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Biomedical subjects

J R Hageman

Publications and source records attributed to J R Hageman.

At least 37 records · Page 2Linked to original sources
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

Perinatal management of meconium staining of the amniotic fluid.

The pathogenesis of meconium passage and the pathophysiology of meconium aspiration are reviewed. Intrapartum and neonatal strategies for the prevention of meconium aspiration syndrome are presented in historical perspective, and newer interventions are appraised.

Amniotic Fluid↗
PubMed1988

Outcome of persistent pulmonary hypertension in relation to severity of presentation.

Since the initial description of persistent pulmonary hypertension of the newborn (PPHN), the management of these infants has been controversial. A variety of therapeutic modalities, such as extracorporeal membrane oxygenation, have been utilized. Early recognition of a group of patients with PPHN who might require aggressive therapy would be clinically useful. Highest alveolar-arterial oxygen gradient at or near diagnosis was evaluated retrospectively in 53 patients with PPHN in relation to survival, aggressiveness of management, and frequency of pulmonary complications (air leak and broncho-pulmonary dysplasia). Highest alveolar-arterial oxygen gradient was a good early predictor of nonsurvival and was significantly higher in nonsurvivors compared with survivors (mean [+/- SD], 618 +/- 23 mm Hg vs 521 +/- 128 mm Hg). Values of 600 mm Hg or greater were more frequent in the nonsurvivors compared with the survivors (92% vs 37%). Air leak also proved to be a good predictor of nonsurvival.

Humans↗
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

Monitoring of critically ill infants and children.

The strategies for monitoring infants and children in the intensive care setting differ from the strategies used to monitor adults. This article highlights the physiologic differences between infants and children and adults that affect these methods. The technical aspects of monitoring infants and children are also discussed.

Adolescent↗
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↗
PubMed1988

Delivery room management of meconium staining of the amniotic fluid and the development of meconium aspiration syndrome.

A 1-year prospective survey of obstetric and pediatric management of meconium staining of the amniotic fluid in 464 patients was undertaken. Pharyngeal suctioning before delivery was performed using bulb syringe (N = 130), De Lee suction catheter (N = 186), or both (N = 98); endotracheal intubation after delivery was also done in 413 instances. Using any of the three suctioning techniques, no differences were seen in Apgar scores, respiratory rates, presence or absence of meconium on or below the vocal cords, or development of meconium aspiration syndrome (MAS). If meconium was present on the vocal cords, it was present below the vocal cords in 76% of the cases. If no meconium was visualized, it was found below the vocal cords in only 7% of the cases. Of the 142 infants with meconium below the vocal cords, 10% developed MAS and all 14 survived.

Amniotic Fluid↗
PubMed1986

The early involvement of pulmonary prostaglandins in hyperoxic lung injury.

To further study the role of arachidonic acid metabolites in the development of hyperoxic lung injury and the function of PMNs and/or alveolar macrophages in facilitating this role, we exposed adult rabbits to greater than 95% O2 or air for 24, 40, 48, or 65 hours. At the end of each study, bronchoalveolar lavage [BAL] of the left lung was performed, and the right lung was inflated and fixed for light and electron microscopy. PGE2, 6-keto-PGF1 alpha and thromboxane B2 were measured by RIA in arterial and venous plasma at the beginning and end of each study and in BAL fluid obtained at sacrifice. Production of these three PGs by BAL cells placed in cell culture was also measured. Significant hyperoxic lung injury did not develop until 65 hours, as evidenced by significant increase in BAL total protein and percent PMNs, and by morphologic findings. At 40 hours, however, BAL fluid PGE2 and 6-keto-PGF1 alpha increased and BAL cell production of all 3 PGs was significantly increased (p less than .05). In summary, the early PG increases observed in these studies may directly contribute to the development of hyperoxic lung injury or, rather, may be representative of a generalized increase in all arachidonic acid metabolites, including the lipoxygenase pathway. The increase in BAL cell PG production and increased PG concentrations in BAL fluid prior to any increase in BAL PMNs suggest that the AM may be the source of the early arachidonic acid metabolite increase in response to hyperoxia.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Fat emulsions and lung function.

IVFE infusion can impair lung function in healthy adults, premature infants, and adults with pre-existing lung injury, and in experimental animals with acute injury. Although all observed IVFE-related lung dysfunction was initially attributed to the temporally associated hyperlipemia, this explanation may in fact be correct only with fat overload syndrome. When serum triglyceride levels are in a more appropriate range, all subsequent studies have shown the same alterations in lung function unrelated to triglyceride increases and indomethacin-related blocking of lung function impairment, despite comparable serum triglyceride increases. Furthermore, our studies with Liposyn demonstrated the most significant increases in serum triglyceride levels, but the smallest PaCO2 and PaO2 changes. In general, the lung function abnormalities associated with IVFE infusion have thus been caused by increases in VA/Q inequalities. Although elucidation of the relationship between IVFE-related increased PG production and secondary VA/Q changes may be of significant physiologic import, the PaO2 and PaCO2 changes even with pre-existing lung injury have generally not been of sufficient magnitude to be of much clinical significance. The IVFE-related increases in plasma PG concentrations may, however, still have significant nonpulmonary clinical effects related to known or postulated consequences of increased plasma PG concentrations, including effects on ductus arteriosus patency, retinal and cerebral blood flow, and immune competence.

