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Biomedical subjects

H Hagberg

Publications and source records attributed to H Hagberg.

At least 145 records · Page 8Linked to original sources
PubMed1991

Changes in extracellular amino acids and spontaneous neuronal activity during ischemia and extended reflow in the CA1 of the rat hippocampus.

This study addresses the possible involvement of an agonist-induced postischemic hyperactivity in the delayed neuronal death of the CA1 hippocampus in the rat. In two sets of experiments, dialytrodes were implanted into the CA1 either acutely or chronically (24 h of recovery). During 20 min of cerebral ischemia (four-vessel occlusion model) and 8 h of reflow, we followed extracellular amino acids and multiple-unit activity. Multiple-unit activity ceased within 20 sec of ischemia and remained zero during the ischemic insult and for the following 1 h of reflow. During ischemia, extracellular aspartate, glutamate, taurine, and gamma-aminobutyric acid increased in both acute and chronic experiments (seven- to 26-fold). Multiple-unit activity recovered to preischemic levels following 4-6 h of reflow. In the group with dialytrodes implanted acutely, the continuous increase in multiple-unit activity reached 110% of basal at 8 h of reflow. In the group with dialytrodes implanted chronically, multiple-unit activity recovered faster and reached 140% of control at 8 h, paralleled by an increase in extracellular aspartate (5.5-fold) and glutamate (twofold). In conclusion, the postischemic increase of excitatory amino acids and the recovery of the neuronal activity may stress the CA1 pyramidal cells, which could be detrimental in combination with, e.g., postsynaptic impairments.

Action Potentials↗
PubMed1991

Extracellular acidic sulfur-containing amino acids and gamma-glutamyl peptides in global ischemia: postischemic recovery of neuronal activity is paralleled by a tetrodotoxin-sensitive increase in cysteine sulfinate in the CA1 of the rat hippocampus.

An excessive activation of the excitatory amino acid system has been proposed as one possible mediator of the ischemia-induced delayed death of CA1 pyramidal cells in the hippocampus. Using dialytrodes in the CA1 of the rat, we have investigated multiple-unit activity and extracellular changes in acidic sulfur-containing amino acids and gamma-glutamyl peptides during ischemia (20-min, four-vessel occlusion) and during 8 h of reflow. Multiple-unit activity was abolished during ischemia and for the following 1 h, but then recovered, gradually reaching preischemic levels after 8 h of reflow. Extracellular cysteate, cysteine sulfinate, and gamma-glutamyltaurine increased (1.5- to threefold) during ischemia, and extracellular glutathione and gamma-glutamylaspartate plus gamma-glutamylglutamine increased during early reflow (two- to threefold). The recovery of neuronal activity at 4-8 h was paralleled by an increase in extracellular cysteine sulfinate (2.5-fold at 8 h of reflow). Perfusion with 10 microM tetrodotoxin at 8 h of reflow abolished the multiple-unit activity and reduced extracellular cysteine sulfinate. Considering the glutamate-like properties of cysteine sulfinate, the observed postischemic increase may be involved in the development of the delayed neuronal death.

Acids↗
PubMed1991

Renal function after autologous bone marrow transplantation.

Seventy-two out of 102 consecutive patients autografted for various hematologic and lymphoid malignancies had a relapse-free survival of greater than 6 months after autologous bone marrow transplantation (ABMT) and were evaluated for long-term effect of the treatment on the renal function. The myeloablative therapy included total body irradiation (TBI) in a single fraction of 7.5 Gy in 41/72 patients. Mean glomerular filtration rate (GFR) showed a significant decrease (p less than 0.01) and serum creatinine and serum urea an increase (p less than 0.05) 6 months after ABMT. Twelve of 72 patients (17%) developed renal dysfunction defined as greater than 25% decrease in GFR, in most cases accompanied by hematuria and proteinuria. Onset was 3-6 months after ABMT. Some patients have later improved considerably, but others continue to deteriorate in renal function. The single most important risk factor for renal dysfunction after ABMT was irradiation. Renal damage was most frequent in lymphoma patients conditioned with BEAC (carmustine [BCNU], etoposide, cytarabine, cyclophosphamide) followed by irradiation, suggesting that this drug combination might have potentiated the toxicity of irradiation. Nephrotoxic antibiotics probably contributed to renal damage in individual cases. Young age did not appear to be a risk factor. Our data indicate that combined treatment with BEAC and TBI should be used with caution and that renal function should be monitored in all patients after bone marrow transplantation to detect any new toxicity patterns of the various conditioning regimens currently used.

