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B Robertson

Publications and source records attributed to B Robertson.

At least 235 records · Page 13Linked to original sources
PubMed1990

[Effect of natural porcine surfactant (Curosurf) on the function of neutrophilic granulocytes].

In this study we have analyzed various phagocytic functions of human neutrophils exposed to either biochemically well defined porcine surfactant (Curosurf) or a phospholipid preparation. Adherence, random migration and chemotactic response to zymosan activated serum and formyl-methionyl-leucyl-phenylalanine were normal in surfactant treated neutrophils; surfactant was not a chemotactic stimulus. In contrast, phagocytosis of S. aureus by neutrophils exposed to surfactant (100 micrograms/ml) or phospholipids (100 micrograms/ml) was impaired (surfactant: t30 49.5 +/- 9.0%, t60 65.0 +/- 8.0%; phospholipids: t30 66.3 +/- 12.6%, t60 78.0 +/- 7.8%; controls: t30 78.1 +/- 8.9%, t60 90.1 +/- 6.2%; p less than 0.001 at t30, t60 for surfactant, p less than 0.05 at t60 for phospholipids). Due to the smaller number of S. aureus ingested, bactericidal activity of surfactant or phospholipid treated neutrophils was slightly reduced when compared to controls (surfactant t30 p less than 0.05, surfactant t60 p less than 0.001, phospholipids t60 p less than 0.05). Surfactant or phospholipids had no bactericidal activity. Uptake of candida was identical in surfactant or phospholipid treated neutrophils with untreated controls; the same was true with the number of candida per cell ingested. Phagocytosis-associated chemiluminescence and production of superoxide anion by neutrophils of either source in response to phorbol myristate acetate and opsonized zymosan was also identical.

Adult↗
PubMed1990

[Treatment of severe hyaline membrane disease with a single-dose of natural exogenous surfactant of porcine origin. A randomized trial: immediate effects and outcome at 28 days of life].

The results obtained with porcine surfactant (Curosurf) administration for the treatment of hyaline membrane disease (HMD) are reported. Thirty premature infants weighing 700 to 2,000 g with severe HMD (mechanical ventilation and oxygen requirement (FiO2) greater than 60% were randomly allocated at 2 to 15 hours postnatal age. Eight of the 30 patients included in this group participated in a multicenter european trial. The fifteen infants with mean gestational age (GA) of 29.5 weeks included in the treatment group (T), were treated at 8.6 hours of life with a single dose of 200 mg/kg Curosurf given intratracheally while 15 infants of mean GA 30 weeks formed the control group (C). Infants in the T group showed an immediate, dramatic and sustained improvement of oxygenation as reflected by increased PaO2/FiO2 and arterial to alveolar PO2 ratios within 1 hour. This significant improvement in favor of T group (p less than 0.005) persisted for 2 days when control infants began to recover. This improvement in oxygenation allowed a significant decrease of FiO2 (p less than 0.005) and mean airway pressure (p less than 0.01) in the T group within 1 hour and up till the second day. Despite this early improvement obtained with Curosurf the survival rate at 28 days of life and the incidence of associated HMD complications were not significantly modified. However the tendency was towards decreased respiratory morbidity. The discussion will consider the value of multiple doses.

Animals↗
PubMed1989

Immunocytochemical evidence for the localization of the GM1 ganglioside in carbonic anhydrase-containing and RT 97-immunoreactive rat primary sensory neurons.

Localization of GM1 ganglioside, the receptor for cholera toxin, and choleragenoid, which is the binding subunit of cholera toxin, was studied in the rat L5 dorsal root ganglion. Sections were incubated with choleragenoid and treated immunocytochemically. Choleragenoid-like immunoreactive cells were then examined for possible co-localization with carbonic anhydrase-like, RT 97 (antibody to neurofilament proteins), substance P-like, somatostatin-like and calcitonin gene-related peptide-like immunoreactivity and fluoride-resistant acid phosphatase (FRAP) activity, using adjacent sections. A subpopulation of dorsal root ganglion neurons exhibited choleragenoid-like immunoreactivity. The majority of these were medium-sized and large neurons. The strongest immunoreactivity was found in the area of the plasma membrane, but strong reactivity was also seen in the cytoplasm. The majority of the choleragenoid-like immunoreactive cells showed carbonic anhydrase-like and RT 97 immunoreactivity. Cells showing co-localization of choleragenoid-like and neuropeptide-like immunoreactivity or activity for FRAP were rarely observed. Our results suggest that the GM1 receptor is localized primarily on carbonic anhydrase-containing and RT 97-immunoreactive primary sensory neurons.

Animals↗
PubMed1989

Inhibition of exogenous surfactant in ventilated immature newborn rabbits.

