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Biomedical subjects

J Lundgren

Publications and source records attributed to J Lundgren.

At least 37 records · Page 2Linked to original sources
PubMed1996

Epidemiology of AIDS-related Kaposi's sarcoma in Europe over 10 years. AIDS in Europe Study Group.

OBJECTIVES: To determine the incidence and risk factors associated with Kaposi's sarcoma (KS) occurrence as an AIDS-defining condition or after the diagnosis of AIDS. DESIGN: Multicentre retrospective cohort study of AIDS in Europe database from 52 clinical centres in 17 European countries. METHODS: Patients' charts (n = 6546) were reviewed and collected in the database of the AIDS in Europe Study Group from 1979 to 1989. At the time of AIDS diagnosis 1394 patients had KS, whereas an additional 525 others developed KS after AIDS diagnosis. Univariate analysis and development of multivariate models determined factors associated with KS occurrence. RESULTS: Frequency of KS as an AIDS-defining condition significantly declined over time (P < 0.0001). In our cohort of patients, homo-/bisexual men from central Europe with CD4 cell counts > 150 x 10(6)/l were statistically more likely to develop KS at the time of AIDS diagnosis (P < 0.0001). For patients with an AIDS diagnosis other than KS, the probability of developing KS during the follow-up was 10 and 24% after 12 and 36 months, respectively. Variables significantly associated with a further KS development were transmission group, central European residence, previous herpes simplex infection other than ulcers, and low CD4 cells (< 150 x 10(6)/l). Previous zidovudine therapy had no influence on KS appearance. For patients who developed KS subsequent to AIDS diagnosis, there was no significant decline of the incidence over the 10-year time period. CONCLUSIONS: This large cohort study clearly shows that demographic data such as sex, transmission group and region of Europe have a major influence on KS development. It also suggests that KS as an AIDS-defining disease occurs earlier in the course of the chronic HIV infection than other opportunistic diseases. Reasons for geographical variations and its declining frequency as an initial AIDS diagnosis remain undetermined.

AIDS-Related Opportunistic Infections↗
PubMed1996

Characteristics of postischemic seizures in hyperglycemic rats.

Normoglycemic animals subjected to 10-20 min of transient ischemia survive without major neurological symptoms, but incur delayed neuronal damage selectively affecting vulnerable neuronal populations. If the animals are hyperglycemic before ischemia is induced, cell damage develops more rapidly, and postischemic seizures appear after a delay of 18-24 h. This study was designed to assess whether the primary insult, i.e., transient ischemia in hyperglycemic animals, triggers early epileptogenic activity which 'matures' into clinical seizures, or if the seizures arise as a result of secondary events occurring after many hours of recirculation. EEG activity during 20-24 h of postischemic recirculation was recorded from electrodes implanted in the neocortex and hippocampus of freely moving rats which had been subjected to 10 min of ischemia under normoglycemic or hyperglycemic conditions. Normoglycemic animals showed a transient postischemic reduction of EEG amplitude and frequency, and sparse and temporary epileptiform activity. In contrast, hyperglycemic animals showed a more pronounced reduction of EEG amplitude and frequency, and early appearing epileptiform activity which was sustained, and ultimately transformed into overt electrographic seizures. The EEG changes were more pronounced in the neocortex than in the hippocampus. The results thus demonstrate that the initial ischemic insult, and not the secondary damage appearing many hours after the initiation of recirculation, triggers epileptiform activity that 'matures' into status epilepticus.

Analysis of Variance↗
PubMed1994

Hyperthermia aggravates and hypothermia ameliorates epileptic brain damage.