Adolescent↗
PubMed1991

Superparamagnetic particles as oral contrast medium in MR imaging of malignant lymphoma.

Non-biodegradable superparamagnetic particles, in plain and viscous aqueous suspensions, were used as an oral contrast medium in 34 patients with known or suspected malignant lymphoma. The contrast effect, the occurrence of artifacts, and the distribution were evaluated in the plain and the viscous aqueous suspensions, and the diagnostic information received from abdominal MR examinations performed without bowel contrast medium was compared with that of post-contrast examinations. Magnetic particles in the concentration of 0.5 g/l displayed a good contrast effect at 0.5 T, and helped in differentiating the intestine from adjacent tissues, resulting in increased diagnostic information in abdominal MR imaging. In the patients given the viscous aqueous suspension the occurrence of artifacts caused by the magnetic particles decreased considerably, and the distribution was homogeneous and improved compared with that in patients given the plain aqueous suspension.

Abdomen↗
PubMed1990

Evaluation of brain damage in a rat model of neonatal hypoxic-ischemia.

In spite of improvements in obstetric and neonatal care, hypoxic-ischemic brain damage with severe neurologic disability is still a clinical reality. A model in 7-day-old rats has been introduced to study the pathophysiology of perinatal hypoxic-ischemic brain damage. Unilateral brain damage is produced in the cerebral cortex, striatum and hippocampus, i.e. a similar distribution as is often seen in human asphyxiated neonates. In the present investigation the model was evaluated further by comparing three different methods to assess the brain damage: weighing the hemispheres, morphometry and somatosensory evoked potentials. Seven-day-old rats were subjected to unilateral carotid artery ligation followed by 2 h of hypoxia (7.7% O2 at 36 degrees C). After 2 h of hypoxic-ischemia pCO2 and pO2 decreased in mixed arterial/venous blood. The evaluation of the damage 2 weeks after the insult, demonstrated close correlation between morphometry and weighing (r = 0.836, P less than 0.01). The amplitude of evoked potentials correlated to the other parameters (r = 0.814, P less than 0.01 and r = 0.824, P less than 0.01 respectively) and displayed a greater relative attenuation than the other methods but with a more pronounced variability. These results indicate that the degree of brain damage can be assessed by weighing for screening purposes.

Aging↗
PubMed1990

Autoantibodies to epithelial cells in patients on long-term therapy with leucocyte-derived interferon-alpha (IFN-alpha).

During routine screening for anti-nuclear antibodies, using rat liver tissue as substrate, a reactivity against bile duct epithelium was observed in sera from carcinoid tumour patients given human leucocyte-derived IFN-alpha (HuLe IFN-alpha). In a retrospective study, initiated by this observation, the development of serum antibodies to bile duct epithelium was observed in nine out of 12 patients with carcinoid tumours and in three out of 14 patients with hairy-cell leukaemia during their treatment with HuLe IFN-alpha. However, no bile duct reactivity was observed in sera from carcinoid or hairy-cell leukaemia in patients given recombinant IFN-alpha. When analysing the reactivity of positive sera against a panel of rat and human tissues, a uniform reactivity was observed against simple epithelial cells lining the gastrointestinal tract, pancreatic secretory ducts, fallopian tube, kidney tubuli, mesothelium and also against carcinoid tumour cells. The mechanisms promoting autoreactivity against this simple epithelial cell autoantigen is so far unknown. The cytoplasmic as well as the restricted staining pattern of simple epithelial cells may indicate autoreactivity against certain cytoskeletal intermediate filaments, such as cytokeratin 19, 18 and 8, known to be exclusively present in simple epithelial cells and tumours derived from them.

