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Biomedical subjects

J M Fiascone

Publications and source records attributed to J M Fiascone.

8 recordsLinked to original sources
PubMed2000

Strategies for prevention of neonatal chronic lung disease.

Chronic lung disease (CLD) of prematurity remains a substantial problem despite modern perinatal and neonatal care. CLD remains related to gestational age and lung immaturity, although it has become clear that severe initial lung disease is not a prerequisite for CLD to develop. Attempts to prevent CLD to date have not adequately addressed the multifactorial nature of the complex pathophysiology that leads to CLD. Thus, results have been modest at best. Prevention of CLD will require a multifaceted approach with specific interventions and care practices focused on different aspects of the pathway that leads to CLD. This review considers new information related to causation of CLD and the magnitude of the effect of prevention strategies tested to date. This article also advances the hypothesis that CLD is preventable with a global strategy of minimizing inciting events, optimizing management, and specific therapies aimed at intrinsic vulnerabilities.

Anti-Inflammatory Agents↗
PubMed1992

Terbutaline does not improve lung function in preterm rabbits.

OBJECTIVE: We used the premature rabbit model of surfactant deficiency to test the hypothesis that perinatal administration of terbutaline would lead to increased secretion of surfactant into the alveolar space and increase lung compliance during mechanical ventilation. STUDY DESIGN: Fetuses underwent delivery at a gestational age of 28 days (term 31 days) followed by mechanical ventilation. Fetuses were subdivided into four treatment protocols: control, fetuses given terbutaline at birth, fetuses of mothers given terbutaline 1 hour before delivery, and fetuses of mothers given terbutaline intramuscularly 12 hours before delivery. Dynamic compliance was determined. After this, alveolar lavage fluid was obtained for phosphatidylcholine content determination. Some fetuses were killed at birth and their alveolar lavage phosphatidylcholine was determined. RESULTS: Among the fetuses undergoing mechanical ventilation, perinatal terbutaline exposure did not alter either dynamic compliance or alveolar lavage phosphatidylcholine. Mechanical ventilation was associated with large increases in alveolar lavage phosphatidylcholine content. CONCLUSION: Perinatal beta-adrenergic agonist exposure does not alter in vivo lung function following preterm delivery.

Animals↗
PubMed1989

Bronchopulmonary dysplasia: a review for the pediatrician.

In this review we have attempted to introduce bronchopulmonary dysplasia as a new chronic lung disease of infancy and childhood. The major risk factors for this illness are preterm birth and the respiratory distress syndrome. The precise etiology of BPD is not understood but trauma from mechanical ventilation and toxicity from exposure to supplemental oxygen are thought to be important. Problems in diagnosis and diagnostic criteria have been discussed as have the details of the unfavorable pulmonary mechanics. We have mentioned some of our own practices in regard to a large and successful home oxygen therapy program. Suggestions have been made for establishing readiness for discharge and for follow-up of these children. Medical management of these patients presently suffers from a lack of prospective and controlled studies. Medical care draws heavily from experience with pediatric asthma. What is known about the long-term outcome of these children has been reviewed with an attempt to highlight controversies between published reports and underscore the need for further investigation. The greatest future success in this area would be the prevention of premature birth. Prior to this, we must await the completion of future controlled and prospective studies.

Aftercare↗
PubMed1989

Surface tension and pulmonary compliance in premature rabbits.

In vitro surface properties of pulmonary surfactant thought to be essential to its ability to increase pulmonary compliance include minimum surface tension less than 10 dyn/cm and large surface tension variability and hysteresis. We tested four surface-active agents (Tween 20, a detergent; and FC-100, FC-430, and FC-431, industrial fluorocarbons), all lacking these properties, for their ability to increase pulmonary compliance in surfactant-deficient premature rabbits. Fetal rabbits were delivered by cesarean section at 27 days (full term = 31 days) and injected via tracheostomy with 50% lactated Ringer solution, adult rabbit surfactant, or one of the four experimental agents. Dynamic compliance was measured using 1 h of mechanical ventilation followed by alveolar lavage. Each experimental agent produced a dynamic compliance significantly higher than 50% lactated Ringer solution and statistically equal to or greater than natural surfactant. Equilibrium surface tension of the agents and minimum and equilibrium surface tension of the alveolar washes each correlated with compliance (P less than 0.05). This suggests that some surface properties of pulmonary surfactant believed to be essential are not, although surface tension does seem to play a role in pulmonary compliance.

Animals↗
PubMed1988

Reutilization of surfactant phosphatidylglycerol and lysophosphatidylcholine by adult rabbits.