Adult↗
PubMed1985

Epiglottitis: a recurrent episode in a youth.

Epiglottitis should be suspected in the adolescent with throat pain and dysphagia out of proportion to pharyngeal inflammation. Endolateral neck radiographs or indirect laryngoscopy will confirm the diagnosis. Blood and throat or epiglottic cultures always should be obtained. Therapy consists of airway stabilization and antibiotic administration. Although epiglottitis in adolescents is often less acute and less severe than in younger children, it may be life-threatening.

Adult↗
PubMed1985

Pulmonary complications of hyperventilation therapy for persistent pulmonary hypertension.

Hyperventilation has become a primary therapeutic modality in the management of neonates with persistent pulmonary hypertension (PPH). Of 51 PPH infants undergoing hyperventilation therapy, 45% developed pneumothorax. The subgroup which developed pneumothorax was exposed to assisted ventilation for significantly longer time periods and at higher peak inspiratory pressures. They were also exposed to longer periods of oxygen therapy at higher oxygen concentrations. Survival in the pneumothorax group was significantly lower. The incidence of bronchopulmonary dysplasia (BPD) in the 35 survivors was only 6%. These data indicate that the use of hyperventilation to treat PPH is associated with a significant incidence of pneumothorax but a low incidence of BPD.

Bronchopulmonary Dysplasia↗
PubMed1984

Persistent pulmonary hypertension of the newborn. Trends in incidence, diagnosis, and management.

Persistent pulmonary hypertension of the newborn ( PPHN ) has become a more commonly recognized problem in neonatal intensive care nurseries. In 62 neonates, 27 from 1980 and 35 from 1981, we compared classification, methods of diagnosis, modes of therapy, and survival. Thirty neonates (48%) had primary and 32 (52%) had secondary PPHN . Overall survival was 71% with significant differences in primary v secondary PPHN . Survival was also higher in 1981 than 1980 and was related to earlier diagnosis and to the more rapid initiation of therapy.

Humans↗
PubMed1983

Intralipid alterations in pulmonary prostaglandin metabolism and gas exchange.

To assess the role of Intralipid as a prostaglandin (PG) precursor, we infused Intralipid into 40 rabbits with long-term arterial and venous catheters; 24 other rabbits received a control saline infusion. One-half of the rabbits in both experimental and control groups had oleic acid-damaged lungs, and at least 5 in each of the 4 groups (Intralipid/saline in normal/damaged lungs) received indomethacin. Two vasodilating PGs (E2 and 6KF1 alpha) and one vasoconstricting PG (F2 alpha) were measured. Triglyceride levels increased significantly in all Intralipid groups, averaging 580 mg/dl. Intralipid-related alterations in PG levels and arterial oxygen tension (PaO2) were significant only in the lung-damaged group. The mean (+/- sem) decrease in PaO2 was 12 +/- 1.5 torr (p less than .001). For both vasodilating PGs, Intralipid infusion increased the pulmonary arteriovenous gradients for PG E2 and PG 6KF1 alpha by 960 pg/ml (p less than .05) and 697 pg/ml (p less than .10), respectively. Both the PaO2 decrease and the vasodilating PG increases were blocked by indomethacin. In summary, Intralipid infusion in lung-damaged rabbits increased pulmonary production of vasodilating PGs and associated hypoxemia, presumably caused by an unblocking of hypoxic vasoconstriction and resultant increase in intrapulmonary right-to-left shunt.

Animals↗
PubMedDate not supplied

Liposyn infusion increases plasma prostaglandin concentrations.

To determine whether Liposyn infusion results in increased plasma prostaglandin (PG) concentrations, the following study was performed in 33 adult rabbits with chronically implanted arterial and venous catheters. Plasma PG concentrations were determined by radioimmunoassay for two vasodilators, PGE2 and PGI2 (as measured by its metabolite 6-keto-PGF1 alpha), and two vasoconstrictors, thromboxane (TX) A2 and PGF2 alpha, as measured by their metabolites TXB2 and PGF2 alpha-M, respectively. A 1-hour infusion of Liposyn at 4 ml per kg resulted in statistically significant increases in arterial and venous concentrations of PGE2 and 6-keto-PGF1 alpha (p less than 0.001) and of TXB2 (p less than 0.04). There were no significant changes in PGF2 alpha-M plasma concentrations. Liposyn infusion also resulted in a small but statistically significant increase in PaO2 of 4.7 +/- 1.5 torr (p less than 0.01). It is concluded that Liposyn infusion results in statistically significant increases in plasma concentrations of PGE2, 6-keto-PGF1 alpha, and TXB2.

6-Ketoprostaglandin F1 alpha↗