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Biomedical subjects

G Enhorning

Publications and source records attributed to G Enhorning.

At least 55 records · Page 3Linked to original sources
PubMed1986

Pulmonary surfactant films affected by solvent vapors.

Pulmonary surfactant obtained from rabbit lung lavage was evaluated with the pulsating bubble surfactometer. Because surfactant forms a monomolecular film at the air-liquid interface consisting mainly of phospholipids, solvent vapors, which might be inhaled, could have a destructive influence on the surfactant monolayer. To assess the risk of such an inhalation, vapors from five solvents--halothane, chloroform, enflurane, acetone, and diethyl ether--were made to flow into the bubble of the surfactometer as it pulsated for 30 sec, i.e., during 10 pulsations. The vapors from halothane and chloroform, excellent solvents of dipalmitoyl-phosphatidylcholine (DPPC), had a destabilizing effect evidenced by the fact that surface tension at minimal bubble size increased from 0 to as high as 20 mN/m. When the vapors were replaced with a flow of room air, the pressure tracing promptly returned to normal. The concentration of halothane vapor, however, had to be at least 20%, a concentration much higher than that used for anesthesia, to have a destabilizing effect on pulmonary surfactant. Twenty-five percent enflurane vapor had a less pronounced yet conspicuous impact. With 25% acetone and diethyl ether vapors, poor solvents of DPPC, surface tension at minimal bubble size remained unaffected. We conclude that vapors of halothane and chloroform, if inhaled in high concentration, might instantaneously obliterate the stabilizing effect of pulmonary surfactant but that anesthetic concentrations of halothane have no effect.

Acetone↗
PubMed1985

Glucocorticoids and beta-adrenergic-receptor agonists: their combined effect on fetal rabbit lung surfactant.

In a previous study on pregnant rabbits (Am J Obstet Gynecol 1983; 147:437) we found that a prolonged infusion of the beta 2-adrenergic-receptor agonist terbutaline would first cause a release of fetal pulmonary surfactant, so that more was available in the airways. However, the airway fluid then contained less surfactant, indicating a depletion of stores. Since terbutaline is often used in high doses as a tocolytic agent, surfactant depletion could be a serious side effect. With further studies on rabbits, we wanted to test the hypothesis that with an accelerated surfactant synthesis, achieved with glucocorticoids, the increased release, evoked with the terbutaline, would never cause a depletion of the surfactant stores. Our results supported this hypothesis. Betamethasone, administered to the pregnant doe on the twenty-sixth and twenty-seventh days of gestation, 0.1 mg/kg, increased compliance of the fetal lungs, and more phospholipid phosphorus could be lavaged from the airways. These effects were further increased when, following steroid administration, the doe was infused with terbutaline. Depletion of the surfactant stores was never seen when betamethasone was given prior to the beta-adrenergic-receptor agonist.

Animals↗
PubMed1985

Composition and surface activity of normal and phosphatidylglycerol-deficient lung surfactant.

The possibility that pulmonary surfactant, characterized by a phosphatidylglycerol deficiency, as in early fetal life, might have inferior surface properties was evaluated. We obtained this specific surfactant from adult rabbits by withholding glucose and giving them an excess of myoinositol by mouth and intravenously. Controls were given a similar quantity of glucose. The myoinositol resulted in a drastic reduction of surfactant phosphatidylglycerol, from 7.2 to 0.3% of phospholipids, and a corresponding increase in phosphatidylinositol from 4.8 to 11.3%. In addition, the myoinositol treatment increased the myoinositol that was disaturated from 18.5 to 27.3% (p less than 0.05). The corresponding figures for disaturated phosphatidyl-choline were 56.0 and 60.5%, respectively (NS). The myoinositol treatment for 4 days increased the pool size of alveolar surfactant by 32% (p less than 0.01). The surface activity was studied with modified Wilhelmy balance and the pulsating bubble surfactometer. Surfactant containing phosphatidylinositol rather than phosphatidylglycerol was not inferior, as compared to surfactant that contained phosphatidylglycerol (minimum surface tension: 2.0 versus 2.2 mN X m-1; collapse rate at 10 nM X m-1: 1.85 versus 1.95 min-1; rate of adsorption from subphase to surface: 32 versus 35 mN X m-1 X 30 s-1), nor was there a difference in the ability of the two surfactants to improve lung stability of 27-day-old rabbit fetuses (air retention at 35 cm H2O: 1.8 versus 1.8 ml/30 g; air retention at 0 cm H20: 0.8 versus 0.9 ml/30 g). We conclude that phosphatidylinositol surfactant does not have inferior surface properties.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Pulmonary surfactant release in fetal rabbits as affected by enprofylline.

