Effects of propofol with EDTA on cell damage induced by oxygen and glucose deprivation (OGD) in PC12 cell cultures and middle cerebral artery (MCA) occlusion in mice

2006 ◽  
Vol 23 (Supplement 37) ◽  
pp. 155
Author(s):  
H. Hara ◽  
Y. Kotani ◽  
Y. Nakajima ◽  
M. Shimazawa
Keyword(s):  
Middle Cerebral Artery ◽  
Cell Cultures ◽  
Cerebral Artery ◽  
Pc12 Cell ◽  
Cell Damage ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation ◽  
Mca Occlusion

scholarly journals ARL 17477, a Potent and Selective Neuronal NOS Inhibitor Decreases Infarct Volume after Transient Middle Cerebral Artery Occlusion in Rats

1996 ◽  
Vol 16 (4) ◽  
pp. 599-604 ◽  
Author(s):  
Zheng G. Zhang ◽  
David Reif ◽  
James Macdonald ◽  
Wen Xue Tang ◽  
Dietgard K. Kamp ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cell Damage ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Arterial Blood ◽  
Mca Occlusion ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Cerebral Artery Occlusion

We tested the effects of administration of a selective neuronal nitric oxide synthase (nNOS) inhibitor, ARL 17477, on ischemic cell damage and regional cerebral blood flow (rCBF), in rats subjected to transient (2 h) middle cerebral artery (MCA) occlusion and 166 h of reperfusion (n = 48) and in rats without MCA occlusion (n = 25), respectively. Animals were administered ARL 17477 (i.v.): 10 mg/kg; 3 mg/kg; 1 mg/kg; N-nitro-L-arginine (L-NA) 10 mg/kg L-NA 1 mg/kg; and Vehicle. Administration of ARL 17477 1 mg/kg, 3 mg/kg and 10 mg/kg reduced ischemic infarct volume by 53 (p < 0.05), 23, and 6.5%, respectively. L-NA 1 mg/kg and 10 mg/kg increased infarct volume by 2 and 15%, respectively (p > 0.05). Administration of ARL 17477 (10 mg/kg) significantly (p < 0.05) decreased rCBF by 27 ± 5.3 and 24 ± 14.08% and cortical NOS activity by 86 ± 14.9 and 91 ± 8.9% at 10 min or 3 h, respectively, and did not alter mean arterial blood pressure (MABP). L-NA (10 mg/kg) significantly reduced rCBF by 23 ± 9.8% and NOS activity by 81 ± 7% and significantly (p < 0.05) increased MABP. Treatment with 3 mg/kg and 1 mg/kg ARL 17477 reduced rCBF by only 2.4 ± 4.5 and 0%, respectively, even when NOS activity was reduced by 63 ± 13.4 and 45 ± 15.7% at 3 h, respectively, (p < 0.05). The data demonstrate that ARL 17477 inhibits nNOS in the rat brain and causes a dose-dependent reduction in infarct volume after transient MCA occlusion.

scholarly journals Photothrombotic Occlusion of Rat Middle Cerebral Artery: Histopathological and Hemodynamic Sequelae of Acute Recanalization

1988 ◽  
Vol 8 (3) ◽  
pp. 357-366 ◽  
Author(s):  
Hitoshi Nakayama ◽  
W. Dalton Dietrich ◽  
Brant D. Watson ◽  
Raul Busto ◽  
Myron D. Ginsberg
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cortical Neurons ◽  
Cell Damage ◽  
Thrombus Formation ◽  
Infarct Volume ◽  
Brain Regions ◽  
Mca Occlusion ◽  
Temporary Occlusion ◽  
Mixed Pattern