The influence of hyperthermia and hypothermia on epileptic brain damage was studied in rats, in which status epilepticus was induced by flurothyl. Histopathological changes were examined by light microscopy after 1 or 7 days of recovery. Two series of animals were studied. In the first, short periods of seizures (20 and 25 min) were employed to examine whether moderate hyperthermia (39.5 degrees C) would aggravate epileptic brain damage, and a longer period (45 min) was used to investigate whether moderate hypothermia (32.5 degrees C) would ameliorate the damage. The second series investigated whether brief periods of status epilepticus (10 min) would cause brain damage if hyperthermia were high or excessive. For this series, animals with body temperatures of 37.0, 39.0, and 41.0 degrees C were studied. Data from normothermic animals (37.5 degrees C) confirmed previously described neuronal damage. Although hyperthermic animals failed to show increased damage in the CA1 sector, or in the hilar region of the dentate gyrus, they showed enhanced damage in the neocortex and globus pallidus (GP). In substantia nigra pars reticulata (SNPR) four out of five hyperthermic animals had bilateral infarcts after 20 min of status epilepticus, whereas no normothermic animal showed such damage. Hypothermia seemed to ameliorate epileptic brain damage in the neocortex (n.s.) and GP (P < 0.05) following status epilepticus for 45 min. Three out of seven hypothermic animals had mild SNPR involvement compared to severe infarction of the nucleus in five out of six normothermic animals (P < 0.05). Thus, hyperthermia aggravated and hypothermia ameliorated epileptic brain damage both in regions showing selective neuronal necrosis (neocortex) and in regions developing pan-necrosis (GP and SNPR). The second series displayed an unexpected result of excessive hyperthermia. Animals subjected to only 10 min of status epilepticus at a temperature of 41 degrees C showed not only neocortical lesions, but also moderate to extensive damage to the hippocampus (CA1, subiculum, and dentate gyrus). It is concluded that at high body and brain temperature, brief periods of status epilepticus can yield extensive brain damage, primarily affecting the hippocampus.

Animals↗
PubMed1994

The dynamics of local tissue damage induced by Bothrops asper snake venom and myotoxin II on the mouse cremaster muscle: an intravital and electron microscopic study.

The acute tissue damaging effects of Bothrops asper snake venom and a myotoxic Lys-49 phospholipase A2 (myotoxin II) on the mouse cremaster muscle were studied by intravital and electron microscopy. Both venom and myotoxin induced local contractions of the muscle fibres within 10-60 sec after exposure, which disappeared after 1-2 min. This observation is consistent with the hypothesis that Bothrops myotoxins act initially at the sarcolemma by affecting its permeability and allowing an influx of calcium. The venom also induced an early but transient vasoconstriction of arterioles. The development of edema was monitored using i.v. FITC-dextran as a marker. Plasma leakage started after about 2 min of exposure to venom or myotoxin, was extensive by 4-5 min, and originated from small venules and their adjoining capillary segments. The venom induced formation of thrombi and emboli in venules, but not in arterioles. Haemorrhage appeared after 4-6 min of exposure, the bleedings always originating from capillaries and small venules. The microbleedings were explosive, appearing as rapid bursts of erythrocytes into the extravascular space, and suggesting a per rhexis type of haemorrhage. This was confirmed by electron microscopy evaluation of the same microvessels observed intravitally, which showed erythrocyte extravasation through gaps in damaged endothelial cells. Other phenomena in the microcirculation included blood-flow disturbances, crenation and sphering of erythrocytes, and stasis with dense packing of cells in capillary networks. Muscle necrosis, caused by either venom or myotoxin, started 3-4 min after application. The first sign of damage in the fibres was the development of a narrow, transverse band with local loss of striation. This was followed by slow retraction of myofibrils until there was a complete transverse rupture of the fibre. This process was often repeated along the same fibre, leaving a row of fragments separated by spaces apparently devoid of myofibrillar material. The results confirm the rapid tissue damaging effects of B. asper venom, implying that potentially useful blocking agents must be administered early and have the ability to diffuse rapidly into the tissues.

Animals↗
PubMed1994

Controversies in the management of laryngeal cancer: results of an international survey of patterns of care.

Cancer of the larynx is the most prevalent non-cutaneous malignancy of the head neck region and its treatment presents a threat to both natural speech and survival. This study examines the manner in which two separate specialties in the same and different geographic regions vary in their opinions about the treatment of glottic laryngeal cancer. The goal was to define options available to patients and to classify controversies about optimal treatment which might be resolved in clinical trials. Questionnaires depicting different presentations of glottic larynx cancer were mailed to 1649 otolaryngologists and radiation oncologists in North America, Europe and Australasia. Half the doctors were asked to describe their preferred treatment for a patient while the others were asked to imagine that they themselves were the patient. In all the disease situations opinions varied significantly with respect to the treatment modality advised (whether to employ surgical or radiotherapy approaches) and in more extensive disease situations the intention of treatment also varied depending on whether a curative approach should involve conservation or loss of the larynx. Doctors also recommended similar treatment for their patients as they would for themselves. Apart from disease extent the most significant variables influencing recommendations were the physicians' specialty (P = 0.0001) and where they practice (P = 0.0001). These findings demonstrate diversity of opinion which is influenced more profoundly by the traditions of the specialties and geographic location of practice than by the reported results of treatments for laryngeal cancer. Convictions about optimal management have become barriers to the assessment of the relative value of different treatments and to ensuring that patients are fully informed about management options. The profession should regard as a high priority efforts to resolve these therapeutic conflicts which are associated with major differences in quality of life.

