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Biomedical subjects

O Kempski

Publications and source records attributed to O Kempski.

At least 55 records · Page 3Linked to original sources
PubMed1999

Modelling of the ischemic penumbra.

What happens to the ischemic penumbra--defined as a territory of critically reduced blood flow in the close neighborhood of an ischemic core--determines outcome after stroke. Currently the pathophysiology of the penumbra is studied predominantly in rat models with occlusion of the middle cerebral artery. Here we propose two other rat models with distinct advantages. One produces a large territory of critical flow reduction in the cortex of one hemisphere without presence of an infarct core: this model is suited to study mediator mechanisms that may transform the penumbra into necrotic tissue. It is produced by occluding one carotid artery and in addition reducing arterial pressure to 50 mm Hg using the hypobaric hypotension technique. Cortical flow is assessed by laser Doppler scanning. The second mode involves the photochemical occlusion of two adjacent cortical veins and goes along with a rather widespread reduction of cortical flow and the development of small infarcts of 2-5 mm3 infarct volume. Like the first model it is suited to administer mediators causing the infarct to grow in size, and thereby to evaluate the pathophysiologic significance of individual mediator mechanisms. In addition the model can be used to study specific therapeutic approaches.

Animals↗
PubMed1999

Surgical procedure affects physiological parameters in rat myocardial ischemia: need for mechanical ventilation.

Several surgical approaches are being used to induce myocardial ischemia in rats. The present study investigated two different operative procedures in spontaneously breathing and mechanically ventilated rats under sham conditions. A snare around the left coronary artery (LCA) was achieved without occlusion. Left lateral thoracotomy was performed in spontaneously breathing and mechanically ventilated rats (tidal volume 8 ml/kg) with a respiratory rate of 90 strokes/min at different levels of O2 supplementation (room air and 30, 40, and 90% O2). All animals were observed for 60 min after thoracotomy. Rats operated with exteriorization of the heart through left lateral thoracotomy while breathing spontaneously developed severe hypoxia and hypercapnia despite an intrathoracic operation time of <1 min. Arterial O2 content decreased from 18.7 +/- 0.5 to 3.3 +/- 0.9 vol%. Lactate increased from 1.2 +/- 0.1 to 5.2 +/- 0.3 mmol/l. Significant signs of ischemia were seen in the electrocardiogram up to 60 min. Mechanically ventilated animals exhibited a spectrum ranging from hypoxia (room air) to hyperoxia (90% O2). In order not to jeopardize findings in experimental myocardial ischemia-reperfusion injury models, stable physiological parameters can be achieved in mechanically ventilated rats at an O2 application of 30-40% at 90 strokes/min.

Animals↗
PubMed1998

In vitro and in vivo porphyrin accumulation by C6 glioma cells after exposure to 5-aminolevulinic acid.

Several malignant tissues synthesize endogenous porphyrins after exposure to 5-aminolevulinic acid (5-ALA). The present experiments have been designed to elucidate whether the C6 glioma cell, a model cell for human malignant glioma, similarly synthesizes porphyrins when exposed to 5-ALA, and whether specific synthesis occurs when C6 cells are inoculated into rat brains to form a tumor. In this situation the blood-brain barrier may interfere with 5-ALA availability, and spreading of porphyrins with edema outside the tumor may occur. Flow cytometry is used to determine the course of cell volume and porphyrin fluorescence intensities in cultured C6 cells which are incubated in 1 mM 5-ALA. For the induction of experimental brain tumors, 10(4) untreated C6 cells are inoculated into the brains of rats. After 9 days animals receive 100 mg 5-ALA/kg body weight. Brains are removed after 3, 6, or 9 h and frozen coronal sections obtained for H/E staining or fluorescence spectography. Cultured C6 cells show a linear increase of protoporphyrin IX fluorescence after exposure to 5-ALA, which begins to plateau after 85 min. Marked fluorescence is also observed in solid and infiltrating experimental tumor. However, faint fluorescence also occurs in normal tissue, basal pia, choroid plexus, and, more obviously, in white-matter tracts bordering the tumor (maximal distance: 1.5 +/- 0.7 mm). The observations demonstrate that C6 cells synthesize protoporphyrin IX after exposure to 5-ALA in vitro and in vivo. However, when utilizing 5-ALA for fluorescence detection or photodynamic therapy of brain tumors, attention should be paid to the possibility of protoporphyrin IX occurring outside the tumor.

