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Biomedical subjects

T W Hansen

Publications and source records attributed to T W Hansen.

At least 91 records · Page 5Linked to original sources
PubMed1991

[Children and diseases in the Third World].

Each year approximately 137 million children are born, 70 million of them in countries where the mortality rate for under-fives exceeds 100 per 1,000. In worst-off Afghanistan 300 per 1,000 children under five die. We review some of the most common causes of this catastrophy: diarrhoea, acute respiratory infections, measles, malaria, and neonatal tetanus. All of the numerically significant contributors to under-five mortality are treatable and/or preventable by simple and inexpensive methods. Medical personnel from industrialized countries, and there is an increasing need for transfer of financial resources from highly developed to developing countries. The living conditions of children in the third world involve many factors that are detrimental to both physical and mental health. In order to effect a change, all countries and societies must become involved.

Age Factors↗
PubMed1990

Differences in magnitude and duration of opioid-induced respiratory depression and analgesia with fentanyl and sufentanil.

The magnitude and duration of analgesia and respiratory depression induced by fentanyl (1.0, 2.0, and 4.0 micrograms/kg) and sufentanil (0.1, 0.2, and 0.4 microgram/kg) after intravenous administration over 30 s were measured in 30 healthy young adult male volunteers divided into three groups and studied in a double-blind, randomized fashion. Each volunteer received one dose of fentanyl or sufentanil and no sooner than 48 h later, the corresponding equipotent dose of the other opioid. End-tidal CO2 and ventilatory and occlusion pressure responses to CO2 rebreathing were used to measure drug-induced respiratory effects. Analgesic effects were assessed by changes in the pain threshold to electric shock applied to the forearm. Plasma levels of fentanyl and sufentanil were measured by radioimmunoassay. Testing and sampling intervals were 5, 30, 60, 90, 120, 240, 300, and 360 min after drug administration. The magnitude and duration of depression of the ventilatory and occlusion pressure response were significantly less with sufentanil compared with fentanyl, irrespective of dose. Ventilatory and occlusion pressure responses returned to control values by 30 and 30 min, respectively, after sufentanil and by 240 and 120 min, respectively, after fentanyl. Statistically significant elevations of the pain threshold were, however, greater and longer lasting after sufentanil compared with fentanyl. Pain threshold returned to control values 180 min after sufentanil but only 90 min after fentanyl. These results suggest that sufentanil may provide better patient comfort with less respiratory depression than does fentanyl.

Adolescent↗
PubMed1990

Pericardial tamponade secondary to central venous catheterization and hyperalimentation in a very low birthweight infant.

A very low birthweight infant developed pericardial tamponade secondary to leakage of fat emulsion through a catheter lodged in the right atrial appendage. At autopsy examination a thrombus was lodged in the appendage, which presumably resulted in immobilization of the catheter and leakage of the fluid through an attenuated and necrotic myocardial wall.

Cardiac Tamponade↗
PubMed1989

Cerebral blood flow during experimental hypoxaemia and ischaemia in the newborn piglet.

The effect of selective hypoxaemia or ischaemia on cerebral blood flow was studied in 14 newborn piglets with the microsphere method. Surgery and experiments were performed under general anesthesia with 70% nitrous oxide. The spontaneously breathing piglet was then exposed to either low (zero) oxygen in the inspired air (hypoxaemia), or a graded tourniquet (3-5 kg string weight) of the neck above the level of the tracheostomy (ischaemia). Cerebral blood flow was measured at baseline, during the hypoxaemic/ischaemic insult, and 30 and 60 min thereafter. Brainstem blood flow was remarkably stable during both ischaemia and hypoxaemia. The reduction in blood flow to the cerebrum and to the cerebellum was greater during ischaemia than during hypoxaemia. Reactive hyperaemia followed hypoxaemia but was not obvious after selective ischaemia. Ischaemia and hypoxaemia thus seem to have different effects on cerebral blood flow.

Animals↗
PubMed1989

Effect of light and hyperoxia on ocular blood flow in the newborn piglet.

Ocular blood flow was studied in newborn piglets during light exposure and light combined with hyperoxia. Light caused a significant increase in ocular blood flow which returned to values not significantly different from baseline levels during superimposed hyperoxia. None of these experimental conditions changed total cerebral blood flow or cardiac output. The findings indicate that light might be a regulator of ocular blood flow. This influence of light on ocular blood flow may be of importance in the pathophysiology of retinopathy of prematurity.