The histopathological and hemodynamic consequences of photochemically induced middle cerebral artery (MCA) thrombosis and recanalization were studied in the rat. Recanalization of the thrombosed MCA segment was achieved by the topical application of nimodipine at 1 h following photochemically induced occlusion. Pathological consequences of permanent and temporary occlusion were compared by morphometric procedures 7 days following thrombus formation. Rats with permanent thrombosis exhibited consistent infarction of both striatum and cortex. MCA recanalization at 1 h was associated with a significant reduction in total infarct volume. In recanalized rats, small cortical infarcts, confined to the peripheral MCA territory, were observed in only three of six rats. In contrast, a mixed pattern of infarction and ischemic cell damage was documented throughout the striatum in all rats. Local CBF (ICBF), measured autoradiographically, was significantly reduced in the MCA territory following 1 h of MCA occlusion, especially within the striatum. At 1 h after recanalization, lCBF recovered within the previously ischemic brain regions to >50% of control. Perfusion deficits were detected by carbon black infusion within focal areas of the striatum following reperfusion. Thus, cortical neurons appear to tolerate 1 h of MCA occlusion in this model. In contrast, reperfusion following 1 h of photochemically induced MCA occlusion gives rise to selective injury to the striatum.

scholarly journals Prevention of Ischemic and Postischemic Brain Edema by a Novel Calcium Antagonist (PN200-110)

1988 ◽  
Vol 8 (3) ◽  
pp. 436-439 ◽  
Author(s):  
Koji Abe ◽  
Kyuya Kogure ◽  
Takao Watanabe
Keyword(s):  
Calcium Antagonist ◽  
Middle Cerebral Artery ◽  
Brain Edema ◽  
Cerebral Artery ◽  
Cell Damage ◽  
Brain Cells ◽  
Mca Occlusion ◽  
Massive Influx ◽  
Occlusion Model ◽  
Excessive Accumulation

The effect of PN200-110, a novel calcium antagonist, on the formation of brain edema was examined with rats using a middle cerebral artery (MCA) occlusion model. PN200-110 was effective in preventing the formation of brain edema in 6-h ischemia and in 3-h reperfusion following 3-h ischemia, which were cases in which great accumulations of calcium were autoradiographically observed. Furthermore, PN200-110 diminished the excessive accumulation of calcium in the MCA area involved. These results indicate that an inhibition of the massive influx of calcium into brain cells by PN200-110 may partially ameliorate cell damage, resulting in prevention of brain edema.

Acute Middle Cerebral Artery Occlusion: Experience with Volume Expansion Therapy

Neurosurgery ◽  
1986 ◽  
Vol 18 (4) ◽  
pp. 397-401 ◽  
Author(s):  
Bruce I. Tranmer ◽  
Cordell E. Gross ◽  
Ted S. Keller ◽  
Glenn W. Kindt
Keyword(s):  
Cardiac Output ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Volume Expansion ◽  
Artery Occlusion ◽  
Neurological Deficits ◽  
Life Styles ◽  
Arterial Blood ◽  
Mca Occlusion ◽  
The Mean

Abstract Five consecutive patients with acute neurological deficits after middle cerebral artery (MCA) occlusion were given emergency treatment with colloidal volume expansion. In each case, the diagnosis was confirmed promptly by computed tomography and cerebral angiography. Aggressive volume expansion therapy was started 2 to 18 hours (mean, 11 hr) after the onset of the neurological deficit. The mean colloidal volume used was 920 ml/day for an average of 4 days. During volume expansion, the mean cardiac output increased 57% from 4.6 + 0.6 to 7.2 + 1.9 litres/min (P &lt; 0.05). The mean hematocrit decreased 19% from 46 + 3% to 37 + 4% (P &lt; 0.01). The mean arterial blood pressure remained stable, and the pulmonary artery wedge pressure was maintained at &lt; 15 mm Hg. Three patients improved dramatically with volume expansion therapy and have returned to their previous life-styles. Two patients made partial recoveries and manage at home with nursing care. The three patients who improved dramatically were young (aged &lt;34) and, when compared to the older patients, they had greater increases in cardiac output (67% vs. 19%). No major complications or deaths were attributed to the volume expansion therapy. We propose that intravascular volume expansion and its concomitant augmentation of the cardiovascular dynamics may be effective in the treatment of acute neurological deficits after acute MCA occlusion.