Aminolevulinic Acid↗
PubMed1998

Superior sagittal sinus thrombosis: a clinical and experimental study.

Sinus-vein thrombosis is increasingly recognized as a much more frequent neurological disorder than was anticipated before. We examined the pathophysiology of superior sagittal sinus thrombosis (SSST) from 19 patients and a rat SSST model. We treated 19 cases with SSST who were diagnosed by angiography. The symptoms of nine patients, who suffered multiple intracerebral hemorrhage, were abrupt. In another ten patients who recovered satisfactorily, the condition progressed slowly and they were treated with heparin and urokinase. Multivariate analysis demonstrated that female, sudden onset (<24 hours) and posterior 1/3 occlusion are related to bad outcome. Experimentally, SSST was induced by ligation and slow injection of kaolin-cephalin suspension into SSS in rats. Regional cerebral blood flow (rCBF) and tissue hemoglobin oxygen saturation (Hb Sao(2)) using a "scanning" technique were measured at 48 locations, and fluorescence angiography was performed before and until 90 min after SSST induction. After 48 hours the animals were sacrificed for histological studies. Decrease of rCBF and tissue Hb SO(2) and brain damage were seen in group B (n = 10) with an extension of thrombosis from SSS into cortical veins. Brain injury was not observed in group A (n = 8) with SSS thrombus alone and sham-operated animals (n = 5). In conclusion, a brain with acute extension of thrombus from SSS into cortical veins becomes critical for cerebral blood supply and metabolism. CBF, tissue HbSO(2) and repeated angiography can be helpful monitors for the early detection of critical conditions after SSST. As to the therapy, restraint on the ongoing thrombus is essential to protect the brain with SSST, and we encourage the use of combination therapy of heparin and urokinase as early as possible in cases without intracerebral hemorrhage.

Journal Article↗
PubMed1998

Laser-Doppler scanning of local cerebral blood flow and reserve capacity and testing of motor and memory functions in a chronic 2-vessel occlusion model in rats.

BACKGROUND AND PURPOSE: An animal model of incomplete forebrain ischemia resembling human hemodynamic insufficiency was established. The model allows examination of acute and chronic changes of local cerebral blood flow (lCBF) and reserve capacity in correlation with behavioral parameters. METHODS: Anesthetized male Wistar-Kyoto rats underwent bilateral carotid occlusion (BCO). Laser-Doppler scanning of lCBF at baseline conditions and after acetazolamide was done 30 minutes after BCO, motor and memory function tests were administered after 1 and 2 days, and both investigations were repeated after 1, 2, 4, and 6 weeks. A sham-operated and a control group without any vessel manipulation served as controls. RESULTS: lCBF dropped within 60 minutes after surgery by 62% (P<0.001) in 10 animals surviving BCO (BCOsurvival) and by 69% in 5 rats that died within 9 days (BCOlethal). Acetazolamide increased lCBF to 142.33% in controls, to 136.66% in sham-operated rats (both significant), and to 104.80% in BCOsurvival (not significant), and it decreased flow by 23.1% in BCOlethal rats (P<0.001). Baseline lCBF normalized within 4 weeks. Total motor function scores were significantly reduced from 9 points preoperatively to 5.80+/-0.65 in BCOlethal and 6.68+/-0.54 points in BCOsurvival rats 1 day after occlusion. Memory retention function remained impaired after BCO, as did the acetazolamide response, which correlated with motor score and was inversely related to maze exploration time. CONCLUSIONS: This model allows long-term follow-up of cerebral function, lCBF, and reserve capacity in a pathophysiological setting similar to hemodynamic insufficiency in humans.

Acetazolamide↗
PubMed1998

Postischemic application of lipid peroxidation inhibitor U-101033E reduces neuronal damage after global cerebral ischemia in rats.

