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O Kempski

Publications and source records attributed to O Kempski.

At least 37 records · Page 2Linked to original sources

Plasma protein loss during surgery: beneficial effects of albumin substitution.

Plasma protein loss during abdominal surgery is a known phenomenon, but its possible pathophysiological relevance has remained unknown. The present study evaluates the effects of albumin substitution on systemic and local hemodynamics and cellular interactions in the mesenteric microcirculation. Rats underwent median laparotomy and exteriorization of an ileal loop for intravital microscopy of the mesenteric microcirculation. Plasma protein concentrations, systemic and local hemodynamics were recorded during the follow up period, with or without albumin substitution. Depending on the time course of plasma protein loss in control experiments, 80% of the calculated protein loss was infused during the first 2 h of surgery, and the other 20% over the following 5 h of intravital microscopy. The control group received a continuous infusion of normal saline. Plasma protein loss was mainly due to loss of albumin. A significant increase in adherent and rolling leukocytes was observed during the course of mesenteric exteriorization, which was almost entirely reversed by albumin replacement. Albumin substitution led to stabilisation of mean arterial pressure and abdominal blood flow and also attenuated reductions in arterial base excess. Albumin infusions to replace plasma protein loss may be a simple and effective measure to attenuate microcirculatory disturbances and may be of benefit in patients undergoing abdominal surgery.

Abdomen↗

Early-onset tolerance in rat global cerebral ischemia induced by a mitochondrial inhibitor.

It was studied whether a subtoxic dose of the mitochondrial neurotoxin, 3-nitropropionic acid (3-NPA), can initiate early-onset tolerance induction for subsequent ischemic injury. Wistar rats were pretreated for 3 h by intraperitoneal 3-NPA (20 mg/kg body weight; n=13) or solvent (n=12). Fifteen minutes global cerebral ischemia was induced by bilateral carotid artery occlusion and hypobaric hypotension. rCBF and tissue hemoglobin oxygen saturation were measured by laser Doppler scanning and a microspectrophotometric method. Ischemic insult and brain temperature were identical in both groups. Body weight and neurological scores recovered in the pretreated group but further deteriorated in the non-treated group (P<0.05). Quantitative histology demonstrated a better neuronal density in neocortex and hippocampal CA2, CA3, and CA4 of pretreated animals (P<0.05).

Animals↗

Mechanisms of arachidonic acid induced glial swelling.

Accumulation of arachidonic acid (AA) in the brain during ischaemia may contribute to development of brain oedema. In this study we investigated the effect of selected drugs on AA-induced cytotoxic brain oedema in C6 glioma cells. Suspended C6 glioma cells were preincubated with drugs and AA (0.1 mM) was added. When no drug was administered cell volume increased immediately after the addition of AA with a maximum cell swelling of 13.1+/-1.9% at 15 min (mean +/- S.E. M.). Preincubation of cells with BW 755C, a dual inhibitor of cyclo- and lipoxygenases, showed no reduction in cell swelling from AA, whereas superoxide dismutase, amiloride and the protein kinase inhibitor H-9370 led to a significant attenuation of volume increase (p<0.05). The role of Na(+) ions during cell swelling from AA was evaluated after pretreatment of C6 glioma cells with ouabain. This resulted in a reversal of cell swelling (p<0.01). We conclude that there is potential involvement of free radicals, signal transduction systems and intracellular accumulation of Na(+) ions in glial cell swelling from AA.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗

Effects of cortical spreading depression on cortical blood flow, impedance, DC potential, and infarct size in a rat venous infarct model.