Animals↗
PubMed1989

Cerebral blood volumes in young rats with and without in situ saline flushing of cerebral vasculature. Implications for in vivo studies of brain substance uptake.

In recent studies of bilirubin encephalopathy, in situ flushing of the cerebral vessels has been used to clear blood from the brain. The effectiveness of such procedures has not been adequately documented. Herein young, male Sprague-Dawley rats were given about 750 KBq of 51Cr-labelled rat erythrocytes 3 min prior to sacrifice. There were four experimental groups: control, displacer (sulfisoxazole), hyperosmolality, and hypercarbia. Half of the rats in each group had the brain vasculature flushed in situ, while the remaining rat brains were not flushed. The brains were dissected into seven regions, and the radioactivity in the tissues was compared to that of blood drawn from the rats immediately before death. Significant amounts of blood (22-42%) remained after in situ flushing. Retention was significantly higher in the hyperosmolar animals, and significantly lower in the hypercarbic animals as compared to controls. Interregional differences in blood volumes per gram wet weight were significant without, but not with flushing. Similar observations were made using 125I-IgM as a marker for the plasma compartment. In studies of brain uptake of substances with high plasma concentrations, substance remaining within the cerebral vessels may contribute significantly to the apparent brain uptake values.

Animals↗
PubMed1989

Effects of sulfisoxazole, hypercarbia, and hyperosmolality on entry of bilirubin and albumin into brain regions in young rats.

We have studied the entry of 3H-bilirubin and 125I-albumin into brain regions in young rats during short-term (1 h) hyperbilirubinemia. Bilirubin enters the brain both under control, displacer (sulfisoxazole 50 mg/kg), hypercarbic (PCO2 18-21 kPa; pH approximately 6.9), and hyperosmolar (serum osmolality approximately 400 mosm/l) conditions. No significant differences in bilirubin uptake were found between brain regions. Thus preferential staining of basal ganglia ('kernicterus') may not be a phenomenon related to uptake. Albumin does not cross the blood-brain barrier under control or displacer conditions, but does enter the brain to some extent in hypercarbia, and to a greater extent in hyperosmolality. During control and displacer conditions, only unbound bilirubin appears to enter the brain. In hypercarbia bilirubin enters primarily in the unbound form, but some is also albumin-bound. In hyperosmolality a significant fraction of the bilirubin entering the brain is albumin-bound.

Animals↗
PubMed1989

The effect of arterial PCO2-variations on ocular and cerebral blood flow in the newborn piglet.

The response of ocular and cerebral blood flow to different arterial PCO2 levels was studied in ventilated paralyzed newborn piglets with the radionuclide-labeled microsphere method. The retina and the choroid have different blood flow responses to variations in arterial PCO2 levels. Retinal blood flow (ml/g/min) was increased during hypercarbia, from 0.26 +/- 0.03 at baseline to 0.51 +/- 0.07 (PaCO2 8.7 +/- 0.2 kPa) and 0.62 +/- 0.07 (PaCO2 11.0 +/- 0.2 kPa). However, no significant change was found in choroidal blood flow during hypercarbia. Cerebral blood flow was more responsive to PaCO2 than retinal blood flow, increasing from 0.71 +/- 0.03 at baseline to 2.25 +/- 0.25 (PaCO2 8.7 +/- 0.2) and 1.77 +/- 0.13 (PaCO2 11.0 +/- 0.2). Hypocarbia did not influence either retinal or choroidal blood flow.

Animals↗
PubMed1988

Bilirubin decreases phosphorylation of synapsin I, a synaptic vesicle-associated neuronal phosphoprotein, in intact synaptosomes from rat cerebral cortex.

