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K A Hossmann

Publications and source records attributed to K A Hossmann.

At least 109 records · Page 6Linked to original sources
PubMed1995

A modified rat model of middle cerebral artery thread occlusion under electrophysiological control for magnetic resonance investigations.

Previous magnetic resonance (MR) investigations of middle cerebral artery (MCA) occlusion in rats were limited by the lack of early post-occlusion MR measurements and/or electrophysiological monitoring. Therefore, we have developed a technique which allows to perform MCA occlusion inside the magnet under simultaneous recording of EEG and direct current (DC) potentials for monitoring the ischemic insult. Rats underwent intraluminal thread occlusion of the right MCA inside the MR tomograph via a catheter extension device, while EEG and DC potentials were recorded by non-magnetic graphite electrodes. The thread was slowly advanced until electrophysiological changes appeared. Diffusion-weighted MR images (DWI) were obtained before and repeatedly after MCA occlusion for up to 7 h. Thereafter, rat brains were frozen in situ or fixed by transcardiac perfusion and investigated by biochemical and histological techniques. In 15 of 18 animals (83%), MCA thread insertion caused immediate EEG changes and a negative DC potential shift at 4.4 +/- 1.8 min (mean +/- SD) after occlusion. In all animals with electrophysiological changes, signal intensity of DWI began to increase within the MCA territory at 12-14 min post-occlusion (the end of the first measurement), and continued to rise throughout the observation period. Ischemia was confirmed by demonstrating focal areas of energy depletion on ATP images. In the animals without electrophysiological changes, DWI or biochemical alterations were absent or confined to the central part of caudate-putamen. The histological lesion area of successfully occluded animals amounted to 70.1 +/- 5.8% of the ipsilateral hemisphere at the level of caudate-putamen.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1995

Imaging of the apparent diffusion coefficient for the evaluation of cerebral metabolic recovery after cardiac arrest.

The apparent diffusion coefficient (ADC) of water is a sensitive indicator of water and ion homeostasis of brain. Resuscitation of the brain after cardiac arrest, the most frequent reason for global cerebral ischemia under clinical conditions, depends critically on the reversal of disturbances of water and ion homeostasis. We, therefore, investigated whether ADC imaging can be used to monitor the development and reversal of ischemic brain injury during and after cardiac arrest. Ten adult mongrel normothermic cats were anesthetized with alfentanil and midazolam, immobilized with pancuronium, and mechanically ventilated with O2/N2O. Arterial, left ventricular, central venous, and intracranial pressures were monitored throughout the experiment. Magnetic resonance imaging was performed in a 4.7T MR scanner with a shielded gradient system. Diffusion-weighted images (DWI) were obtained by pulsed gradient spin echoes (diffusion weighting factor b: 0, 500, 1000, 1500 s/mm2). Quantitative ADC images were calculated from DWIs by fitting signal intensities against b-factors. Fifteen minute cardiac arrest was induced in the magnet by electrical fibrillation. Resuscitation was also carried out in the magnet, using a pneumatic vest for remotely controlled closed chest cardiac massage. Seven of 10 animals were resuscitated successfully and subsequently monitored for 3 h. During cardiac arrest, ADC declined from 678 +/- 79 x 10(-6) to 430 +/- 128 x 10(-6) mm2/s (63% of baseline). In the successfully resuscitated animals ADC returned to 648 +/- 108 x 10(-6) mm2/s within 30 min and remained at this level throughout the 3 h of recirculation. Regional evaluations of ADC revealed a transient overshoot in brainstem and basal ganglia to 114% of control at 15 min before returning to baseline values after 40 min. Failure of cardiac resuscitation prevented ADC normalization and led to its further decline to below 50% of control. Postcardiac arrest normalization of ADC maps correlated with homogeneous return of ATP, glucose, and lactate to near normal, whereas failure of ADC normalization was associated with depletion of ATP and glucose and severe lactate accumulation. In conclusion, our data indicate, that normalization of ADC is a reliable indicator of cerebral recovery after resuscitation from cardiac arrest.

Animals↗
PubMed1995

Evolution of regional changes in apparent diffusion coefficient during focal ischemia of rat brain: the relationship of quantitative diffusion NMR imaging to reduction in cerebral blood flow and metabolic disturbances.