A cortical venous infarction model has been evaluated as to the degree of regional flow reduction and by studying effects of cortical spreading depression (CSD). Two adjacent cortical veins were occluded photochemically with rose bengal and fiberoptic illumination. Seven rats served to demonstrate effects on regional cortical blood flow using laser Doppler scanning. In 36 rats local CBF, DC potential, and brain tissue impedance were measured continuously for 75 min after vein occlusion. No, 3, or 10 CSD waves were induced by potassium chloride injection during the initial 75 min. Rats were compared for spontaneous CSDs; baseline local CBF, CBF, and impedance response to CSD; and infarct volume. Seventy-five minutes after vein occlusion regional cortical flow in a 3.5x7-mm window was reduced to 34.3+/-13.2%. At 45% of the 840 measured locations in 7 rats flow was <40% baseline and at 27.3% <30%, indicating a widespread penumbra territory. During the initial 75 min 2.1+/-1.1 spontaneous CSDs were observed. There was a positive correlation between the number of spontaneous CSDs seen acutely and infarction volume after 5 days. Moreover, brain injury was significantly increased in the group with 10 KCl-induced CSDs. A reduced 1CBF response and an overshooting tissue impedance change during CSD were predictors of ischemic damage. This study demonstrates a CSD-related growth of the venous infarct. Second, the data indicate that flow after two-vein occlusion resembles that seen under penumbra conditions, allowing for studies of damage mechanisms responsible for infarct growth.

Acute Disease↗

Plastic foil technique attenuates inflammation in mesenteric intravital microscopy.

BACKGROUND: Interpretation of intravital microscopic observations is complicated by the "inflammatory"-type response to the trauma inflicted on the tissue by the surgical preparation. The present study evaluates different experimental conditions for prolonged observations of the mesenteric microcirculation in the rat. METHODS: The mesentery was exteriorized through a median laparotomy and subjected to an organ bath or a modified plastic foil technique. Hemodynamic, metabolic, respiratory, and microcirculatory data were analyzed. RESULTS: In contrast to the plastic foil technique, which yielded stable baseline values over a 5-h observation period, venular velocity and wall shear rates decreased significantly in the organ bath technique, and leukocyte adhesion to the endothelium was significantly increased. Likewise, abdominal blood flow decreased significantly by 35% and base excess declined (-10.0+/-0.4 mmol/L) in the organ bath, with reduced pco(2) (26.4+/-2.5 mm Hg vs. 33.7+/-1.1 mm Hg in plastic foil technique) due to respiratory pH compensation. CONCLUSIONS: The plastic foil technique was found clearly superior to the organ bath technique for maintenance of stable baseline metabolic, hemodynamic, and microcirculatory conditions in mesenteric intravital microscopy.

Animals↗

Laser Doppler scanning: how many measurements are required to assess regional cerebral blood flow?

This study was initiated to determine the optimal number of measuring sites necessary to estimate regional cerebral blood flow (CBF) under pathophysiological conditions. 25 rats were exposed to 15 minutes of global cerebral ischemia. Local CBF was sequentially measured by laser Doppler (LD) at 32 locations during baseline conditions, ischemia and reperfusion using a computer-controlled scanning technique. A simulation study was performed based on 800 local measurements at each time point: random samples (size 1-100) were repeatedly drawn to estimate the variability of median flow. Accuracy was defined as probability that the simulated median differed less than +/- 5 LD-units from the true median of the 800 data. Above a single location, CBF was measured with an accuracy of 21.6 +/- 0.4% (baseline conditions, n = 100 simulations, mean +/- SEM), 85.8 +/- 0.4% (ischemia) and 11.1 +/- 0.3% (30th min. reperfusion). Accuracy increases to 75.2 +/- 0.5% (baseline conditions), 100 +/- 0% (ischemia) and 41.8 +/- 0.6% (30th min. reperfusion) if 24 locations are scanned. Scanning, therefore, improves accuracy and reduces variability of CBF measurements. With enough local CBF measurements laser Doppler assessment of regional CBF is possible. Single location CBF assessment is sufficiently accurate only during ischemia. During reperfusion, when accuracy is half reduced compared to baseline conditions, larger sample sizes are required.

Animals↗

Spreading depression induces permanent cell swelling under penumbra conditions.