Attitude of Health Personnel↗
PubMed1994

Possible errors in diagnosis of bacterial sinusitis in tracheal intubated patients.

Bacterial sinusitis is recognized as a complication of prolonged nasotracheal intubation. Verification of the diagnosis, however, requires culture findings from a "true" sample from the maxillary antrum. A "true" antral sample can only be obtained after passing either the nasal or oral mucosae with their rich aerobic and anaerobic bacterial flora. No properly controlled study has been made into the problem of contaminated samples in bacterial sinusitis complicating prolonged nasotracheal intubation. The design of the study was a case series in an intensive care unit. The patients had either had endotracheal tube or tracheal cannula for seven days or were septic, having an endothracheal tube or a tracheal cannula and therefore due to an investigation of infection foci. Antral cultures obtained via the canine fossa were compared with oral cultures to exclude the contribution of oral bacterial contamination and thereby to improve the reliability of diagnosis based on culture results. The contamination rate was lowered significantly from 67% to 5% when an area of free bone was prepared in the canine fossa thus avoiding instrument contact with the oral mucosa. A high contamination risk can be dealt with by adjusting the technique of sampling thereby increasing the culture reliability.

Adolescent↗
PubMed1994

Preischemic hyperglycemia leads to delayed postischemic hyperthermia.

BACKGROUND AND PURPOSE: Temperature alterations are known to influence the outcome of transient ischemia, even when instituted in the postischemic period. Since preischemic hyperglycemia aggravates ischemic brain damage, the question of whether hyperglycemic animals become hyperthermic arose. To explore this possibility, we measured body temperature telemetrically in normoglycemic and hyperglycemic rats subjected to 10 minutes of forebrain ischemia at a body (and brain) temperature of 37 degrees C. METHODS: Isoflurane-anesthetized animals were subjected to 10 minutes of forebrain ischemia under normoglycemic or hyperglycemic conditions. Temperature changes after ischemia were measured by means of a telemetric temperature coil. RESULTS: In normoglycemic animals, temperature decreased to 35.6 +/- 1.1 degrees C (mean +/- SD) during the first 4 hours of recovery, after which it gradually increased to normal values (38 degrees C). Hyperglycemic animals behaved differently in that they remained normothermic for approximately 10 hours during recovery and later became hyperthermic, with core temperatures rising above 39 degrees C. The rise in temperature was not due to the osmotic load of the glucose administered because infusion of mannitol, which gave a comparable increase in plasma osmolality, failed to cause delayed postischemic hyperthermia. Excessive hypercapnia during ischemia in normoglycemic animals, which produces cerebral acidosis of a magnitude similar to that of hyperglycemia and is known to aggravate ischemic lesions, likewise failed to induce hyperthermia. When post-ischemic seizures ensued in hyperglycemic subjects, temperature was 39.8 +/- 0.6 degrees C. Animals with seizures invariably died. To evaluate the influence of postischemic hyperthermia on the outcome, an additional series of experiments was performed in which delayed hyperthermia was avoided by gentle cooling (n = 6) or by acetaminophen administration (n = 5). Although these procedures prevented delayed hyperthermia, they neither blocked seizure induction nor affected the fatal outcome. Postischemic seizures developed when the core temperatures of animals were 37.9 +/- 0.1 degrees C and 37.8 +/- 0.2 degrees C in the cooled and acetaminophen-treated groups, respectively. CONCLUSIONS: The results suggest that both delayed hyperthermia and delayed seizures in hyperglycemic animals are caused by the aggravated damage incurred by these animals during or immediately after the ischemic insult.

Acetaminophen↗
PubMed1992

Frontal cortex lesion prior to hyperglycemic ischemia: no decrease in ensuing substantia nigra pars reticulata damage or fatal post-ischemic seizures.