Middle cerebral artery occlusion was performed in rats while the animals were inside the nuclear magnetic resonance (NMR) tomograph. Successful occlusion was confirmed by the collapse of amplitude on an electrocorticogram. The ultrafast NMR imaging technique UFLARE was used to measure the apparent diffusion coefficient (ADC) immediately after the induction of cerebral ischemia. ADC values of normal cortex and caudate-putamen were 726 +/- 22 x 10(-6) mm2/s and 659 +/- 17 x 10(-6) mm2/s, respectively. Within minutes of occlusion, a large territory with reduced ADC became visible in the ipsilateral hemisphere. Over the 2 h observation period, this area grew continuously. Quantitative analysis of the ADC reduction in this region showed a gradual ADC decrease from the periphery to the core, the lowest ADC value amounting to about 60% of control. Two hours after the onset of occlusion, the regional distribution of ATP and tissue pH were determined with bioluminescence and fluorescence techniques, respectively. There was a depletion of ATP in the core of the ischemic territory (32 +/- 20% of the hemisphere) and an area of tissue acidosis (57 +/- 19% of the hemisphere) spreading beyond that of ATP depletion. Regional CBF (rCBF) was measured autoradiographically with the iodo[14C]antipyrine method. CBF gradually decreased from the periphery to the ischemic core, where it declined to values as low as 5 ml 100 g-1. When reductions in CBF and in ADC were matched to the corresponding areas of energy breakdown and of tissue acidosis, the region of energy depletion corresponded to a threshold in rCBF of 18 +/- 14 ml 100 g-1 min-1 and to an ADC reduction to 77 +/- 3% of control. Tissue acidosis corresponded to a flow value below 31 +/- 11 ml 100 g-1 min-1 and to an ADC value below 90 +/- 4% of control. Thus, the quantification of ADC in the ischemic territory allows the distinction between a core region with total breakdown of energy metabolism and a corona with normal energy balance but severe tissue acidosis.

Adenosine Triphosphate↗
PubMed1995

Glial expression of the beta-amyloid precursor protein (APP) in global ischemia.

The beta-amyloid precursor protein (APP) bears characteristics of an acute-phase protein and therefore is likely to be involved in the glial response to brain injury. In the brain, APP is rapidly synthesized by activated glial cells in response to comparatively mild neuronal lesions, e.g., a remote peripheral nerve injury. Perfusion deficits in the brain result largely in neuronal necrosis and are a common condition in elderly patients. This neuronal necrosis is accompanied by a pronounced reaction of astrocytes and microglia, which can also be observed in animal models. We have therefore studied in the rat, immunocytochemically, the induction of APP after 30 min of global ischemia caused by four-vessel occlusion. The postischemic brain injuries were examined at survival times from 12 h to 7 days. From day 3 onward, APP immunoreactivity was strongly induced in the CA1 and CA4 regions of the rat dorsal hippocampus as well as in the dorsolateral striatum. In these areas, the majority of APP-immunoreactive cells were reactive glial fibrillary acidic protein (GFAP)-positive astrocytes, as shown by double-immunofluorescence labeling for GFAP and APP. Additionally, small ramified cells, most likely activated microglia, expressed APP immunoreactivity. In contrast, in the parietal cortex, APP immunoreactivity occurred focally in clusters of activated microglia rather than in astrocytes, as demonstrated by double-immunofluorescence labeling for APP and the microglia-binding lectin Griffonia simplicifolia isolectin B4. In conclusion, following global ischemia, APP is induced in reactive glial cells with spatial differences in the distribution pattern of APP induction in astrocytes and microglia.

Amyloid beta-Protein Precursor↗
PubMed1995

Delayed neuronal death after brief histotoxic hypoxia in vitro.

The effect of three metabolic inhibitors--iodoacetate, potassium cyanide, and potassium arsenate--on neuronal viability was studied in primary rat cortical and hippocampal CA1 neuronal cultures. Iodoacetate (0.1 mM) applied for 5 min to 8-day-old cultures resulted in delayed neuronal death within 3-24 h in cortical and hippocampal CA1 neurons. Neuronal degeneration was preceded by transient inhibition of energy metabolism to approximately 40% and a permanent inhibition of protein synthesis to approximately 50%. The inhibition of protein synthesis and the neuronal death were prevented by the free radical scavenger vitamin E but not by the glutamate antagonist MK-801. Removal of calcium during iodoacetate exposure could not protect against toxicity, and there was no increase of intracellular calcium concentration during and shortly after iodoacetate treatment. Cyanide and arsenate produced only partial neuronal degeneration, even at a dose of 10 mM. These observations demonstrate that brief exposure of neurons to low concentrations of iodoacetate produces a delayed type of neuronal death that is not mediated by either calcium or glutamate. The therapeutic effect of vitamin E points to a free-radical mediated injury and suggests that this type of pathology may also be involved in delayed neuronal death after transient energy depletion in vivo.