At a gestational age of 27.9 days, pregnant rabbits were infused with enprofylline, a new xanthine with potent antiasthmatic effects. Following a priming dose of 5 mg/kg, 20 mg/kg were infused over a 2-h period. Controls received Ringer's solution. On completion of the infusion, the fetuses were delivered and the effect on their surfactant system was evaluated. Surface tension in airway fluid, measured with the pulsating bubble surfactometer, at minimal bubble size in the third cycle, was 21.8 +/- 2.2 (mean +/- SE) versus 28.7 +/- 1.7 mN m-1 (p less than 0.01). Pressure-volume loops of the lungs of the fetuses showed that at a deflation pressure 10 cm H2O the volume was 64 +/- 3 versus 49 +/- 3% (p less than 0.0005). The lung lavage fluid had a phospholipid phosphorus content of 41.9 +/- 3.8 versus 18.5 +/- 1.3 micrograms/g dry lung (p less than 0.0005). The values indicate that enprofylline caused a release of surfactant into the fetal airways.

Animals↗
PubMed1985

Prevention of neonatal respiratory distress syndrome by tracheal instillation of surfactant: a randomized clinical trial.

With a randomized clinical trial, the possibility was assessed that a tracheal instillation of pulmonary surfactant prior to the first breath might prevent the development of some of the signs of neonatal respiratory distress syndrome. Of the 72 infants in the trial, all born at a gestational age of less than 30 weeks, 39 received 3 or 4 mL of surfactant, prepared from the lipids extracted from calf lung lavage. The treatment resulted in a significantly improved gas exchange during the first 72 hours of life. On the average, the arterial/alveolar PO2 ratio was 0.15 higher for the treated infants, and only about half as much extra oxygen had to be supplied. The respiratory support (peak inspiratory pressure X frequency) could be lowered significantly. Pulmonary interstitial emphysema occurred in 13 of the 33 control infants, but in only three of the 39 treated infants. Six of the control infants died in the neonatal period, but only one treated infant died. It is concluded that surfactant supplementation prior to the first breath is feasible and is of value as protection against the respiratory distress syndrome and the negative effects of hypoxia and ventilatory support.

Clinical Trials as Topic↗
PubMed1984

Pre-eclampsia: a hypothesis for its pathogenesis.

A hypothesis is presented according to which the pathogenesis of pregnancy-induced hypertension can be attributed to disturbances in renal function caused by the upright posture of the human. In pregnancy, glomerular filtration rate (GFR) and tubular reabsorption, the latter stimulated by aldosterone, are working in high gear. A diminished GFR with continued stimulation of tubular reabsorption would lead to sodium retention. That situation could result, particularly in the primigravida, from the enlarged uterus of late pregnancy exerting pressure on and interfering with venous return, arterial blood flow to kidneys, and/or ability of ureters to transport urine and maintain low pressure in the kidney pelvis. At an early stage, pre-eclampsia can be controlled by bed rest, quite likely by removing dangerous uterine compression. Animal studies are required to test the hypothesis.

Aldosterone↗
PubMed1983

Pulmonary surfactant release in fetal rabbits: immediate and delayed response to terbutaline.