Preischemic hyperglycemia worsens brain damage after ischemia, and characteristically leads to post-ischemic seizures and a pan-necrotic lesion in substantia nigra pars reticulata (SNPR). The excitatory input to SNPR could contribute to the damage observed. By performing a unilateral frontal cortex lesion 6-19 days prior to the ischemia, we wanted to explore whether a decrease in excitatory input to the ipsilateral SNPR ameliorate the seizures or alter the light microscopical damage in SNPR. Our results demonstrate that unilateral frontal cortex lesion did not alter the development of fatal post-ischemic seizures after 10 min of ischemia in hyperglycemic subjects. Thus, 7/8 animals developed seizures and died within 20 h of recovery. This study also failed to show any difference between the left and right side in post-ischemic SNPR damage after 15 h of recovery in animals with preischemic unilateral frontal cortex lesion. Furthermore, no side difference was observed in any other brain region evaluated. The results thus suggest that the pan-necrotic lesion in SNPR after hyperglycemic ischemia is not caused by excessive excitatory input from frontal cortex. A decrease in the GABA-ergic inhibitory input from caudoputamen to SNPR may be a more important mechanism for the ensuing excitotoxic post-ischemic SNPR damage, and for seizure development.

Amino Acids↗
PubMed1992

Effects of dimethylthiourea on ischemic brain damage in hyperglycemic rats.

Hyperglycemia is known to worsen the outcome of transient global or forebrain ischemia. The aggravating effect is believed to be mediated by the additional formation of lactate- and of H+. Recent evidence suggests that reactive oxygen species contribute to the damage after brain ischemia. Since acidosis accelerates free radical damage in vitro, we decided to explore if ischemic damage in hyperglycemic subjects is ameliorated by dimethylthiourea (DMTU), an established free radical scavenger. In one series of hyperglycemic rats, we studied whether preischemic administration of DMTU alters the clinical outcome, notably the incidence and frequency of seizures. In two different series, the effect of DMTU on tissue damage was assessed by light microscopy after 15 h of recovery. Longer periods could not be studied since seizures developed. In the first of these series the animals were anesthetized with isoflurane, and in the second with halothane. The latter anesthesia largely suppressed the "early" postischemic seizures, i.e. those occurring after 1-4 h. Dimethylthiourea treatment altered the clinical outcome after ischemia. Thus, the "late" postischemic seizures appeared milder and occurred significantly later than in untreated animals. The fatal outcome was also delayed since treated animals died after 35.5 +/- 8.2 h (mean +/- SD) of recirculation, as compared to 19.8 +/- 3.6 h of recirculation in control animals. However, all DMTU-treated (and control) animals died. In the first morphological series (isoflurane anesthesia) the histopathological analysis was complicated by the occurrence of prefixation seizures; such seizures were recognized in 4/16 animals. When these 4 animals were excluded from the analysis (2 treated and 2 control animals), DMTU pretreatment did not ameliorate the damage, except in the substantia nigra pars reticulata (P < 0.05). In the second series, comprising animals anesthetized with halothane, only one animal out of 16 had "early" seizures, and none showed "late" seizures before death. Among these animals DMTU treatment significantly ameliorated damage to caudoputamen and cingulate cortex (P < 0.01). We conclude that treatment with the free radical scavenger DMTU partly ameliorates ischemic brain damage associated with excessive acidosis, and marginally delays the development of post-ischemic seizures. However, the effects were moderate and could, at least in part, have been caused by nonspecific effects of DMTU. Furthermore, all DMTU-treated animals died. The results thus give little support to the notion that the aggravating effects of acidosis is due to enhancement of free radical production.

Animals↗
PubMed1992

Ischemic brain damage is not ameliorated by 1,3-butanediol in hyperglycemic rats.

BACKGROUND AND PURPOSE: Treatment with the ketone body precursor 1,3-butanediol has been suggested to ameliorate hypoxic/ischemic brain damage. Butanediol could provide an alternative energy substrate for the brain, thereby decreasing the amount of glycolytically produced lactate. Hyperglycemia aggravates brain damage after brain ischemia and causes fatal postischemic seizures, probably by increasing the production of lactate and decreasing the pH. We studied whether butanediol treatment altered the adverse consequences following ischemia complicated by hyperglycemia. METHODS: Hyperglycemic adult male rats were given 25 or 50 mmol.kg-1 body wt butanediol intravenously 30 minutes before 10 minutes of transient forebrain ischemia. Morphological evaluation was performed following perfusion-fixation after 15 hours of recovery. Blood concentrations of beta-hydroxybutyrate, acetoacetate, glucose, and lactate and brain tissue concentrations of energy metabolites were measured before and after ischemia. RESULTS: Blood levels of ketone bodies increased in the butanediol-treated rats. Ischemia decreased the blood levels of acetoacetate but increased the levels of beta-hydroxybutyrate by a similar amount, resulting in unchanged high levels of total ketone bodies in the animals that received butanediol. Brain tissue levels of glucose, energy metabolites, and lactate showed no difference between butanediol- and saline-treated rats. Furthermore, compared with saline-treated animals butanediol-treated rats showed no decrease in brain damage and no attenuation in the development of postischemic seizures. CONCLUSIONS: The ketone body precursor 1,3-butanediol offers no protective effect in transient forebrain ischemia complicated by hyperglycemia.