Animals↗
PubMed1990

Effect of propentofylline (HWA 285) on extracellular purines and excitatory amino acids in CA1 of rat hippocampus during transient ischaemia.

1. The adenosine uptake blocker propentofylline (HWA 285) has previously been shown to protect hippocampal CA1 pyramidal cells from ischaemia-induced delayed neuronal death. The influence of propentofylline, on the extracellular concentrations of purines, aspartate and glutamate in the CA1 of the rat hippocampus during transient forebrain ischaemia was investigated. 2. Twenty min of ischaemia was induced by four-vessel occlusion in Wistar rats, extracellular compounds were sampled by use of microdialysis and EEG was recorded by a tungsten electrode attached to the dialysis probe. 3. Propentofylline (10 mg kg-1 i.p.) did not influence the basal levels of any of the compounds in the hippocampal dialysates. 4. The EEG became isoelectric within 20 s after induction of ischaemia. 5. Extracellular adenosine, inosine, hypoxanthine, aspartate and glutamate increased several fold during ischaemia and remained elevated during early reflow. Within 2 h of reperfusion the concentration of all compounds was normalized. Xanthine increased upon reperfusion and remained elevated after 2 h. 6. Propentofylline (10 mg kg-1 i.p.) administered 15 min before ischaemia significantly enhanced the ischaemia-evoked increase of adenosine but attenuated the increases of the other purine catabolites and of glutamate. 7. In separate in vitro experiments, propentofylline did not inhibit adenosine deaminase activity. 8. The present data show that propentofylline enhances extracellular adenosine and lowers extracellular glutamate in vivo during ischaemia. These findings may be important in relation to the neuroprotective properties of propentofylline.

Adenosine Deaminase↗
PubMed1990

Immunophenotype of hairy-cell leukemia.

15 cases of HCL were studied with a panel of monoclonal antibodies against different leukocyte antigens. A B-cell phenotype different from that of B-CLL was observed (CD10-, CD19+, CD20+, CD21-, CD22+, CD37+, CD38-, FMC7+, LN1+, PCA-1+, BLy7+ and CD5-). As expected, CD11c and CD25 were positive and, in addition, a My7 and My9 positivity in varying degree was noted. 3 weeks of in vitro incubation did not significantly alter the phenotype. We conclude that HCL exhibits a unique phenotype among chronic B-cell leukemias, which is closer to the plasma cell stage of differentiation than that of B-CLL. The BLy7 monoclonal antibody seems to be a promising marker for HCL.

Antigens, CD↗
PubMed1990

Methyl-GAG, ifosfamide, methotrexate and etoposide (MIME) as salvage therapy for Hodgkin's disease and non-Hodgkin's lymphoma. The Swedish Lymphoma Study Group.

One hundred and three patients with recurrent or refractory Hodgkin's disease (HD) or non-Hodgkin's lymphoma (NHL) treated with MIME (methyl-GAG, ifosfamide, methotrexate, etoposide) were retrospectively studied. Thirty-seven of the 44 patients with HD, 34/47 with high-grade malignant and 9/12 with low-grade malignant NHL were evaluable for response. Of the 37 evaluable patients with HD, 16 (43%) achieved complete remission (CR) and 4 partial remission (PR), giving a total response rate of 54%. Of the 34 evaluable patients with high-grade NHL, 5 achieved CR and 8 PR, giving a response rate of 38%. Of 9 evaluable patients with low-grade NHL, 2 achieved CR. The main toxicity was leukopenia, thrombocytopenia and infections. Twenty-six per cent of the patients developed septicaemia, which was fatal in 6 cases (6%). We conclude that MIME as salvage regimen can induce complete remissions in lymphoma patients, particularly in HD with previous heavy treatment, and that it is relatively well tolerated.