The fetal lung responds to beta-receptor agonists with a release of surfactant from type II alveolar cells, if such stimulation were intense or long-lasting, the supply might become depleted and, while the supply is being restored, there could be a surfactant deficiency. With experiments on pregnant rabbits, this hypothesis was put to the test and found to be true. At a gestational age of 27.75 days, fetuses received the beta 2-receptor agonist terbutaline, 0.1 or 0.01 mg intramuscularly, or saline only. At the same stage of pregnancy, other does were infused with 7.2 to 9.6 mg of terbutaline or given Ringer's solution. The fetuses were put to death at intervals of 1 to 48 hours, and the lungs were examined. At 1 hour and also at 2 and 3 hours after injection of 0.1 mg of terbutaline, pressure-volume loops demonstrated improved compliance and stability compared to those of controls, but at 24 hours the situation was reversed. At 48 hours there was no difference. At 12 hours from the start of the infusion, pressure-volume loops clearly showed that fetuses of does receiving terbutaline were at a disadvantage. We conclude that terbutaline depleted surfactant stores and, while these stores are being replenished, there is a surfactant deficiency in the alveolar space. Phospholipid analysis supported our conclusion.

Animals↗
PubMed1983

Tricolor photography for assessment of spermatozoa motility.

A rapid and accurate technique for assessment of spermatozoa motility has been developed. With the use of tricolor photography with sequential exposures in green, red, and blue light, spermatozoa were photographed in Makler chambers with a depth of 10 mu. Exposure in green light had a 1-second duration and was immediately followed by the red light from an electronic flash, and 0.05 second later by the blue light from a second flash. With this system, spermatozoa with motility would leave a green track, at the end of which they would appear first red and then blue. The colors and their intensity were chosen so that, when superimposed on nonmotile spermatozoa, the latter would appear white. By projection of the transparent film onto white paper, spermatozoa, motile and nonmotile, were easily counted and the percentage and motility was determined. Also, concentration could be calculated because the photograph represented a semen volume of 0.001 mu. Measurement of the green track and conversion to true length in micrometers gave the velocity in micrometers per second.

Color↗
PubMed1983

Hyaline membrane disease treated with bovine surfactant.

Six preterm infants with severe hyaline membrane disease requiring ventilation were treated, at a median age of 15.5 hours, with a single intratracheal bolus of a bovine surfactant suspension. Arterial oxygenation increased dramatically, and chest radiograms showed improvement after two to four hours. However, a variable degree of deterioration occurred within 24 hours. All of the infants required oxygen therapy for several weeks, and one developed severe bronchopulmonary dysplasia.

Animals↗
PubMed1982

Lung expansion and survival in rabbit neonates treated with surfactant extract.

Preterm rabbit fetuses, delivered on the 27th day of gestation, were studied following upper airway instillation with either natural surfactant (NSA) obtained from the lavage of adult rabbit lungs or with a protein-free suspension of lipids extracted from lung wash (ESA). First, lung compliance was studied postmortem. The administration of 25 microliters of either preparation resulted in greater hysteresis (P less than 0.05) than was observed in control fetuses receiving no surfactant material. Increasing the phospholipid concentration stepwise from 10 to 50 mg/ml improved airway expansion and stability. No further improvement was encountered with concentrations greater than 50 mg/ml. There was no significant difference in compliance response between NSA and ESA. Morphometry of the lungs also indicated that the two preparations had an equal effect on compliance. Second, it was determined how neonatal survival was affected by a pharyngeal deposition, prior to the first breath, of 50 microliters NSA or ESA. Both treatment groups demonstrated improved survival (P less than 0.001) when compared with controls receiving no pharyngeal deposition. These findings offer further support to the concept that protein is not required for the efficacy of a surfactant supplementation. The equivalence of the two preparations suggests that a sterile suspension of a protein-free surfactant extract could be used to prevent or treat respiratory distress in preterm neonates.

Animals↗
PubMed1982

Surfactant supplementation in the preterm rabbit: effects of applied volume on compliance and survival.