Animals↗
PubMed1991

Influence of moderate hypothermia on ischemic brain damage incurred under hyperglycemic conditions.

Preischemic hyperglycemia aggravates brain damage following transient ischemia, and adds some special features to the damage incurred, notably a high frequency of postischemic seizures, cellular edema, and affectation of additional brain structures, such as the substanta nigra pars reticulata (SNPR). We raised the question whether mild intra-ischemic hypothermia (32-33 degrees C), known to reduce selective neuronal vulnerability in normoglycemic subjects, also ameliorates the characteristic damage observed in hyperglycemic animals. To that end, two series of experiments were performed. In the first, normo- and hypothermic animals were subjected to 10 min of ischemia during hyperglycemic conditions (plasma glucose 20-25 mmol.l-1), and allowed either 15 h or 1 week of recovery. In the second, both normo- and hyperglycemic animals were subjected to 15 min of ischemia (at normal or reduced temperature) and surviving animals were studied after 1 week of recovery. All normothermic, hyperglycemic animals developed postischemic seizures and died within the first 24 h. Mild hypothermia afforded substantial protection. Thus, 6/7 hypothermic animals subjected to 10 min of ischemia survived 1 week of recovery and none developed post-ischemic seizures. Of the hypothermic animals subjected to 15 min of ischemia 6/11 survived for 1 week, only one of which developed seizures. Protection by hypothermia was also shown by the histopathological analysis. Experiments with 10 min of ischemia and 15 h of recovery showed the expected damage in normothermic, hyperglycemic subjects. Hypothermia markedly reduced damage in all vulnerable structures, including the cingulate cortex and SNPR. The protection was most pronounced in the caudoputamen, where no affected neurons were seen in the hypothermic subjects. The experiments with 15 min of ischemia confirmed previous findings that mild hypothermia protects normoglycemic animals against the insult. The results also showed that hypothermia prevented most of the exaggeration of damage caused by hyperglycemia. However, under hypothermic conditions hyperglycemia still augmented damage in the cingulate cortex, medial and lateral venteroposterior thalamic nuclei, and SNPR, structures specifically damaged under hyperglycemic, normothermic conditions. This suggests that hypothermia has less of a protective effect on mechanisms causing such damage than on neuronal damage in the classic selectively vulnerable regions, particularly the caudoputamen.

Animals↗
PubMed1991

Neurogenic sarcoma of the sinonasal tract.

Five cases of a rare malignant sinonasal tumour of neurofibromatous nature are described. The term neurogenic sarcoma (or malignant peripheral nerve sheath tumour) is advocated instead of malignant schwannoma. The clinicopathological features of this tumour are described, and the different diagnosis are discussed. The necessity of using immunohistochemistry in the diagnosis of sinonasal tumours of fibromatous nature is emphasized. The clinical management consists of radical surgery and adjuvant radiotherapy. Clinically there seems to be a high-grade and a low-grade type of sinonasal neurogenic sarcoma, however, this could not be distinguished histologically in the present series.

Adult↗
PubMed1991

Acidosis-induced ischemic brain damage: are free radicals involved?