Adenine Nucleotides↗
PubMed1995

Reactive microglia in cerebral ischaemia: an early mediator of tissue damage?

Microglial cell activation is a rapidly occurring cellular response to cerebral ischaemia. Microglia proliferate, are recruited to the site of lesion, upregulate the expression of several surface molecules including major histocompatibility complex class I and II antigens, complement receptor and the amyloid precursor protein (APP) as well as newly expressed cytokines, e.g. interleukin-1 and transforming growth factor beta 1. The ischaemia-induced production of APP may contribute to amyloid deposition in the aged brain under conditions of hypofusion. Ultrastructurally, microglia transform into phagocytes removing necrotic neurons but still respecting the integrity of eventually surviving neurons even in the close vicinity of necrotic neurons. Microglial activation starts within a few minutes after ischaemia and thus precedes the morphologically detectable neuronal damage. It additionally involves a transient generalized response within the first 24 hours post-ischaemia even at sites without eventual neuronal cell death. In functional terms, the microglial reaction appears to be a double-edged sword in ischaemia. Activated microglia may exert a cytotoxic effector function by releasing reactive oxygen species, nitric oxide, proteinases or inflammatory cytokines. All of these cytotoxic compounds may cause bystander damage following ischaemia. Pharmacological suppression of microglial activation after ischaemia has accordingly attenuated the extent of cell death and tissue damage. However, activated microglia support tissue repair by secreting factors such as transforming growth factor beta 1 which may limit tissue damage as well as suppress astroglial scar formation. In line with ultrastructural observations microglial activation in ischaemia is a strictly controlled event. By secreting cytokines and growth factors activated microglia most likely serve seemingly opposed functions in ischaemia, i.e. maintenance as well as removal of injured neurons. Post-ischaemic pharmacological modulation of microglial intervention in the cascade of events that lead to neuronal necrosis may help to improve the structural and functional outcome following CNS ischaemia.

Animals↗
PubMed1995

Diffusion and perfusion MR imaging of cerebral ischemia.

Over the last few years, diffusion and perfusion magnetic resonance (MR) imaging methods have found increasing user for monitoring the effects of cerebral ischemia under clinical and experimental conditions. Blood perfusion can be visualized by studying the patency of the cerebrovascular bed (MR angiography), by recording exchange of diffusible tracers between blood and brain ([2H]water or [19F]trifluoromethane clearance), or by measuring the volume and transit time of the circulating blood (bolus track or spin-tagging imaging). In addition, changes in blood oxygenation level can be visualized by taking advantage of the susceptibility changes of the magnetic field homogeneity (functional or blood-oxygenation-level-dependent imaging). Diffusion imaging is based on the modulation of signal intensity by brain water diffusion. Recording a series of diffusion-weighted images allows calculation of the apparent diffusion coefficient (ADC) and the reconstruction of quantitative ADC images. Brain ADC changes are a function of intra-extracellular water homeostasis and therefore are a sensitive marker of ionic equilibrium. Since disturbances of ion and water homeostasis are among the first pathological alterations induced by brain ischemia, diffusion imaging is able to detect the incipient injury within minutes. Conversely, the reversal of these alterations is able to detect the incipient injury within minutes. Conversely, the reversal of these alterations is an early and reliable predictor of postischemic recovery. Applications of perfusion and diffusion imaging are reviewed in relation to the pathophysiology, the pathobiochemistry, and the therapy of evolving brain infarct after focal ischemia and the manifestation and reversal of ischemic injury during and after global ischemia.

Brain Ischemia↗
PubMed1994

NBQX reduces threshold of protein synthesis inhibition in focal ischaemia in rats.