BACKGROUND AND PURPOSE: The lipid peroxidation inhibitor U-101033E was examined for effects on cerebral blood flow (CBF), cortical tissue hemoglobin oxygen saturation (HbSo2), and neuronal damage. METHODS: Fifteen minutes of global cerebral ischemia was induced by two-vessel occlusion and hypobaric hypotension. Wistar rats (n = 25) were randomized to receive vehicle (n = 9) or 40 mg/kg U-101033E (n = 9) intraperitoneally during 2 hours of reperfusion. A sham group (n = 7) had neither ischemia nor therapy. Histology was evaluated 7 days after ischemia. RESULTS: During late hyperperfusion (at 17 minutes), vehicle-treated animals had a higher (P = 0.044) cortical tissue HbSo2 (72.0 +/- 1.4%) than did U-101033E-treated animals (65.8 +/- 2.5%). Neuronal counts in the superficial cortex layer found after 7 days correlated negatively with rCBF (r = -0.76; P < 0.001) or cortical tissue HbSo2 (r = -0.56; P = 0.028) assessed during the late hyperperfusion phase. U-101033E reduced neuronal damage in hippocampal CA1 from 64.3 +/- 9.2% to 31.2 +/- 8.4% (P = 0.020), as well as in the superficial cortical layer from 53.5 +/- 14.6% to 12.8 +/- 11.7% (P = 0.046). While animals in the vehicle group had reduced counts in all four examined cortex layers (P < 0.05 versus sham group), there was significant cortical neuron loss in the U-101033E group in only one of four areas. U-101033E had no effect on resting CBF or CO2 reactivity. CONCLUSIONS: Postischemic application of U-101033E protects hippocampal CA1 and cortical neurons after 15 minutes of global cerebral ischemia. The results indicate that free radical-induced lipid peroxidation contributes to reperfusion injury, a process that can be inhibited by antioxidants such as U-101033E.

Animals↗
PubMed1998

Local cerebral blood flow autoregulation following "asymptomatic" cerebral venous occlusion in the rat.

OBJECT: Maintenance of cerebral blood flow (CBF) autoregulation in the brain is of major importance for patient outcome in various clinical conditions. The authors assessed local autoregulation after "asymptomatic" cortical vein occlusion. METHODS: In Wistar rats, a single cortical vein was occluded photochemically by using rose bengal and fiberoptic illumination. In rats with bilateral carotid artery occlusion, mean arterial blood pressure (MABP) was lowered in 5-mm Hg increments down to 40 mm Hg by using hypobaric hypotension. Local CBF at each pressure level was assessed by performing laser Doppler (LD) scanning at 25 (5 x 5) locations within bilateral cranial windows. In this manner, the lower limit of autoregulation (LLA) was detected. The LLA was 60 mm Hg in both right and left hemispheres in Group A (five rats), in which the animals received illumination without rose bengal and had no venous occlusion. Of the 11 rats that underwent vein occlusion, three developed severe reductions in local CBF and/or a growing venous thrombus and were distinguished as Group C (symptomatic; three rats); from previous work we know that those animals are bound to experience venous infarction. The remaining rats formed Group B (asymptomatic; eight rats). In this group the LLA remained at 60 mm Hg in the left hemisphere without occlusion, whereas, in the right cortex with the occluded vein, the LLA was found to be 65 mm Hg. Below a carotid stump pressure of 25 mm Hg regional CBF in the affected hemisphere dropped more abruptly to a possibly ischemic range than that in the opposite normal hemisphere. CONCLUSIONS: The results of the present study suggest that cerebral venous circulation disorders are manifested via additional pathways, that is, from a partially impaired local autoregulation in the vicinity of the occluded vein, even under conditions in which the vein occlusion itself does not cause brain damage. Care should be taken in the control of blood pressure in patients with this pathological condition.

Analysis of Variance↗
PubMed1997

Intracoronary application of C1 esterase inhibitor improves cardiac function and reduces myocardial necrosis in an experimental model of ischemia and reperfusion.

BACKGROUND: Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events, including complement activation, leukocyte adhesion, and infiltration and release of diverse mediators, probably play important roles. The present study addresses the possibility of reducing reperfusion damage by the application of C1 esterase inhibitor (C1-INH). METHODS AND RESULTS: Cardioprotection by C1-INH 20 IU/kg IC was examined in a pig model with 60 minutes of coronary occlusion, followed by 120 minutes of reperfusion. C1-INH was administered during the first 5 minutes of coronary reperfusion Compared with the NaCl controls, C1-INH reduced myocardial injury (48.8 +/- 7.8% versus 73.4 +/- 4.0% necrosis of area at risk, P < or = .018). C1-INH treatment significantly reduced circulating C3a and slightly attenuated C5a plasma concentrations. Myocardial protection was accompanied by reduced plasma concentration of creatine kinase and troponin-T. C1-INH had no effect on global hemodynamic parameters, but local myocardial contractility was markedly improved in the ischemic zone. In the short-axis view, 137 degrees of the anteroseptal region showed significantly improved wall motion at early and 29 degrees at late reperfusion with C1-INH treatment. CONCLUSIONS: C1-INH significantly protects ischemic tissue from reperfusion damage, reduces myocardial necrosis, and improves local cardiac function.