Immature newborn rabbits were treated at birth by tracheal instillation of porcine surfactant (100 microliters, phospholipid concentration 80 mg.ml-1), to which [14C]dipalmitoylphosphatidylcholine had been added as a marker. They were kept in a body plethysmograph/pneumotachygraph system at 37 degrees C. During a 120 min period of artificial ventilation with a peak insufflation pressure of 20 cm H2O, there was a gradual decrease in tidal volumes (36%.h-1). This decrease was correlated to an elevation of minimum surface tension (r = 0.81; P less than 0.01) and to a prolongation of the adsorption rate (r = 0.80; P less than 0.01) of surfactant recovered by lung lavage from the same animals. There was also correlations between duration of ventilation and minimum surface tension (r = 0.56; P less than 0.01), and between duration of ventilation and adsorption rate (r = 0.73; P less than 0.01). The surface properties of phospholipids extracted from the lavage fluid were similar to those of the original surfactant preparation. Our data suggest that, in immature newborn rabbits subjected to artificial ventilation, exogenous surfactant may become inactivated, probably due to protein leakage into the airspaces.

Animals↗
PubMed1989

Combined retrograde tracing and enzyme/immunohistochemistry of trigeminal ganglion cell bodies innervating tooth pulps in the rat.

Rat trigeminal neurons innervating tooth pulps were retrogradely labelled with fluorogold and analysed enzyme- and immunohistochemically for their content of substance P, calcitonin gene-related peptide, fluoride-resistant acid phosphatase, GM 1 ganglioside, carbonic anhydrase and neurofilament protein. The data showed that both small, medium-sized and large trigeminal neurons were labelled after fluorogold deposition in maxillary molar pulps, with a majority of the cells being medium-sized and large. Less than 2% of the pulpal neurons showed substance P-like immunoreactivity. Fifty-six per cent of the pulpal nerve cells were calcitonin gene-related peptide-positive. These cells were small, medium-sized and large. Only 1% of the fluorogold-labelled cells contained fluoride-resistant acid phosphatase enzyme activity. This paralleled the finding that the pulpal neurons were unstained by Griffonia simplicifolia isolectin I-B4, a plant lectin which preferentially binds to fluoride-resistant acid phosphatase-positive cells. Choleragenoid-like immunoreactivity, which identifies cells with the GM 1 ganglioside receptor, was found in 70% of the fluorogold-labelled pulpal neurons. Approximately 80% of the fluorogold-labelled cells showed RT 97-immunoreactivity. RT 97 labels neurofilament protein and is present in large light primary sensory neurons. No pulpal neurons appeared to contain carbonic anhydrase, as judged from both enzyme- and immunocytochemical observations. The findings suggest that, in the rat, trigeminal tooth pulp neurons, which according to the classical view are nociceptive, form a heterogeneous group of neurons with a minority of small cells which may contain calcitonin gene-related peptide but rarely either substance P or fluoride-resistant acid phosphatase. However, the vast majority of pulpal nerve cells appear to have sizes and cytochemical characteristics which are not generally associated with nociceptive primary sensory neurons.

Acid Phosphatase↗
PubMed1989

Lung lesions after experimental combined exposure to nickel and trivalent chromium.

Rabbits were exposed to a combination of 0.7 mg/m3 of Ni2+ as NiCl2 and 1.2 mg/m3 of Cr3+ as Cr(NO3)3, to 0.6 mg/m3 of Ni2+ as NiCl2, or to filtered air for 4 months (5 days/week, 6 hr/day). Light microscopy of the lung tissue showed widespread areas with nodular accumulation of macrophages in all rabbits exposed to both metals, in two rabbits exposed to nickel alone, and in none of the controls. Electron microscopy of the lung showed attenuated septa and alveoli stuffed with surfactant-like material in the group exposed to both metals. In two of these rabbits, groups of alveoli were filled with densely packed debris and type I cell borders were obscure. The reaction in the group exposed to nickel alone was less prominent. The volume density of alveolar type II cells showed a fourfold increase after exposure to both metals and a twofold increase following exposure to nickel alone compared to controls. The lung tissue content of total phospholipids and especially phosphatidylcholines and phosphatidylinositols was significantly higher in the groups exposed to both metals than in controls or in animals exposed to nickel only. In lung tissue the molar percentage of 1,2-dipalmitoylphosphatidylcholine was significantly higher in the group exposed to both metals than in the other groups. The results indicate that trivalent chromium potentiates the effect of nickel on the type II cells resulting in an increased surfactant production; in addition, trivalent chromium probably reduces the catabolism of surfactant in alveolar macrophages. Our observations raise the concern that noxious effects might occur also in humans exposed to a combination of nickel and trivalent chromium.

Animals↗
PubMed1989

Experimental obstructive hydronephrosis in newborn rats. XI. A one-year follow-up study of renal function and morphology.