Substantial evidence exists that reactive oxygen species participate in the pathogenesis of brain damage following both sustained and transient cerebral ischemia, adversely affecting the vascular endothelium and contributing to the formation of edema. One likely triggering event for free radical damage is delocalization of protein-bound iron. The binding capacity for some iron-binding proteins is highly pH sensitive and, consequently, the release of iron is enhanced by acidosis. In this study, we explored whether enhanced acidosis during ischemia triggers the production of reactive oxygen species. To that end, enhanced acidosis was produced by inducing ischemia in hyperglycemic rats, with normoglycemic ones serving as controls. Production of H2O2, estimated from the decrease in catalase activity after 3-amino-1,2,4-triazole (AT) administration, was measured in the cerebral cortex, caudoputamen, hippocampus, and substantia nigra (SN) after 15 min of ischemia followed by 5, 15, and 45 min of recovery, respectively (in substantia nigra after 45 min of recovery only). Free iron in cerebrospinal fluid (CSF) was measured after ischemia and 45 min of recovery. Levels of total glutathione (GSH + GSSH) in cortex and hippocampus, and levels of alpha-tocopherol in cortex, were also measured after 15 min of ischemia followed by 5, 15, and 45 min of recovery. The results confirm previous findings that brief ischemia in normoglycemic animals does not measurably increase H2O2 production in AT-injected animals. Ischemia under hyperglycemic conditions likewise failed to induce increased H2O2 production. No difference in free iron in CSF was observed between animals subjected to ischemia under hyper- and normoglycemic conditions. The moderate decrease in total glutathione or alpha-tocopherol levels did not differ between normo- and hyperglycemic animals in any brain region or at any recovery time. Thus, the results failed to give positive evidence for free radical damage following brief periods of ischemia complicated by excessive acidosis. However, it is possible that free radical production is localized to a small subcellular compartment within the tissue, thereby escaping detection. Also, the results do not exclude the possibility that free radicals are pathogenetically important after ischemia of longer duration.

Acidosis↗
PubMed1990

Preischemic hyperglycemia and postischemic alteration of rat brain pyruvate dehydrogenase activity.

Transient cerebral ischemia in normoglycemic animals is followed by a decrease in glucose utilization, reflecting a postischemic cerebral metabolic depression and a reduction in the activity of the pyruvate dehydrogenase complex (PDHC). Preischemic hyperglycemia, which aggravates ischemic brain damage and invariably causes seizure, is known to further reduce cerebral metabolic rate. To investigate whether these effects are accompanied by changes in PDHC activity, the postischemic cerebral cortical activity of this enzyme was investigated in rats with preischemic hyperglycemia (plasma glucose 20-25 mM). The results were compared with those obtained in normoglycemic animals (plasma glucose 5-10 mM). The activated portion of PDHC and total PDHC activity were measured in neocortical samples as the rate of decarboxylation of [14C]pyruvate in crude brain mitochondrial homogenates after 5 min, 15 min, 1 h, 6 h, and 18 h of recirculation following 15 min of incomplete cerebral ischemia. In normoglycemic animals the fraction of activated PDHC, which rises abruptly during ischemia, was reduced to 19-25% during recirculation compared with 30% in sham-operated controls. In hyperglycemic rats the fraction of activated PDHC was higher during the first 15 min of recirculation. However, after 1 and 6 h of recirculation, the fraction was reduced to values similar to those measured in normoglycemic animals. Fifteen of 26 rats experienced early (1-4 h post ischemia) seizures in the recovery period. The PDHC activity appeared unchanged prior to these early postischemic seizures. We conclude that the accentuated depression of postischemic metabolic rate observed in hyperglycemic animals is not coupled to a corresponding postischemic depression of PDHC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Ischemia in normoglycemic and hyperglycemic rats: plasma energy substrates and hormones.

Seizures are a documented complication to cerebral ischemia. After 10 min of forebrain ischemia in rats, preischemic hyperglycemia invariably leads to severe, most often fatal epileptic attacks. This outcome is related to the exaggerated lactic acidosis, which has been suggested as a possible contributor to severe membrane changes and widespread edema. To find out if circulating hormones or plasma energy substrates modulate this additive damage caused by the hyperglycemia, plasma concentrations of of corticosterone, epinephrine, norepinephrine, dopamine, glucagon, insulin, glucose, free fatty acids (FFA), 3-hydroxybutyrate, and acetoacetate were measured before and in the early recirculation period after 15 min of forebrain ischemia in the rat. Plasma corticosterone levels did not differ between the normo- and hyperglycemic groups. Although not significantly different from control, the catecholamine levels showed a tendency to be higher in the hyperglycemic groups. Therefore, because catecholamines have been reported to have a protective effect during ischemia the present result cannot explain why hyperglycemia aggravates the ischemic damage. Insulin levels seemed to increase during ischemia but not significantly. Levels quickly returned to normal after 30 min of recirculation. FFA concentrations were reduced after the induction of ischemia and appeared lower in all hyperglycemic groups. The level of one of the ketone bodies, 3-hydroxybutyrate, showed a significant decrease in hyperglycemic ischemia in all groups compared with normoglycemic ischemia. The same tendency was seen for acetoacetate. Results are compatible with a protective role of ketone bodies in ischemia. It is concluded that among the hormones and substrates studied only the ketone body concentrations qualify as a modulator of the exaggerated brain damage after ischemia in hyperglycemic subjects.

Animals↗