Anaphylatoxins↗
PubMed1997

[Effect of ketamine on global cerebral ischemia].

This review focuses on the significance of S-(+)-ketamine as a neuroprotective agent. Evidence in the literature supporting or contradicting a neuroprotective or even therapeutic role of ketamine in global cerebral ischaemia is critically reviewed, and data from an ongoing study in a rat global cerebral ischaemia model (15 min ischaemia with S(+)-ketamine administered 15 min after reperfusion) are reported. The number of experimental studies available so far limited, however, and therefore results cannot be considered conclusive at the present time. Only at higher ketamine dosages was protection found reliably, especially in models of complete forebrain ischaemia lasting over 10 min. In our own study, only after 90 mg/kg S(+)-ketamine was there significantly better preservation of cortical neurons than without treatment; 30 and 60 mg/kg did not produce this effect.

Animals↗
PubMed1997

An experimental model of intraoperative venous injury in the rat.

Intraoperative obliteration of cerebral veins occasionally causes unexpected severe complications, especially in elderly patients. However, very title information is available on the pathophysiology of cerebral venous circulation disturbance. Occlusion of cortical veins in rats by a photochemical thrombotic technique is a less invasive, clinically relevant and reproducible model that is suitable for the study of venous circulation disturbance. In the present study, 54 male Wistar rats were used. We examined changes of the cerebral venous flow pattern by fluorescence anglography and brain damage histologically in a one- or two-(cortical) vein occlusion model using a photochemical thrombotic technique. Approximately 30% (9 of 27) of animals in the single-vein occlusion group and 90% (15 of 17) of those in the two-vein occlusion group had microcirculation perturbation, which results very soon in the formation of venous thrombus accompanied by severe venous infarction. In addition, infarction size in the two-vein occlusion group (9.7 +/- 3.2%) was significantly larger than in the single-vein group (2.9 +/- 1.3%) (unpaired T-test, P < 0.01).In conclusion, the photochemical dye technique of attaining cerebral venous occlusion is a worth while addition to the study of circulation perturbations of the brain.

Journal Article↗
PubMed1997

Increased hypoxic tolerance by chemical inhibition of oxidative phosphorylation: "chemical preconditioning".

A short ischemic episode preceding sustained ischemia is known to increase tolerance against ischemic cell death. We report early-onset long-lasting neuroprotection against in vitro hypoxia by preceding selective chemical inhibition of oxidative phosphorylation: "chemical preconditioning." The amplitude of CA1 population spikes (psap) in hippocampal slices prepared from control animals (control slices) was 31 +/- 27% (mean +/- SD) upon 45-min recovery from 15-min in vitro hypoxia. In slices prepared from animals treated in vivo with 20 mg/kg 3-nitropropionate (3-np) 1-24 h prior to slice preparation (preconditioned slices), psap improved to 90 +/- 15% (p < 0.01). Posthypoxic oxygen free radicals were reduced to 65 +/- 10% (mean +/- SD) of control in preconditioned slices (p < 0.05). Posthypoxic neuronal density improved from 52 +/- 15% (mean +/- SD) in control slices to 97 +/- 23% in preconditioned slices (p < 0.001). Glibenclamide, an antagonist at KATP-channels, partly reversed increased hypoxic tolerance. We conclude that chemical preconditioning induces early-onset long-lasting tolerance against in vitro hypoxia. Ultimately, this strategy may be applicable as a neuroprotective strategy in humans.

Adenosine Triphosphate↗
PubMed1997

Endothelial cell swelling and brain perfusion.

BACKGROUND: Whereas the contribution of glial swelling to no-reflow conditions in the ischemic penumbra or during reperfusion after after global ischemia is widely discussed, little is known about cell volume control of endothelial cells under reperfusion conditions. METHODS: The effect of extracellular acidosis-a key mediator of secondary brain damage-on cell volume was studied in the GM7373 endothelial cell line. Experiments were performed at pH = 6.0 in the presence or absence of bicarbonate, and during exposure to inhibitors of specific transport systems such as ethyl isopropyl amiloride or 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid. RESULTS: Endothelial swelling to 111.1 +/- 3.4% was found at pHe = 6.0 in bicarbonate-buffered media. In hydroxyethyl piperin ethanesulfonic acid-buffered media, swelling was only 107.9 +/- 0.3%. 4,4'-Diisothiocyanatostilbene-2,2'-disulfonic acid reduced swelling to 102.8 +/- 0.6% in bicarbonate media, whereas swelling was completely prevented in the presence of ethyl isopropyl amiloride in hydroxyethyl piperin ethanesulfonic acid-buffered media. CONCLUSIONS: Endothelial swelling can be expected to occur in severely ischemic tissue sections and may then advance no-reflow. Therapeutic strategies should be established to prevent acidosis-induced endothelial swelling, e.g., by specific antagonists of the transport systems involved, or to reduce swelling by osmotic treatment such as hypertonic-hyperoncotic solutions.