BACKGROUND: Spreading depression (SD) is known to go along with temporary breakdown of ion gradients and cell swelling which spontaneously normalizes. Here, the effects of SD at reduced flow conditions as encountered in the ischemic penumbra are examined. METHODS: In rats the right carotid artery was permanently occluded. MABP was lowered to 50 mmHg for 30 min. This is sufficient to reduce CBF to penumbra-like conditions in the right hemisphere. The following parameters were assessed: rCBF, DC potential, and tissue impedance. 5 or 15 min after onset of flow reduction one SD wave was initiated by microinjection of KCl. Histology was performed after 7 days. RESULTS: In animals with hypotension there was depolarization resembling anoxic depolarization after SD induction and an uncoupling of CBF and metabolism only in the right hemisphere. Impedance increased with SD but did not recover spontaneously as long as rCBF remained reduced. 15 min of SD-induced cell swelling was tolerated without permanent damage, whereas 25 min were followed by severe neuron loss in the affected cortex after 7 days. CONCLUSIONS: The study demonstrates the induction of penumbra conditions in the cortex of one hemisphere. SD is followed by cell swelling which persists as long as flow is critically reduced. The experiments illustrate how peri-infarct depolarizations may detrimentally affect the penumbra.

Animals↗

Investigation of iodine-123-labelled amino acid derivatives for imaging cerebral gliomas: uptake in human glioma cells and evaluation in stereotactically implanted C6 glioma rats.

In developing iodine-123-labelled amino acid derivatives for imaging cerebral gliomas by single-photon emission tomography (SPET), we compared p-[123I]iodo-L-phenylalanine (IPA), L-[123I]iodo-1,2,3,4-tetrahydro-7-hydroxyisoquinoline-3-carboxylic acid (ITIC) and L-3-[123I]iodo-alpha-methyltyrosine (IMT) with regard to their uptake in human glioblastoma T99 and T3868 cells, and thereafter studied the mechanisms promoting the cellular uptake. The potential of the 123I-iodinated agents for use as SPET radiopharmaceuticals was evaluated in healthy experimental rats as well as in rats with stereotactically implanted C6 gliomas. The radiopharmaceutical uptake into glioblastoma cells was rapid, temperature and pH dependent, and linear during the first 5 min. Equilibrium was reached after 15-20 min, except in the case of ITIC, the initial uptake of which gradually decreased from 15 min onwards. The radioactivity concentration in glioma cells following 30-min incubation at 37 degrees C (pH 7.4) varied from 11% to 35% of the total activity per million cells (ITIC < IMT < or = IPA). Competitive inhibition experiments using alpha-(methylamino)-isobutyric acid and 2-amino-2-norbornane-carboxylic acid, known as specific substrates for systems A and L, respectively, as well as representative amino acids preferentially transported by system ASC, indicated that IPA, like IMT, is predominantly mediated by the L and ASC transport systems, while no significant involvement of the A transport system could be demonstrated. By contrast, none of the three principal neutral amino acid transport systems (A, L and ASC) appear to be substantially involved in the uptake of ITIC into glioblastoma cells. Analysis of uptake under conditions that change the cell membrane potential, i.e. in high K+ medium, showed that the membrane potential plays an important role in ITIC uptake. Alteration of the mitochondrial activity by means of valinomycin or nigericin induces a slight increase or decrease in the radiopharmaceutical uptake, suggesting a minor contribution of the mitochondria in the uptake. IPA, IMT and ITIC passed the blood-brain barrier, and thereafter showed efflux from the brain. The radioactivity concentration in healthy rat brain 15 min following intravenous injection varied from 0.07% (ITIC) to 0.27% ID/g (IPA). In comparison, the brain uptake in the stereotactically implanted C6 glioma rats was substantially higher (up to 1.10% ID/g 15 min p.i.), with tumour-to-background ratios greater than 4. These data indicate that IPA and ITIC, like IMT, exhibit interesting biological characteristics which hold promise for in vivo brain tumour investigations by SPET.

Alanine↗

Migratory activity of human glioma cell lines in vitro assessed by continuous single cell observation.