Preterm rabbit neonates, delivered on the 27th day of gestation, were treated before the first breath with a tracheal instillation of ESA, a suspension of lipids extracted from pulmonary surfactant. Lung compliance development and neonatal survival were studied after treatment to determine the effect of suspension volume and concentration. Compliance development was not dependent on either delivery volume or suspension concentration, but rather on the quantity of phospholipids instilled. Indices of improved expansion and stability demonstrated a dose response relationship up to 1.1 mg phospholipid per g lung. Larger doses neither improved nor detracted from the response. The ability of the neonates to survive and adapt to an air breathing environment was influenced by the instillation volume. Viability was reduced when the treatment volume exceeded 16% of the functional residual capacity. Prophylactic surfactant supplementation therapy may be useful in preventing the development of neonatal respiratory distress syndrome. Surfactant extract may prove acceptable for both prophylaxis and treatment of established respiratory distress syndrome.

Animals↗
PubMed1980

Results of a double-blind controlled study on the use of betamethasone in the prevention of respiratory distress syndrome.

A double-blind controlled study on the prenatal use of betamethasone in the prevention of respiratory distress syndrome (RDS) was carried out on 137 patients from 24 to 34 weeks' gestation. The incidence of RDS was less in the treated group (5%) than in control group (17%). The neonatal mortality rate was lower in the treated group (5%) than in the control group (18%) due to an excess of neonatal deaths in the placebo group.

Betamethasone↗
PubMed1979

Isoxsuprine infusion to the pregnant rabbit and its effect on fetal lung surfactant.

Rabbit does, pregnant on the 28th day, were infused with isoxsuprine 2.5 mg/kg body weight/h in 50 ml 5% glucose, or with glucose only. The isoxsuprine caused maternal heart rate to increase and blood pressure, mean and diastolic, to decrease. The volume of fetal pulmonary fluid (FPF) and the wet lung weight/body weight ratio were significantly lowered by isoxsuprine. Lecithin/sphingomyelin ratio of FPF in isoxsuprine-infused animals was higher, compared with controls, not infused. Minimal surface tension of FPF, evaluated with pulsating bubble, was significantly lower in treated fetuses. Histologic examination of the fetal lungs after fixation with potassium dichromate and mercuric chloride showed that in isoxsuprine-treated litters FPF contained more granular and sudanophilic material. The results offer further evidence that isoxsuprine causes dehydration of fetal lungs and a release of pulmonary surfactant.

Animals↗
PubMed1978

Improved ventilation of prematurely delivered primates following tracheal deposition of surfactant.

Twelve rhesus monkeys were delivered prematurely at 129, 130, or 131 days. The first breath was inhibited while tracheotomy was performed and a catheter introduced into the umbilical artery. Into the tracheal tubes of six of the newborn monkeys was instilled 0.20 to 0.27 ml. of a natural surfactant (SA) suspension, obtained from lung wash of adult rabbits. Nothing was given to six control monkeys. Breathing was then supported with a ventilator. Although its settings were adjusted in attempts to maintain normal blood gases, the control monkeys developed severe hypercapnia and acidosis, and two died after 4 1/2 and 5 1/2 hours. The remaining four control monkeys and the six treated monkeys were killed after six hours. Pulmonary pressure-volume characteristics were conspicuously better following SA treatment. It was concluded that instillation of SA in the upper airways of premature primates prior to their first breath holds promise as an effective way of preventing respiratory distress.

Animals↗
PubMed1977

Isoxsuprine-induced release of pulmonary surfactant in the rabbit fetus.

Rabbit fetuses were injected intramuscularly with 0.5 mg. of isoxsuprine on the twenty-eighth day of gestation. They were killed in utero four hours after the injection, and fetal pulmonary fluid (FPF) was collected through a tracheal catheter. The quantity of FPF and the lung weight/body weight ratio were both significantly less in the isoxsuprine-treated fetuses than in control fetuses. Surface activity, evaluated with pulsating bubble, and the lecithin/sphingomyelin (L/S) ratio were greater in FPF from isoxsuprine-treated animals than in control samples. We concluded that isoxsuprine is able to dehydrate the fetal lung and cause a release of surfactant stored in type II pneumocytes. This latter conclusion was supported by a significant decrease in the number of lamellar inclusions observed in these cells.

Amniotic Fluid↗