Adult↗
PubMed1989

Extracellular increase of hypoxanthine and xanthine in the cortex and basal ganglia of fetal lambs during hypoxia-ischemia.

A microdialysis procedure was used to sample purine catabolites from the extracellular compartment of two areas of the fetal brain, the cerebral cortex and the striatum region. Seven exteriorized, anesthetized fetal sheep were studied during conditions of normal oxygenation and during asphyxia induced by stepwise lowering of maternal placental perfusion pressure. Fetal cerebral blood flow (CBF) was measured with the 133Xe washout method. Somatosensory evoked potentials were recorded during tactile stimulation of the fetal snout. The purine catabolites hypoxanthine (HX), xanthine (Xan), guanosine (Gua), inosine (Ino) and adenosine (Ade) were measured in arterial and venous plasma and in the dialysate by a HPLC method. During gradually increasing asphyxia HX increased 4-6-fold both in cerebral tissue and in arterial plasma, while Xan rose 1.5-3 times in cerebral tissue and arterial plasma. Gua did not change in either tissue or blood and Ino did not rise until at the most extreme degree of asphyxia it rose 2-4-fold. Ade concentrations remained unaltered during moderate asphyxia (when CBF rose 3-fold), but demonstrated a significant (2-3-fold) augmentation at the most extreme degrees of asphyxia. The results thus suggests a significant accumulation of oxypurines, especially HX, in the interstitium of the fetal brain during asphyxia. The rise in xanthine concentration demonstrates the presence of an activity of xanthine oxidase in brain tissue. A discrepancy between the elevation of CBF and of the tissue concentration of Ade does not support a direct role of Ade in the asphyctic cerebral vasodilation in the fetus.

Animals↗
PubMed1989

Rupture and dehiscence of cesarean section scar during pregnancy and delivery.

A prospective study was undertaken to evaluate the risk of uterine rupture or dehiscence after cesarean section. During the 10 years of the study, 24,644 patients were delivered of infants. Of these women, 2036 (8.3%) had previously undergone cesarean section. A trial of labor was allowed in 1008 of these patients, and 92.2% were delivered vaginally. The incidence of uterine rupture in this trial of labor group was 0.6%, compared with 0.4% in the total group. Cesarean section scar rupture caused no serious complications in either the mothers or the offspring in the trial of labor group. Uterine rupture in this group was not associated with use of oxytocin or epidural analgesia. Patients with lower-segment scar rupture had no history of puerperal pyrexia. The incidence of uterine dehiscence was 4%. In summary, the risk of uterine rupture in patients who have previously undergone cesarean section but are allowed a trial of labor is low and not associated with serious complications. Vaginal delivery is therefore considered the safest route of delivery in these patients.

Adult↗
PubMed1989

Relative cerebral ischemia in SHR due to hypotensive hemorrhage: cerebral function, blood flow and extracellular levels of lactate and purine catabolites.

Cerebral blood flow (CBF, by laser Doppler flowmetry) and extracellular cortical concentrations (by microdialysis) of adenosine, inosine, xanthine, hypoxanthine, and lactate were measured together with somatosensory evoked potentials (SEP) in chloralose-anaesthetized spontaneously hypertensive rats (SHR) during relative cerebral ischemia induced by hypotensive hemorrhage. Reduction of mean arterial blood pressure (MABP) to 40-50 mm Hg, which decreased SEP to about 50% of prebleeding control level, decreased CBF only to about 75% of control due to cerebrovascular "autoregulation." A secondary, marked rise in cerebrovascular resistance (CVR) occurred after about 15 min in parallel with a striking increase in heart rate (after initial bradycardia). This late rise in heart rate is probably elicited by relative ischemia in medullary centers. The increase in CVR might indicate increased sympathetic nerve activity to the circle of Willis and large cerebral arteries. Cortical lactate increased initially but started to decline after about 30 min, and after 2 h it was not significantly higher than control. Cortical adenosine, inosine, hypoxanthine, and xanthine increased slowly and were significantly elevated after 50 min of hemorrhage. After 80 min, adenosine and inosine had returned to initial levels, while hypoxanthine and xanthine were further elevated. Despite the apparent partial recovery of metabolic disturbances during late hemorrhage, and with a blood flow maintained at 75% of resting control, SEP did not improve. It is suggested that the depression of SEP is not primarily caused by circulatory-metabolic derangements, but instead by activation of specific inhibitory systems.