A new migration assay, the time-lapse individual cell migration assay (TIM-assay), was developed, which allows the observation of cells over 24 h under controlled conditions. Using this technique, the migratory behavior of 8 human glioblastoma cell lines in vitro was studied. Special features are simultaneous documentation of migratory parameters of individual cells, i.e., migration velocities and migration paths of individual cells. Migration velocity for cell populations of the same cell line ranged from 0 to 24 microm/h. The migration paths were examined for being directional. Two thirds of all cells showed directional migration. Migration paths were further classified according to visual judgements for being linear, oscillating or mixed. The migration index had a mean of 91%. The presented TIM-assay allows the assessment of several new parameters. that may be useful to identify subgroups of gliomas with different biological characteristics.

Adult↗

Tolerance-Inducing dose of 3-nitropropionic acid modulates bcl-2 and bax balance in the rat brain: a potential mechanism of chemical preconditioning.

Many studies have reported ischemia protection using various preconditioning techniques, including single dose 3-nitropropionic acid (3-NPA), a mitochondrial toxin. However, the cellular signal transduction cascades resulting in ischemic tolerance and the mechanisms involved in neuronal survival in the tolerant state still remain unclear. The current study investigated the mRNA and protein expression of the antiapoptotic bcl-2 and the proapoptotic bax. two antagonistic members of the bcl-2 gene family, in response to a single dose of 3-NPA, to global cerebral ischemia-reperfusion. and to the combination of both 3-NPA-pretreatment and subsequent global cerebral ischemia-reperfusion. Brain homogenates of adult Wistar rats (n = 25) were analyzed for bcl-2 and bax mRNA expression using a new highly sensitive and quantitative polymerase chain reaction (PCR) technique that allows real-time fluorescence measurements of the PCR product (LightCycler; Roche Diagnostics, Mannheim, Germany). Animals for mRNA analysis received 3-NPA (20 mg/kg, intraperitoneal; "chemical preconditioning") or vehicle (normal saline), and were either observed for 24 plus 3 hours or were subjected to 15 minutes of global cerebral ischemia 24 hours after the pretreatment and observed for 3 hours of reperfusion. Immunohistochemistry was applied to serial brain sections of additional rats (n = 68) to determine amount and localization of the respective Bcl-2 and Bax protein expression in various brain areas. One set of animals was injected with 3-NPA and observed for 3, 12, 24, and 96 hours; a second set was exposed to 15 minutes global cerebral ischemia, 3, 12, and 24 hours reperfusion; and a third set was pretreated with 3-NPA or saline 24 hours before the ischemic brain insult and observed for 96 hours of reperfusion. The authors found single dose 3-NPA treatment to be associated with an elevated bcl-2:bax ratio (increased bcl-2 expression, decreased bax expression), both on the transcriptional (mRNA) and the translational (protein) level. The differential influence of 3-NPA was maintained during early recovery from global cerebral ischemia (3 hours), when 3-NPA pretreated animals showed higher bcl-2 and lower bax mRNA levels compared with rats with saline treatment. Respective changes in protein expression were localized predominately in neurons vulnerable to ischemic damage. Compared with baseline, Bcl-2 protein was significantly higher in surviving neurons at 96 hours after the insult, whereas Bax protein remained unchanged. However, at this late time of postischemic recovery (96 hours), the protein expression pattern of surviving neurons was not different between animals with and without 3-NPA pretreatment. To the authors' knowledge, the current study is the first report on the differential expression of pro- and antiapoptotic genes after a single, nonlethal dose of 3-NPA. The current results suggest alterations in the balance between pro- and antiapoptotic proteins as a potential explanation for the reported protection provided by chemical preconditioning using 3-NPA in rats.

Animals↗

Significance of resting and stimulated cerebral blood flow for predicting the risk of hemodynamic cerebral ischemia in a model of chronic hemodynamic insufficiency.