Adult rabbits reutilize the phosphatidylcholine (PC) of surfactant much less efficiently than developing rabbits (22% vs. 95%). Comparisons of reutilization efficiency of other components of surfactant in adult rabbits have not been determined. We injected adult rabbits intratracheally with [3H]dipalmitoylphosphatidylcholine (DPPG) mixed with [14C]lysophosphatidylcholine (lysoPC) and natural surfactant or [14C]DPPC mixed with [3H]dipalmitoylphosphatidylglycerol (DPPG) and natural surfactant. Recovery in the alveolar wash and lamellar bodies of labelled DPPC, lysoPC and DPPG was determined at different times after injection. By plotting the ratio of [3H]DPPG to [14C]DPPC in the alveolar wash versus time after injection we found that phosphatidylglycerol was reutilized with an efficiency of only 0-7% which was much less than the reutilization of PC in these animals. At early times after injection, adult rabbits injected with [14C]lysoPC had a ratio of [14C]PC in their alveolar wash to lamellar bodies that was larger than 1.0. By comparison, 3-day old rabbits injected intratracheally with [14C]lysoPC had a ratio of [14C]PC in alveolar wash to lamellar bodies less than 1.0 at the earliest times measurable. Thus adult rabbits demonstrate a pathway for accumulation of PC in their alveolar space prior to its appearance in lamellar bodies. This was not detected in developing rabbits. As in developing rabbits, adult rabbits reutilize the phosphatidylglycerol of surfactant less efficiently than the PC of surfactant.

Aging↗
PubMed1987

Betamethasone increases pulmonary compliance in part by surfactant-independent mechanisms in preterm rabbits.

Antenatal exposure to corticosteroids is known to increase the pulmonary compliance of preterm animals. We wished to determine whether this was due solely to alteration in lung surfactant content. Rabbit does were injected with either vehicle alone or betamethasone on days 25 and 26 of gestation. Fetuses were delivered at 27 days and given either 50% lactated Ringer's or intratracheal natural surfactant prior to their first breath. Fetuses were mechanically ventilated at a tidal volume of 12 ml/kg for 60 min with periodic compliance measurements. Following ventilation an alveolar lavage was collected for phosphatidylcholine determination. Some fetuses did not undergo ventilation but had saline compliance studies instead. Fetuses given intratracheal surfactant had a higher dynamic compliance than fetuses exposed to antenatal corticosteroids (0.55 +/- 0.01 versus 0.48 +/- 0.02 ml/cm H2O/kg, respectively). Fetuses exposed to antenatal corticosteroids and given intratracheal surfactant had a dynamic compliance (0.66 +/- 0.02) that was greater than those exposed to either single therapy. This was found despite an alveolar surfactant content equal to that in fetuses receiving intratracheal surfactant alone. Saline compliance at birth was significantly greater for fetuses exposed antenatally to steroids. These data imply the existence of a nonsurfactant mechanism by which antenatal corticosteroids increase fetal pulmonary compliance.

Animals↗
PubMedDate not supplied

Corticosteroids and intratracheal surfactant both alter the distribution between the airways and lung tissue of intratracheally administered radiolabeled phosphatidylcholine in the preterm rabbit.

Developmental differences exist regarding quantitative aspects of surfactant phosphatidylcholine clearance from the alveolar space and its subsequent reutilization. We wished to further extend observations of this nature to prematurely delivered rabbits undergoing mechanical ventilation. In addition we tested the hypothesis that prenatal corticosteroid exposure and/or intratracheal surfactant at birth would produce alterations in the lung's clearance of phosphatidylcholine from the airways. Pregnant does were injected with either Ringer's lactate or betamethasone on days 25 and 26 of gestation. Fetuses were delivered at 27 days and given by intratracheal injection either surfactant or one-half strength Ringer's lactate, both of which were trace labeled with [3H]phosphatidylcholine. Fetuses then underwent mechanical ventilation for periods of time ranging from 10 to 120 min. Following ventilation, alveolar lavage and lung tissue were examined to determine the distribution of [3H]phosphatidylcholine between these two compartments. Antenatal corticosteroid exposure was associated with decreased recovery of the radiolabel from the alveolar space and increased recovery of the label from the lung tissue in comparison to control fetuses. Intratracheal surfactant was associated with persistence of the radiolabel within the alveolar space. Therapy with both of these modalities produced a radiolabel distribution that resembled that seen in fetuses receiving intratracheal surfactant alone.

Adrenal Cortex Hormones↗