Adenosine↗
PubMed1989

Ischemic damage in hippocampal CA1 is dependent on glutamate release and intact innervation from CA3.

The removal of glutamatergic afferents to CA1 by destruction of the CA3 region is known to protect CA1 pyramidal cells against 10 min of transient global ischemia. To investigate further the pathogenetic significance of glutamate, we measured the release of glutamate in intact and CA3-lesioned CA1 hippocampal tissue. In intact CA1 hippocampal tissue, glutamate increased sixfold during ischemia; in the CA3-lesioned CA1 region, however, glutamate only increased 1.4-fold during ischemia. To assess the neurotoxic potential of the ischemia-induced release of glutamate, we injected the same concentration of glutamate into the CA1 region as is released during ischemia in normal, CA3-lesioned, and ischemic CA1 tissue. We found that this particular concentration of glutamate was sufficient to destroy CA1 pyramids in the vicinity of the injection site in intact and CA3-lesioned CA1 tissue when administered during control (non-ischemic) conditions. In contrast, the same amount injected during ischemia in the CA3-lesioned CA1 region destroyed pyramidal cells in a widely distributed zone around the injection site in the CA1 region. It is concluded that the ischemia-induced damage of pyramidal cells in CA1 is dependent on glutamate release and intact innervation from CA3.

Amino Acids↗
PubMed1989

Bone marrow morphology during alpha-interferon treatment in hairy cell leukemia.

14 patients with HCL were started on alpha-interferon (IFN) treatment. Bone marrow changes were followed in trephine biopsies every 3rd month. Differential counting was performed according to the point counting method and fiber content was evaluated. At the start of treatment all patients had 80% or more of tumor cells in the bone marrow. The reduction of granulopoiesis was more pronounced than for erythropoiesis. During treatment cellularity decreased in 6/13 patients already after 3 months; later, cellularity was normalized in most patients. Only 1 patient showed a complete remission. 12/14 patients showed a significant but slow reduction of tumor cells. Also, between 12 and 18 months an improvement was seen in some patients. The megakaryocytes improved rapidly and the erythropoiesis was normalized before the granulopoiesis. Only 1 patient did not show a bone marrow response. 5/14 patients showed a reduction of bone marrow fibers, first seen after 6 months of treatment. IFN was discontinued in 9/14 patients. 7 of these relapsed during the observation period (18 months).

Adult↗
PubMed1989

Primarily asymptomatic low-grade non-Hodgkin lymphomas: prediction of symptom-free survival and total survival.

Low-grade non-Hodgkin lymphomas (NHL) constitute a group of tumours with an often long survival time but, at present, with little--or no--chance of cure if the disease is not strictly local. In primarily asymptomatic patients, treatment may either be started immediately after diagnosis or deferred until symptoms occur. The possibility of predicting the symptom-free time was investigated in 64 non-selected initially asymptomatic patients with advanced low grade NHL, all of whom had treatment deferred until symptoms occurred. The most powerful predictor was the histopathological subgroup. Lymphocytic (LC) and follicular centroblastic-centrocytic (fCBCC) lymphomas had a median symptom-free period of 2 years, which was four times longer than that for immunocytoma (IC) and follicular and diffuse CBCC (fdCBCC). In addition, the serum levels of deoxythymidine kinase (S-TK) and lactic dehydrogenase (S-LDH) could predict the symptom-free period. This did not apply to S-Haptoglobin, S-Orosomucoid or stage. In a multivariate analysis, only S-TK gave additional information to histopathology. The only variable that predicted the overall survival time was the length of the symptom-free period.

Follow-Up Studies↗