OBJECTIVE: It has been postulated that patients with a compromised cerebrovascular reserve capacity (RC), defined as cerebral blood flow (CBF) response to acetazolamide (ACZ) (by percent), are at higher risk for ischemic stroke. The value of CBF and RC for predicting the risk of hemodynamically induced impairment of cerebral function is examined. METHODS: Both common carotid arteries were occluded in 22 Wistar-Kyoto rats. Thirty-one days later, mean arterial blood pressure was reduced to 40 mm Hg for 30 minutes. Laser Doppler scanning of CBF at resting conditions and after intraperitoneal administration of ACZ (0.1 mg/g body weight) was performed 30 minutes and 28 days after occlusion as well as before and during hypotension. Memory and motor functions were examined before and after CBF measurements. RESULTS: After occlusion, CBF dropped significantly and ACZ did not increase CBF. Four weeks later, resting CBF had significantly improved but remained impaired, as did RC, showing a distinct interindividual variability. Hypotension reduced CBF by 57 +/- 4% (P < 0.001) and significantly impaired memory and motor functions. CBF during hypotension correlated with resting CBF before hypotension (r = 0.495, P = 0.027) and with CBF before (r = 0.392, P = 0.048) and after (r = 0.476, P = 0.034) ACZ, as determined 4 weeks after occlusion. There was no correlation with RC (r = 0.091, P = 0.702). Neurological tests performed 1 day after hypotension correlated with CBF during hypotension (memory function, P = 0.03; motor function, P = 0.02) but not with RC. CONCLUSION: In this model of chronic hemodynamic insufficiency, the risk of impairment to global cerebral function was predicted by resting CBF and CBF after ACZ but not by RC determined with ACZ.

Acetazolamide↗

Tightness of duraplasty in rabbits: a comparative study.

OBJECTIVE: The purpose of this study was to test, in rabbits, the tightness of seven dural substitution materials commonly used in neurosurgery, i.e., Lyodura (B. Braun Melsungen AG, Melsungen, Germany), Tutoplast dura (Tutogen Medical, Inc., Parsippany, NJ), Tutoplast fascia lata (Tutogen Medical, Inc.), autologous periosteum, Neuropatch (B. Braun Melsungen AG), Dacron (E.I. du Pont de Nemours and Co., Wilmington, DE), and Ethisorb (Ethicon, Inc., Somerville, NJ). METHODS: Duraplasties were performed with sutures alone or were additionally fixed with fibrin glue. Leakage pressures were assessed by infusion of artificial cerebrospinal fluid, containing sodium fluorescein, into the cisterna magna and detection of fluorescence using a charge-coupled display camera with background substraction, 3 days, 3 weeks, or 3 months after surgery. RESULTS: Three days after implantation, the mean tightness values of duraplasties with Lyodura or Neuropatch were significantly higher (P = 0.007) than the values for the other substitutes. A significant improvement of tightness with increasing implantation time could be demonstrated for autologous periosteum (P = 0.0063). Improvement of tightness with the use of fibrin glue could be proven only for the heterologous grafts (P = 0.0071). The tightness values for Neuropatch fixed only with sutures were similar to those for the best heterologous substitutes implanted with additional fibrin glue. Lyodura, Tutoplast dura, and Neuropatch demonstrated favorable implantation characteristics; they were thin, flexible, and easily suturable. Neither adhesions to the brain nor space-occupying scars were noted. CONCLUSION: These results confirm the excellent suitability of Lyodura and Neuropatch for dural substitution.

Animals↗

Hypertonic/hyperoncotic resuscitation after intestinal superior mesenteric artery occlusion: early effects on circulation and intestinal reperfusion.