Acidosis↗
PubMed1996

Swelling, intracellular acidosis, and damage of glial cells.

Cerebral ischemia and severe head injury among others are associated with a limited availability of oxygen, leading to cell catabolism as well as anaerobic glycolysis. Resulting metabolites, such as arachidonic- and lactic acid, can be expected to leak into perifocal brain areas, contributing there to cytotoxic swelling and damage of neurons and glia. Since elucidation of mechanisms underlying cell swelling and damage in the brain is difficult in vivo, respective investigations were carried out in vitro using suspended glial cells. Thereby, effects of arachidonic acid (AA) and of lactacidosis on glial cell volume, intracellular pH (pHi), and cell damage were analyzed utilizing flow cytometry. AA led to an immediate, dose dependent swelling and intracellular acidosis of glial cells. A concentration of 0.1 mM increased cell volume to 110% of control and decreased pHi to 7.05. Whereas glial swelling was permanent, pHi recovered to baseline after 90 min. Cell viability of 90% remained unchanged after addition of AA up to 0.1 mM, while at 0.5 mM it was significantly decreasing. Glial swelling from AA was nearly completely inhibited by the aminosteroid U-74389F or by using a Na(+)-free suspension medium for the experiment. Acidification of the medium to pH 6.8 or 6.2 led to a cell volume of 110% or 120% of control without affecting cell viability. The cells were not capable to defend their normal pHi during lactacidosis of the suspension medium but became acidotic as well. Addition of amiloride or utilization of Na(+)-free medium inhibited cell swelling from lactacidosis, while intracellular acidosis was even more pronounced. The results indicate that AA as well as acidosis are potent mediators of glial swelling and damage at levels found under pathophysiological conditions in the brain in vivo. Whereas intracellular acidification caused by AA was reversible, glial cells were unable to regulate their pHi during maintenance of extracellular acidosis. Concerning the mechanisms of glial swelling by AA, the production of oxygen- and lipid radicals might play a major role in the swelling process. The results indicate a role of the Na+/H(+)-antiporter in acidosis-induced glial swelling, whereas the exchanger has a limited significance for maintenance of pHi. As seen, the final pathway of glial swelling from both, AA and lactacidosis, requires a net influx of Na(+)-ions, probably together with Cl-ions, and osmotically obliged water.

Acid-Base Equilibrium↗
PubMed1996

"Small volume resuscitation" as treatment of cerebral blood flow disturbances and increased ICP in trauma and ischemia.

"Small volume resuscitation" (SVR) is a promising concept for the treatment of shock and trauma patients. SVR utilizes the fast infusion of a small volume of hypertonic saline to mobilize intraendothelial and parenchymal water to expand and restitute intravascular volume. Therefore it seems warranted to also consider SVR for the treatment of disturbances of the cerebral circulation and of increased intracranial pressure (ICP). The current study uses a rabbit model of global cerebral ischemia combined with mild hemorrhage to test SVR. Somatosensory evoked potentials (SEPs) serve as a short-term outcome parameter. The data demonstrate a beneficial effect treatment with hypertonic/hyperoncotic saline/hydroxyethylstarch as compared to volume replacement with starch or blood.

Animals↗
PubMed1996

[Reperfusion shock after occlusion of the superior mesenteric artery and accumulation of leukocytes within the wall of the small intestine].