Partial obstruction of the left ureter was created in two-day-old rats and its effects on kidney function were studied with 99mTc-DMSA and 99mTc-DTPA after one, two, three and six weeks, and after one year. Kidneys from animals sacrificed at the age of six weeks or one year were also examined histologically. The obstructed renal pelvis was enlarged by about 35 times and there was a delayed excretion of 99mTc-DTPA during forced diuresis, indicating significant, chronic obstruction. The renal DMSA-uptake ratio (left kidney/(left and right kidney] was reduced to about 40% from the first week of obstruction. The parenchymal weight ratio (expressed as above) was reduced to about 45% after both six weeks and one year. The glomerular filtration rate, examined during forced diuresis and calculated on the basis of uptake capacity, was lowered to 42% after six weeks but was not significantly reduced after one year of obstruction. The incidence figures for medullary hemorrhage or accumulation of iron pigment, and chronic inflammatory changes in the cortex were somewhat higher after one year of obstruction than after 6 weeks, but the lesions were patchy in both groups. We conclude that partial unilateral ureteric obstruction, created in the neonatal period, leads to a slight but permanent functional disturbance and parenchymal weight reduction without prominent structural parenchymal damage.

Animals↗
PubMed1989

Actions of anaesthetics and avermectin on GABAA chloride channels in mammalian dorsal root ganglion neurones.

1. The gamma-aminobutyric acid (GABA)-mimetic actions of some anaesthetics and the antehelminthic avermectin B1a were examined on freshly isolated mammalian dorsal root ganglion (DRG) neurones by use of suction electrodes and a single electrode voltage clamp. 2. Pentobarbitone (60 microM-3 mM), chloralose (600 microM-1 mM), etomidate (10-100 microM), alphaxalone (10-60 microM) and avermectin (10-60 microM) directly activated chloride channels in GABA-sensitive DRG neurones. The agonist action was sensitive to block by bicuculline and picrotoxinin. 3. Steady-state current-voltage (I-V) curves for the anaesthetics were either linear, or rectified in the opposite direction to steady-state I-V curves obtained with GABA. Current relaxations in response to voltage jumps were also of the opposite direction. An extra surge of current ('bounce') was commonly observed on washout of some of these agonists. 4. Pentobarbitone was ineffective as an agonist at alkali pH (10.4 and 9.4), but was approximately twice as effective at acid (5.4) than at normal (7.4) pH values. 5. These results suggest that some anaesthetics and avermectin are capable of 'blocking' GABA channels in addition to activating them.

Anesthetics↗
PubMed1989

Cardiorespiratory collapse and pulmonary oedema due to intravascular absorption of prostaglandin F2 alpha administered extraamniotically for midtrimester termination of pregnancy.

A case of severe reaction to extraamniotically administered prostaglandin F2 alpha, with cardiorespiratory collapse and pulmonary oedema necessitating transfer to an intensive care unit, is presented. Attention is drawn to the profound haemodynamic effects of systemically administered prostaglandin, and the need for caution and ready availability of facilities for resuscitation when this potent substance is administered. Treatment for the effects of intravascular absorption of prostaglandin F2 alpha is discussed.

Abortion, Therapeutic↗
PubMed1989

Characteristics of GABA-activated chloride channels in mammalian dorsal root ganglion neurones.

1. The properties of gamma-aminobutyric acid (GABA)-activated chloride channels in dorsal root ganglion (DRG) neurones obtained from rats and cats were examined using the single-electrode voltage clamp in conjunction with suction-electrode techniques. 2. GABA-evoked currents showed voltage-sensitive kinetics. Time constants (tau D) were measured from voltage-jump relaxations and tau D became briefer with membrane hyperpolarization. tau D was 33 ms at -120 mV with 60 microM-GABA and changed e-fold for 188 mV. tau D decreased as GABA concentration was increased - the extrapolated tau D at 'zero' GABA concentration was approximately equal to 50 ms at -120 mV. 3. The steady-state current in GABA was curvilinear, rectifying at negative potentials. The instantaneous current was linear with symmetrical chloride concentrations (140 mM) on both sides of the cell membrane. 4. Muscimol was a more effective agonist than GABA, while piperidine-4-sulphonic acid and ethylenediamine monocarbamate were only weakly effective agonists. Taurine and glycine had no detectable agonist activity. 5. Ion substitution experiments revealed the permeability sequence I- greater than Br- greater than Cl- greater than F- greater than propionate (1.88 greater than 1.21 greater than 1.0 approximately equal to 0.1 approximately equal to 0.1). 6. The presence of iodide and bromide ions externally caused an increase in chloride efflux at membrane potentials more negative than -40 mV, and caused a prolongation of voltage-jump relaxations. Relaxations in fluoride and propionate solutions were faster than those seen in chloride.