The objective of the study was to determine the early effects of hypertonic/hyperoncotic starch resuscitation after 2 h occlusion of the superior mesenteric artery (SMA) in comparison to animals reperfused without treatment and isotonic resuscitation. SMA was clamped (18 pigs, 19-23 kg) for 2 h followed by a 2-h reperfusion period, which was initiated with isotonic (ISO) (35 mL/kg 0.9% NaCl and 5 mL/kg 10% hydroxyethyl starch within 30 min) or hypertonic/hyperoncotic resuscitation (HHES) (7.5% NaCl/10% hydroxyethyl starch within 5 min). Cardiac output (CO), mean arterial blood pressure (MAP), serum lactate, antimesenteric serosal Laser-Doppler values (LD), and intramural pHi (tonometry) were measured. Without resuscitation at the onset of reperfusion MAP (70 +/- 3 mmHg) decreased to 40 +/- 3 mmHg and CO to 31% of baseline values after 30 min. Serum lactate increased to 5.1 +/- 1.6 mmol/L without improvement. The decrease of CO was attenuated only during the initial 30 min of reperfusion in the ISO group, but significantly better counteracted by hypertonic/hyperoncotic resuscitation. Without treatment, LD flow of the ileum (baseline 23-27 LD units) recovered but intramural pH (pHi) remained significantly decreased (7.26 +/- 0.05). With isotonic resuscitation LD values (21.8 +/- 2.1 LD units) and intramural pHi (7.09 +/- 0.14) decreased even more (P < 0.05) whereas the HHES group showed a significant hyperemic reaction and a normalization of the intramural pHi and serum lactate within 30 min. Hypertonic/hyperoncotic resuscitation significantly improves MAP and CO during reperfusion shock and induces an immediate hyperemic reperfusion reaction of the intestinal microcirculation. Adequate isotonic fluid replacement in order to restore the postischemic plasma volume loss may cause a pronounced deterioration of intestinal perfusion.

Animals↗

Mechanisms of endothelial cell swelling from lactacidosis studied in vitro.

One of the early sequelae of ischemia is an increase of circulating lactic acid that occurs in response to anaerobic metabolism. The purpose of the present study was to investigate whether lactic acidosis can induce endothelial swelling in vitro under closely controlled extracellular conditions. Cell volume of suspended cultured bovine aortic endothelial cells was measured by use of an advanced Coulter technique employing the "pulse area analysis" signal-processing technique (CASY1). The isosmotic reduction of pH from 7.4 to 6.8 had no effect on cell volume. Lowering of pH to 6.6, 6.4, or 6.0, however, led to significant, pH-dependent increases of cell volume. Swelling was more pronounced in bicarbonate-buffered media than in HEPES buffer. Specific inhibition of Na(+)/H(+) exchange by ethylisopropylamiloride completely prevented swelling in HEPES-buffered media. Pretreatment with ouabain to partially depolarize the cells did not affect the degree of acidosis-induced swelling. In bicarbonate-buffered media, the inhibition of transmembrane HCO(3)(-) transport by DIDS reduced swelling to a level comparable with that seen in the absence of bicarbonate ions. Lactacidosis-induced endothelial swelling, therefore, is a result of intracellular pH regulatory mechanisms, namely, Na(+)/H(+) exchange and bicarbonate-transporting carriers.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

Effect of age on cerebral venous circulation disturbances in the rat.

OBJECT: Mild cerebral venous circulation disturbances (CVCDs) in aged patients are frequently known to cause unexpectedly severe postoperative complications in neurosurgical practice. The object of the present study was to determine whether there are age-related differences involved in vulnerability to CVCDs. METHODS: Thirty-eight male Wistar rats were used. A single cortical vein with a 100-microm diameter was occluded photochemically by using rose bengal dye and fiberoptic illumination in young (Group Y, 19 animals aged 10-14 weeks) and aged (Group A, seven animals aged 80-100 weeks) rats. Five young and seven aged animals served as sham-operated controls. Regional cerebral blood flow (rCBF) was determined from local CBF, which was measured at 25 (5 x 5) identical locations, with the occluded vein located central to the scanning field, by using a laser Doppler scanning technique every 15 minutes for 90 minutes after venous occlusion. The cerebral venous flow pattern was examined using fluorescence angiography until 90 minutes after occlusion. Histological specimens were examined 24 hours after occlusion. In Group Y, rCBF did not change significantly after venous occlusion. However, in Group A, rCBF decreased rapidly beginning 15 minutes after occlusion. Significant intergroup differences were observed 30, 60, and 90 minutes after occlusion. Venous flow arrest, which resulted in venous infarct, was observed on angiography 90 minutes after occlusion in two (10.5%) of 19 young and six (85.7%) of seven aged rats. The venous thrombus in Group A rats was significantly larger than that in Group Y rats 90 minutes after occlusion. Venous infarction was seen in all aged rats (100%) and in six young rats (31.6%); the infarct size, expressed as a percentage of the size of the ipsilateral hemisphere, was significantly larger in aged rats than in young rats. CONCLUSIONS: This study demonstrated an age-related increase in the rate and size of venous infarct following vein occlusion, suggesting that the greater vulnerability to CVCDs in the aged brain might be attributed to early and extensive hypoperfusion of circumscribed brain areas drained by the occluded vein. The larger thrombus formation in aged animals indicates that a shift in the thrombogenetic/thrombolytic equilibrium is responsible for the observed effect.