The epithelial damage and the accumulation of the leucocytes within intestinal wall layers after ischemia and reperfusion was investigated in a pig model. Superior mesenteric artery (SMA) was occluded for 1 h (group 2, n = 9), 2 h (group 3, n = 6) and 3 h (group 4, n = 7) with a consecutive 2 h reperfusion period. The histological evaluation was performed on hematoxylin-eosine and Naphtol AS-D chloracetate stained preparations. The intensity of reperfusion shock depended on the duration of the intestinal ischemia. After 1 h SMA occlusion systolic blood pressure stabilized at a lower level with a normalization of the serum lactate level and the intestinal intramural pHi within the reperfusion period. After 2 h SMA occlusion the decrease of the systolic blood pressure was intensified (54-69 mm Hg) with a persistent elevated serum lactate concentration and a delayed increase of the ischemic pHi values. Reperfusion after 3 h SMA occlusion caused an irreversible shock. The epithelial damage also depended on the duration of the SMA occlusion. There were no significant changes of the leucocytic accumulation within the submucosa. But a significant increase of the number of the leucocytes was seen within the inner and the outer layer of the muscularis after 1 h SMA occlusion (106+/-5/mm2 resp. 280/mm2; p<0.05). This increase was less pronounced after 2 h (92+/-5/mm2*resp. 189+/-4/mm2; *p<0.05) and 3 h of SMA occlusion (84+/-5/mm2 resp. 185+/-23/mm2). Intestinal ischemia and reperfusion caused no changes of the leucocytic accumulation within the submucosa but a significantly increased accumulation within the muscularis after 1 h SMA occlusion, which was not seen after a more elongated occlusion period. A reperfusion shock without normalization of the serum lactate level and the intramural pHi suggesting intestinal perfusion disturbances may also lead to a depression of the leucocytic accumulation within the muscularis.

Animals↗
PubMed1996

Photodynamic therapy within edematous brain tissue: considerations on sensitizer dose and time point of laser irradiation.

Photosensitizer is known to spread with vasogenic edema fluid arising from a cerebral lesion (Neurosurg 33:1075-1082, 1993), which may be essential for sensitizing malignant cells outside the main tumor mass. The present experiments seek to elucidate whether resultant necrosis of perifocal brain tissue after laser irradiation follows a corresponding time pattern and whether damage depends on the photosensitizer dose. Male Wistar rats were anaesthetized with chloralhydrate for venous cannulation, craniotomy and focal cold lesion in order to induce vasogenic edema. Simultaneously, Photofrin II (PF II) was administered at a dose of 5 mg kg-1. The animals were re-anaesthetized after either 4, 12 or 24 h for the irradiation of lesion and perifocal tissue with 200 J cm-2 of laser light (630 nm). The brains of other animals were irradiated 4 h after cold lesion with 200 J cm-2 after receiving either 0, 2.5 or 5 mg kg-1 PF II (all groups: n = 6). Resultant necrosis was assessed planimetrically in serial coronal cryosections of brains perfusion fixed 24 h after irradiation. Necrosis was significantly enhanced with irradiation 4 h after cold lesion and photosensitizer (avg. area +/- SD: 4.3 +/- 0.7 mm2) compared with lesion only (0.84 +/- 0.2 mm2). Maximal necrosis (6.3 +/- 1.6 mm2) occurred with irradiation 12 h after lesion, whereas necrosis was only slightly increased with irradiation at 24 h (2.8 +/- 0.4 mm2). Furthermore, the area of necrosis was dependent on the sensitizer dose (0 mg kg-1: 0.7 +/- 0.3 mm2, 2.5 mg kg-1: 2.09 +/- 0.2 mm2, 5 mg kg-1: 4.3 +/- 0.7 mm2; all differences p < 0.05). Therefore, to prevent unwanted side-effects such as necrosis of edematous but otherwise healthy, peritumoral tissue in the treatment of malignant cerebral tumors by PDT, tribute should be paid to the possibility of time and dose dependent sensitization of the perifocal tissue after i.v. administration of photosensitizer.

Animals↗
PubMed1996

Monitoring of cortical blood flow: clinical relevance of experimental laser Doppler studies.

Continuous monitoring of cortical blood flow provides real time information of CBF-changes during neurosurgical operations and on the neurointensive care unit. Laser Doppler flowmetry is a continuous, noninvasive technique suitable for measurement of the cortical microcirculation. In a number of experimental studies we have analyzed the characteristics of this method for cortical blood flow monitoring. The high spatial resolution of laser Doppler flowmetry and the heterogeneity of the cortical microvascular network results in a scatter of flow values over a wide range depending on the site of measurement. Data collection from different spots and calculation of frequency histogram may serve as a measure of cortical blood flow. For clinical application instead of single fiber probes a multispot measurement approach will provide a reliable cortical blood flow monitoring. The use of continuous techniques will lead to a better understanding of cerebral hemodynamics under pathological conditions.

Animals↗