The effect of the AMPA antagonist NBQX on peri-infarct inhibition of cerebral protein synthesis (CPS) was studied in rats subjected to 3 h occlusion of the left middle cerebral artery (MCA). Cerebral blood flow and CPS were measured with double tracer autoradiography and local ATP content was monitored by bioluminescence imaging. In untreated MCA-occluded animals the perfusion threshold of ATP depletion in cerebral cortex was 17 +/- 5 ml 100 g-1 min-1 and that of CPS inhibition was 49 +/- 13 ml 100 g-1 min-1. NBQX treatment (2 x 30 mg kg-1 after vascular occlusion) reduced the perfusion threshold of CPS inhibition to 16 +/- 6 ml 100 g-1 min-1 (p < 0.05) whereas that of ATP depletion was not affected (11 +/- 6 ml 100 g-1 min-1). The NBQX-induced pharmacological improvement of peri-infarct CPS is similar to the previously described amelioration of peri-infarct CPS by MK-801 and may contribute to the reduction of infarct size by this treatment.

Adenosine Triphosphate↗
PubMed1994

Viability thresholds and the penumbra of focal ischemia.

The classic concept of the viability thresholds of ischemia differentiates between two critical flow rates, the threshold of electrical failure and the threshold of membrane failure. These thresholds mark the upper and lower flow limits of the ischemic penumbra which is thought to suffer only functional but not structural injury. Recent studies of the functional and metabolic disturbances suggest a more complex pattern of thresholds. At declining flow rates, protein synthesis is inhibited at first (at a threshold of about 0.55 ml/gm/min), followed by a stimulation of anaerobic glycolysis (at 0.35 ml/gm/min), the release of neurotransmitters and the beginning disturbance of energy metabolism (at about 0.20 ml/min), and finally the anoxic depolarization (< 0.15 ml/gm/min). The penumbra, as defined by the classic flow thresholds, does not remain viable for extended periods. Since viability of the tissue requires maintenance of energy-dependent metabolic processes, penumbra is redefined as a region of constrained blood supply in which the energy metabolism is preserved. Imaging of the penumbra by combining autoradiographic cerebral blood flow measurements with bioluminescent images of adenosine triphosphate (ATP) demonstrates a gradual expansion of the infarct core (in which ATP is depleted) into the penumbra until, after a few hours, the penumbra has disappeared. It is suggested that the limited survival of the penumbra is due to periinfarct depolarizations, which result in repeated episodes of tissue hypoxia, because the increased metabolic workload is not coupled to an adequate increase of collateral blood supply. This explains pharmacological suppression of periinfarct depolarizations lowering the threshold of metabolic disturbances and reducing the volume of the ischemic infarct.

Adenosine Triphosphate↗
PubMed1994

Transient cell depolarization after permanent middle cerebral artery occlusion: an observation by diffusion-weighted MRI and localized 1H-MRS.

Focal cerebral ischemia causes rapid intensity changes in diffusion-weighted images (DWI) and elevated lactate as detected by localized proton spectroscopy (1H-MRS). To investigate whether such changes can also be evoked by perischemic depolarizations, we combined DWI and 1H-MRS measurements with DC potential recordings. About 40 min after occlusion of the middle cerebral artery in a rat, a negative DC deflection was observed indicating transient cell depolarization. Coincidentally with the depolarization a transient increase of the DWI signal intensity and a partially reversible increase of lactate occurred in the periphery of the ischemic territory. These results show that peri-ischemic depolarization, known to contribute to the evolution of cerebral infarction, evokes disturbances that can be detected by DWI and 1H-MRS.

Animals↗
PubMed1994

Quantitative diffusion MR imaging of cerebral tumor and edema.

The detection of brain tumors using standard techniques of qualitative, relaxation-weighted magnetic resonance imaging (MRI) requires the application of contrast agents. We investigated whether or not it is possible to use diffusion-weighted MRI to localize tumors without contrast enhancement. Three different experimental rat brain tumors were studied: F98 glioma, RN6 Schwannoma and E376 neuroblastoma. We found a marked hypointensity in the region of the tumor and edema in heavily diffusion-weighted images, which corresponded well with the histological presentation. Quantitative maps of the apparent diffusion coefficient (ADC) allowed a better localization of the tumor than that obtained by regional presentation of T2 times, particularly under conditions in which peritumoral edema was absent. The ADC differences of the three tumor types were statistically not significant. Based upon regions-of-interest evaluations, tumor could be distinguished from peritumoral edema and normal brain tissue. However, a sharp demarcation between tumor and peritumoral edema was not possible, and this is attributed to a similar enlargement of interstitial space. It was concluded that diffusion-weighted MRI possesses a high potential for the detection of brain tumors but does not allow precise demarcation of the tumor border.