Aging↗

Ex vivo study of the physical effect of coils on pressure and flow dynamics in experimental aneurysms.

BACKGROUND AND PURPOSE: Recent experimental studies and a few case reports reveal that coiling may not lead to permanent occlusion of aneurysms by an organized thrombus. Therefore, biologic long-term prognosis seems to be doubtful, and the physical effect of coils may be important. The purpose of this study was to investigate the physical effect of coils on pressure and flow dynamics in aneurysms. METHODS: Bifurcation aneurysms were created in eight rabbits, explanted after 3 weeks, and tested in a model with pulsatile perfusion with 0.9% saline and heparinized blood. Before and after densely packing with coils, systemic and intraaneurysmal pressure, aneurysmal pulsation, and impact measurements were recorded. RESULTS: The peak and shape of the pressure waves in the aneurysm and in the delivery system were not significantly different before and after coiling. Under physiological intraaneurysmal pressure (while being perfused with saline), significant reduction (P = .022) of aneurysmal wall pulsation after coil embolization was noted. Overall, the aneurysmal impact on surrounding structures was statistically unchanged after coiling. However, in a few cases, after coil embolization, the observed increase of impact was more than doubled compared with the original values before coiling. CONCLUSION: Coils do not physically affect intraaneurysmal pressure. After coiling, there is no significant reduction of flow rates through the aneurysm and no reduction of aneurysmal impact, but aneurysmal wall pulsation may be decreased.

Animals↗

Control of brain temperature during experimental global ischemia in rats.

Temperature control during experimental ischemia continues to be of major interest. However, if exposure of brain tissue is necessary during the experiment, regional heat loss may occur even when the core temperature is maintained. Furthermore, valid non-invasive brain temperature monitoring is difficult in small rodents. This paper describes a method for both monitoring and maintenance of brain temperature during small animal preparations in a stereotaxic frame. The device used includes an ear-bar thermocouple probe and a small near-infrared radiator. The new equipment permitted to maintain peri-ischemic brain temperature at a desired level while carrying out non-invasive continuous recordings of cerebral blood flow (laser Doppler-flowmetry) and of electrical brain function (EEG). In contrast, without extracranial heat application, superficial and basal brain temperatures decreased during global cerebral ischemia by 4.1 +/- 0.1 and 4.6 +/- 0.4 degrees C (mean +/- SEM), respectively, returning to baseline values at 15-30 min of reperfusion while rectal (core) temperature remained stable at baseline values. The ear-bar thermocouple probe (tympanic membrane) reliably reflected basal brain temperature, and temperature in superficial brain areas correlated well with that in the temporal muscle. Our data show that the new system allows to exclude unwanted hypothermic neuroprotection, and does not interfere with optical and electrical measurement techniques.

Animals↗

C1-esterase inhibitor reduces infarct volume after cortical vein occlusion.

In order to clarify the role of complement as a mediator of cerebral infarct growth, we inhibited the classical complement activation pathway in a photochemical cortical vein occlusion model. Immediately after occlusion, rats were infused with either 0.9% saline (vehicle), or C1-esterase inhibitor (C1-INH) over 30 min. Regional cerebral blood flow (rCBF) decreased after occlusion, and was about 50% of baseline after 2 h. No difference was noted between experimental groups. Mean arterial blood pressure (MABP) and arterial blood gases were likewise unaffected by the treatment. However, administration of C1-INH had significantly reduced infarct volume by 72%, as evaluated after 5 days survival. Thus, the neuroprotective effect cannot be explained by an improvement of cerebral perfusion but rather by protection of the parenchyma in the penumbra.

Animals↗