The mechanisms by which bilirubin causes neurotoxicity in newborns have not been well defined, but an involvement in synaptic transmission appears possible. Herein we present evidence for an inhibitory effect of bilirubin on both basal and depolarization-induced (50 mM KCl) phosphorylation of synapsin I, a synaptic vesicle-associated protein that may play a role in neurotransmitter release. Synaptosomes from rat cerebral cortices, prelabeled with 32P in vitro to label the intraterminal ATP pool, were incubated with or without bilirubin and bovine serum albumin (added as a stabilizer) at varying doses and for different time intervals. Some preparations were also depolarized by high KCl concentrations to induce Ca++ influx. The phosphorylation of synapsin I was monitored. Our results show that addition of bilirubin to the medium significantly decreases 32P incorporation into synapsin I, both under basal and depolarizing conditions, in a time- and dose-dependent manner, significant effects being observed already at 10 microM bilirubin after 120-min incubation of the synaptosomes. Separate analysis of the multiple phosphorylation sites in synapsin I showed that the phosphorylation of both the "head" and "tail" regions of the protein was decreased by bilirubin. Removal of the bilirubin-containing incubation medium retarded the decrease in synapsin I 32P content, indicating that the effect observed may be reversible. The nontoxic pyrrole biliverdin had no effect on synapsin I phosphorylation under the experimental conditions used, indicating that the effect was specific to bilirubin. Our results thus suggest that bilirubin may achieve some of its reversible effects on the brain through inhibition of the phosphorylation of the synapsic vesicle-associated protein synapsin I.

Animals↗
PubMed1988

Short-term exposure to bilirubin reduces synaptic activation in rat transverse hippocampal slices.

We evaluated the feasibility of using the in vitro transverse rat hippocampal slice as a model to study the effect of bilirubin on neuronal activity. Bilirubin in concentrations from 100 mumol/liter to 1 mmol/liter with bovine serum albumin as a stabilizer caused a significant decrease in the slope of the field excitatory postsynaptic potentials, concomitant with a significant increase in the peak latency of the population spike. These changes were partially reversible when bilirubin was removed from the incubation fluid. A partially reversible shift to the right of the presynaptic fiber volley/field excitatory postsynaptic potential relationship was interpreted as an expression of a reduction in synaptic activation. A partially reversible shift to the left of the field exitatory postsynaptic potential population spike relationship was interpreted as an expression of increased postsynaptic excitability. In conclusion the in vitro rat hippocampal slice was used successfully to study the effect of bilirubin on neuronal activity. A depressive effect of bilirubin was observed.

Action Potentials↗
PubMed1987

Open-field behavior of rats previously subjected to short-term hyperbilirubinemia with or without blood-brain barrier manipulations.

The aim of this study was to investigate (i) whether bilirubin encephalopathy with lasting sequelae could be created in a rat model, and (ii) putative differences in brain toxicity between bound and unbound bilirubin. Hyperbilirubinemia was produced by infusing bilirubin 20 mg/kg/h during 3 h into 6-week-old male Sprague-Dawley rats. In addition to the hyperbilirubinemia, different groups were created by exposing the rats to hyperosmolality, hypercarbia, and sulfisoxazole. Three weeks after the infusion the rats were studied in an open-field apparatus during 10 daily sessions of 15 min duration. A data collection program was used to study the following measures of activity: crossings in cage, peeks, rearing, latency to enter field, crossings in middle and in outer field, and time outside cage. The data were subjected to multivariate analyses of variance (MANOVA). Generally, the level of activity was higher in the bilirubin-treated rats as compared to the control animals. The difference in activity between bilirubin-treated and control rats changed systematically both between and within sessions. The data show that both unbound and albumin-bound bilirubin are neurotoxic, but they indicate a more pronounced effect of unbound bilirubin. The sequelae of bilirubin brain toxicity appear to include changes in stimulus processing. This is compatible with findings from neuropsychological tests of children who have had significant neonatal hyperbilirubinemia.

Animals↗
PubMed1987

Effects of hyperoxia on entry of bilirubin and albumin into rat brain.

The effects of hyperoxia on the entry of bilirubin and albumin into the brain were studied in five to six-week-old male Sprague-Dawley rats. Bilirubin was infused at 20 mg/kg/hour for three hours through a carotid catheter, resulting in serum bilirubin levels of 200-220 microM at 180 minutes. Group 1 (n = 8) was normoxic at all times. Group 2 (n = 8) was given oxygen (FiO2 = 0.75 -0.80) for the last hour of the three-hour bilirubin infusion. Group 3 (n = 10) was given oxygen (FiO2 = 0.75 -0.80) for 24-27 hours prior to, as well as during the bilirubin infusion. No significant differences were found in brain bilirubin (as measured by chloroform extraction) or brain albumin (as measured by 125I-albumin uptake) between the groups. Under these experimental conditions, hyperoxia does not increase bilirubin deposition in rat brain nor does it cause opening of the blood-brain barrier as measured by albumin entry into the brain.

Animals↗