Animals↗
PubMed1994

Proton MR spectroscopy of experimental brain tumors in vivo.

F98 gliomas, E367 neuroblastomas, and RN6 Schwannomas in rat brain were studied non-invasively in vivo by localized proton MR spectroscopy (MRS). The spectra obtained from homotopic brain contralateral to the tumors were qualitatively indistinguishable from those of normal rat brain in vivo and showed resonance lines assigned to N-acetylaspartate, glutamate, total creatine (creatine and phosphocreatine), choline, glucose, and myo-inositol. The tumor spectra displayed marked differences compared to those obtained from contralateral brain. There were increases in choline, myo-inositol and lipids, which are presumably associated with increased membrane turnover. The presence of lactate indicated anaerobic glycolysis. Other differences included the absence of signals from NAA resulting from the destruction or displacement of neuronal tissue by the tumor. There was also a loss of total creatine. Although the spectra of all three tumor types were distinct from contralateral brain, there were no obvious differences between the different tumor types.

Animals↗
PubMed1994

Protein synthesis in the hippocampal slice: transient inhibition by glutamate and lasting inhibition by ischemia.

Protein synthesis was measured in hippocampal slices which were exposed to glutamate (1 mM or 10 mM) or which were deprived of glucose and oxygen ('in vitro ischemia') for 15 min. Glutamate at 1 mM, a concentration estimated to occur during in vivo ischemia did not affect protein synthesis. Ten mM glutamate inhibited protein synthesis immediately after exposure (50% of control values) and reduced ATP levels to about 30% of the control. After two hours, slices fully recovered their protein synthesis and energy metabolism. The effect of 10 mM glutamate was not receptor-mediated, as NMDA, AMPA, or metabotropic receptor antagonists failed to block the glutamate effect. Immediately after ischemia, protein synthesis was reduced to 30% of control values, and 2 hours later it was still depressed to one-half of control values. Energy charge, however, recovered completely. Ischemic inhibition of protein synthesis was not reversed by glutamate receptor antagonists. The data indicate that inhibition of protein synthesis in hippocampal slices during ischemia is not glutamate-dependent.

Animals↗
PubMed1994

Effect of serum on intracellular calcium homeostasis and survival of primary cortical and hippocampal CA1 neurons following brief glutamate treatment.

Glutamate neurotoxicity was studied in primary neuronal cultures prepared from rat cerebral cortex and hippocampal CA1 sector. Neurons were cultivated with 5% native horse serum and then exposed to 0.1 or 1.0 mM glutamate for 5 min. Subsequently, neurons were allowed to recover for 24 hours either in the presence or in the absence of 5% native horse serum. In the absence of serum, neurons showed morphological signs of degeneration and exhibited marked loss of vitality as tested by vital staining and release of lactate dehydrogenase (LDH). In contrast, when neurons were cultivated in the presence of serum, no degenerative changes were seen and the neurons survived. Heat inactivated serum did not prevent neuronal death but addition of basic fibroblast growth factor (bFGF) or transforming growth factor-beta 1 (TGF-beta 1) had the same protective effect as native serum. Measurements of intracellular calcium activity ([Ca2+]i) with the indicator dye fura-2 revealed a sharp increase during glutamate exposure. In the absence of serum, [Ca2+]i returned to near control within 5 min but it secondarily increased after 1 hour to almost the same level as during glutamate exposure. This delayed increase was more pronounced in CA1 than in cortical neurons, it correlated linearly with the initial rise during glutamate exposure, and it was greatly reduced in the presence of serum. These observations suggest that glutamate neurotoxicity in vitro is a function of the delayed and not of the primary rise of intracellular calcium activity, and that trophic factors prevent neurotoxicity by attenuating this delayed response.

Animals↗
PubMed1994

Prevention of periinfarct direct current shifts with glutamate antagonist NBQX following occlusion of the middle cerebral artery in the rat.

