than 0.025), alveolar lavage fluid phospholipid (5.65 +/- 3.33 mg/g dry lung versus 3.01 +/- 1.84, p less than 0.05), and alveolar lavage fluid disaturated phosphatidylcholine (DPC) (2.47 +/- 1.84 mg/g dry lung versus 1.06 +/- 1.05, p less than 0.05). Incorporation of 14C-palmitate into lung lipid was not influenced by dexamethasone, but a significantly greater portion of the label appeared in the DPC fraction with treatment. Antenatal dexamethasone treatment was successful in reducing the incidence and severity of experimental HMD in this animal model; the beneficial effects of treatment were associated with accelerated maturation of fetal pulmonary functions, including, but not limited to, synthetic metabolism of SAM phospholipid.

Animals↗
PubMed1981

Development of CO2 sensitivity: effects of gestational age, postnatal age, and sleep state.

To determine the independent effects of sleep state, gestational age, and postnatal age on eucapnic ventilation and steady-state CO2 sensitivity, nine premature (146 +/- 3 days) and eight full-term (168 +/- 2 days) monkeys, Macaca nemestrina, from accurately timed conceptions were studied serially over the first 3 wk of life. Minute volume (VE)/kg,tidal volume (VT)/kg, and respiratory frequency were quantitated during rapid-eye-movement sleep (REM) and nonrapid-eye-movement sleep (NREM)in room air and when animals were breathing varied concentrations of cO2 in 21% O2. Eucapnic VE/kg and CO2 sensitivity [(deltaVE/kg)/delta PaCO2] increased progressively with advancing postnatal age during NREM sleep in grouped term and premature animals. CO2 sensitivity was not significantly different between REM and NREM sleep except in full-term animals at the highest postconceptual age studied (189 +/- 2 days) when [(delta VE/kg)/delta PaCO2] was lower in REM sleep than in NREM sleep (209 +/- 54 vs. 301 +/- 71 ml.min-1.kg-1.Torr-1; P less than 0.05, paired-t test). Gestational age had no measurable effect on eucapnic ventilation or CO2 sensitivity. These results support the hypothesis that REM sleep-induced depression of CO2 sensitivity develops in the neonatal monkey with advancing postconceptual age.

Aging↗
PubMed1981

Differential effect of sex in experimental hyaline membrane disease in newborn monkeys.

Data from forty-four infant monkeys of 135 to 150 days' gestation were reviewed for the existence of sex-related differences in the development of hyaline membrane disease, post-mortem lung mechanics, biochemistry, and histologic features. Severity of hyaline membrane disease was scored from 1 (severe) to 6 (none) from chest radiographic appearance and arterial PO2 determination. Female monkeys had a lower score (mean +/- 1 SD = 2.7 +/- 1.6) than males (3.8 +/- 1.6, less than 0.05). Females accounted for 70% of animals with scores of 1 or 2, and 33% of those with scores of 5 or 6 (p = 0.045). There was no difference in lung homogenate phospholipid (PL) concentration. Airway lavage PL and the ratio of lavage PL to homogenate PL were both decreased in the female. Surface activity of the lavage material was also less in the female. No significant differences between males and females were noted for mean maximal lung volume air-tissue ratio, as determined by light microscopy, or number of type II pneumocytes per alveolus. Premature female monkeys appeared to sustain a disadvantage in pulmonary adaptation to postnatal life.

Animals↗
PubMed1980

Sleep and maturation of eucapnic ventilation and CO2 sensitivity in the premature primate.

The effects of sleep state and postnatal maturation on steady-state CO2 sensitivity, "inspiratory drive" (VT/TI), and the inspiratory "duty cycle" (TI/Ttot) were examined in nine unanesthetized premature Macaca nemestrina in the first 3 wk of life. Minute volume (VE) in room air was less in NREM sleep than in the awake state but there were no differences in VE, VT/TI, or TI/Ttot between REM and NREM sleep. VE and VT/TI corrected for body weight increased in REM and NREM sleep with postnatal maturation whereas TI/Ttot did not vary. Concomitant with this increase in room air VE and VT/TI, an increase in CO2 sensitivity (delta V/delta Paco2) with postnatal maturation was documented in NREM sleep. CO2 sensitivity was similar between REM and NREM states at each postnatal age. The increase in VE following inhalation of 2-5% CO2 was mediated by an increase in VT/TI, whereas TI/Ttot remained constant. The differences in the effect of sleep on CO2 sensitivity between neonates and adults are discussed and possible mechanisms for the observed developmental increase in CO2 sensitivity are proposed.

Animals↗
PubMed1979

The immature monkey as a model for studies of bronchopulmonary dysplasia.

The monkey is a potential model for BPD since there is considerable background information on the normal-developing lung, the prematurely delivered infant is viable, HMD can be produced, the infant is large enough to permit physiologic measurements, and it should be possible to test the effects of positive pressure, oxygen, and pharmacologic agents. Clearly further information is needed on the cellular and subcellular changes occurring during the acute and recovery stages of HMD. The monkey has already proven to be of value in this inquiry. Studies on mechanisms of altered lung repair by various injurious agents are needed, and will require an animal model as well as in vitro systems. Basic understanding of the pathogenesis of bronchopulmonary dysplasia with establishment of the relative importance of the contributing factors should help in our efforts to prevent or minimize chronic lung disease in the newborn infant.

Animals↗