Action Potentials↗
PubMed1989

Interacting proteins identified by genetic interactions: a missense mutation in alpha-tubulin fails to complement alleles of the testis-specific beta-tubulin gene of Drosophila melanogaster.

In this paper we demonstrate that failure to complement between mutations at separate loci can be used to identify genes that encode interacting structural proteins. A mutation (nc33) identified because it failed to complement mutant alleles of the gene encoding the testis-specific beta 2-tubulin of Drosophila melanogaster (B2t) did not map to the B2t locus. We show that this second-site noncomplementing mutation is a missense mutation in alpha-tubulin that results in substitution of methionine in place of valine at amino acid 177. Because alpha- and beta-tubulin form a heterodimer, our results suggest that the genetic interaction, failure to complement, is based on the structural interaction between the protein products of the two genes. Although the nc33 mutation failed to complement a null allele of B2t (B2tn), a deletion of the alpha-tubulin gene to which nc33 mapped complemented B2tn. Thus, the failure to complement appears to require the presence of the altered alpha-tubulin encoded by the nc33 allele, which may act as a structural poison when incorporated into either the tubulin heterodimer or microtubules.

Alleles↗
PubMed1989

Effects of experimental obstructive hydronephrosis on the immature nephrons in newborn rats.

Partial obstruction of the left ureter was created in rats less than 36 h of age and its effects were studied at the age of 2-6 days. A considerable hydronephrosis with distension of the kidney developed within 1 day after obstruction, but there was no parenchymal weight reduction. The thickness of the mature, inner cortical layer was significantly decreased, suggesting a delay in the differentiation of the cortex. The parenchymal weight reduction, previously documented in our laboratory after long-standing ureteric obstruction, may thus be caused by a retardation of renal growth, which is never caught up, rather than by an atrophy of renal parenchyma or other destructive tissue lesions.

Animals↗
PubMed1989

Background to neonatal respiratory distress syndrome and treatment with exogenous surfactant.

The neonatal respiratory distress syndrome (RDS), caused by surfactant deficiency, is characterized by a nonuniform distribution of tidal volumes in the lung parenchyma, epithelial necrosis in peripheral airspaces, and leakage of protein into the alveoli from areas of epithelial disruption. Studies on premature experimental animals have shown that the leakage of protein is correlated to the pressure required to ventilate the lungs, i.e. presumably to the degree of surfactant deficiency. Since the leaking material includes potent surfactant inhibitors, the underlying surfactant deficiency may become aggravated, and a vicious cycle is easily established. Lung compliance is improved, epithelial necrosis prevented, and protein leakage significantly reduced by instillation of surfactant into the airways of immature newborn experimental animals. This provides the rationale for surfactant replacement therapy in neonatal RDS.

Animals↗
PubMed1989

Vascular to alveolar leak of iron dextran (120 kD) in the immature ventilated rabbit lung.

Rabbit fetuses were delivered by hysterotomy on day 27 or 28 of gestation. Immediately after birth, the animals were tracheotomized and received by intravenous injection 0.2 mu Ci radiolabeled albumin and 11 mg iron dextran in 0.2 ml saline. The newborn rabbits then were ventilated artificially with a tidal vol of 12 ml/kg for 5-20 min. One group of nonventilated animals served as controls. At the end of the experiment, one lung was lavaged via the airways and the other was fixed for histologic examination. The recovery of labeled albumin and iron dextran in the lavage fluid was quantified. Iron dextran complexes were easily identified in the lung sections by staining with Prussian blue. Iron dextran accumulated in the airspaces of animals delivered on day 27 (about 4% of the injected dose during 10-20 min of ventilation). The albumin leakage was slightly higher than that of the dextran, a result consistent with different mol wt of the markers. The vol density of leaking alveoli in histologic sections increased with time, from 0 at birth to a mean value of 0.36 after 20 min of ventilation. The leakage starts as a focal event, gradually involving more and more terminal airspaces. In the histologic sections, there was no indication of a significant leakage at the bronchiolar level, although the epithelium of terminal and preterminal airways was clearly injured in all ventilated animals.

Albumins↗
PubMed1989

Neonatal respiratory distress syndrome and surfactant therapy; a brief review.

Several randomized clinical trials have now documented a beneficial effect of surfactant replacement in established neonatal respiratory distress syndrome (RDS). These results have been obtained with surfactant isolated from animal lungs or human amniotic fluid. Treatment with exogenous natural surfactant usually reverses the clinical course of severe RDS, reduces the incidence of serious complications including bronchopulmonary dysplasia, and improves survival rate. Prophylactic surfactant treatment at birth reduces the incidence of severe RDS in very premature babies; this effect has been documented with natural as well as synthetic surfactant preparations. Increased incidence of patent ductus arteriosus was reported in one series of RDS patients treated with modified bovine surfactant, but otherwise no adverse effects have been observed.

1,2-Dipalmitoylphosphatidylcholine↗