The effect of the glutamate (AMPA subtype) receptor antagonist NBQX on periinfarct direct current (DC) shifts and cortical ATP depletion volume was examined in rats subjected to 3 h of occlusion of the middle cerebral artery (MCA). MCA occlusion produced an immediate DC shift in the periphery of the ischemic territory. Vehicle-treated (untreated) animals developed one to five additional DC shifts (median, 2) during the 3-h occlusion time. NBQX treatment (2 x 30 mg/kg i.v. immediately after MCA occlusion and 1 h later) significantly reduced the number of DC deflections (median, 0; range, 0-2; p < 0.05) without changing blood flow in the border zone of the infarct (untreated, 50.6 +/- 10.6%; NBQX-treated: 51.9 +/- 7.7% of control; mean +/- SD). NBQX treatment significantly decreased the cortical volume of ATP depletion (untreated, 75.3 +/- 11.4 mm3; NBQX-treated, 47.9 +/- 10.1 mm3; p < 0.05). Moreover, a significant linear relationship between the number of periinfarct DC shifts and the volume of cortical ATP depletion was obtained (y = 38.3 + 9.4x; r = 0.866; p < 0.001). The reduction of brain infarct volume by NBQX treatment is explained by the suppression of DC shifts and the decrease of metabolic workload in hemodynamically compromised cortex.

Animals↗
PubMed1994

Differential expression of the immediate early genes c-fos, c-jun, junB, and NGFI-B in the rat brain following transient forebrain ischemia.

The temporospatial expression pattern of four immediate early genes (IEGs) (c-fos, c-jun, junB, NGFI-B) following 30 min of global ischemia was investigated in rat brains by in situ hybridization and immunohistochemistry (c-fos). All examined IEG mRNAs, as well as Fos-like immunoreactivity, increased transiently in vulnerable and resistant brain regions following ischemia, but the induction profiles were distinct. Ischemia caused a post-ischemic early-onset, transient c-fos induction in wide-spread regions, as well as a late-onset induction restricted to vulnerable regions. Late-onset c-fos induction was observed in the CA1 region and the ventral thalamus but not in the striatum or neocortex, where neurons degenerate at a quicker pace. After recirculation, c-jun mRNA appeared to be initially coinduced with c-fos mRNA, but c-jun mRNA levels remained elevated or increased in various regions, including all vulnerable regions, when c-fos mRNA had already declined to near basal levels. Compared to c-fos and c-jun, junB induction was less pronounced and confined largely to the dentate gyrus. NGFI-B mRNA increased moderately and only in brain regions exhibiting the most dramatic c-fos increases and with similar kinetics. The differential activation of the investigated IEGs suggests that rather complex long-term adaptive processes may be initiated at the genomic level after global ischemia. The present findings provide further evidence that the activation of IEGs forms part of the brain's metabolic response to ischemia, but no simple correlation appears to exist between the induction of the investigated IEGs and the phenomenon of selective vulnerability.

Animals↗
PubMed1994

Cortical negative DC deflections following middle cerebral artery occlusion and KCl-induced spreading depression: effect on blood flow, tissue oxygenation, and electroencephalogram.

In the periphery of ischemic brain lesions, transient spreading depression-like direct current (DC) deflections occur that may be of pathophysiological importance for determining the volume of the ischemic infarct. The effect of these deflections on cerebral blood flow, tissue oxygen tension, and electrophysiology was studied in rats submitted to intraluminal thread occlusion of the middle cerebral artery (MCA) and compared with the changes following potassium chloride (KCl)-induced spreading depression of intact animals. Immediately after MCA occlusion, cortical laser-Doppler flow (LDF) in the periphery of the MCA territory sharply decreased to 35 +/- 14% of control (mean +/- SD; p < 0.05), tissue PO2 declined from 28 +/- 4 to 21 +/- 3 mm Hg (p < 0.05), and EEG power fell to approximately 80% of control. During 7-h occlusion, 3-11 DC deflections with a mean duration of 5.2 +/- 4.8 min occurred at irregular intervals, and EEG power gradually declined to 66 +/- 16% of control (p < 0.05). During the passage of DC deflections, LDF did not change, but PO2 further declined to 19 +/- 4 mm Hg (p < 0.05). KCl-induced depolarizations of intact rats were significantly shorter (1.4 +/- 0.5 min; p < 0.05) and were accompanied by a 43% increase in LDF (p < 0.05) and a slight but significant increase in tissue PO2 from 22 +/- 4 to 25 +/- 4 mm Hg (p < 0.05). The comparison of periinfarct and KCl-induced depolarizations demonstrates that oxygen requirements are not coupled to an appropriate flow response in the periinfarct zone with severely reduced blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