scholarly journals Cerebral Energy Metabolism Measured in vivo by 31P-NMR in Middle Cerebral Artery Occlusion in the Cat—Relation to Severity of Stroke

1987 ◽  
Vol 7 (5) ◽  
pp. 557-562 ◽  
Author(s):  
S. Komatsumoto ◽  
S. Nioka ◽  
J. H. Greenberg ◽  
K. Yoshizaki ◽  
V. H. Subramanian ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cerebral Metabolism ◽  
Recovery Period ◽  
Creatine Phosphate ◽  
Significant Shift ◽  
Mca Occlusion ◽  
Occlusion Model

The energy metabolism of the brain has been measured in a middle cerebral artery (MCA) occlusion model in the cat utilizing 31P-nuclear magnetic resonance (NMR). 31P-NMR spectra were serially obtained during 2 h of ischemia and a subsequent 4-h recovery period. The ratio of creatine phosphate (PCr) to inorganic phosphate (Pi) (PCr/Pi) showed a precipitous decrease in parallel with changes in electroencephalographic (EEG) amplitude in severe strokes during ischemia as well as during recirculation. Animals with mild strokes, as determined by EEG criteria, exhibited a much smaller decrease in PCr/Pi during ischemia. In the severe strokes, there was a splitting and significant shift of the Pi peak immediately after occlusion. In addition, the shifted Pi peak rapidly increased and remained elevated throughout the study. In the mild strokes, Pi also increased, but not as markedly. Intracellular pH determination by chemical shift of the Pi peak revealed a decrease from 7.1 to 6.2–6.3 during ischemia and the subsequent recovery period in the animals with severe strokes, whereas the pH in the animals with mild strokes did not show a significant change. A gradual decrease in adenosine triphosphate (ATP) to 57–79% of the control was exhibited in severely stroked animals during both the ischemia and the recovery period, whereas there was no change in ATP in the mild stroked animals. These results suggest that the dynamic process of pathophysiological changes in an MCA occlusion model in the cat leads to significant differences in cerebral metabolism between animals with mild and severe strokes.

Extracranial-intracranial arterial bypass for middle cerebral artery stenosis and occlusion

1985 ◽  
Vol 62 (6) ◽  
pp. 831-838 ◽  
Author(s):  
Brian T. Andrews ◽  
Norman L. Chater ◽  
Philip R. Weinstein
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Slight Reduction ◽  
Content Type ◽  
Perioperative Stroke ◽  
Arterial Bypass ◽  
Mca Occlusion ◽  
Bypass Patency ◽  
Completed Stroke ◽  
Fine Print

✓ Forty-seven patients with middle cerebral artery (MCA) stenosis and 18 patients with MCA occlusion underwent extracranial-intracranial arterial bypass procedures. Patients presented with a history of transient ischemic attacks (TIA's), reversible ischemic neurological deficits, TIA's after initial stroke, stroke-in-evolution, or completed stroke. Angiography revealed that the MCA stenosis ranged from 70% to over 95%. Two patients (4.3%) in the stenosis group had a perioperative stroke (within 30 days of operation). There was no perioperative mortality. In the occlusion group, no patient had a perioperative stroke, and one patient (5.5%) died from a non-neurological disease. The TIA's resolved completely in 90% of the patients with stenosis and in 91.6% of those with occlusion. No patient with MCA stenosis had a late ipsilateral stroke, although five had a contralateral or vertebrobasilar stroke. One patient with MCA occlusion had a late ipsilateral stroke. The bypass patency rate at late follow-up review was 100%. The results of intracranial-extracranial arterial bypass procedures appear to be similar for patients with either stenosis or occlusion of the MCA. Symptomatic relief of TIA's was excellent and, in two patients with progressive stroke-in-evolution, the deficit was stabilized. The incidence of postoperative ipsilateral stroke was low in patients with TIA's alone or with TIA's after an initial stroke, but among patients with completed stroke, improvement was confined to slight reduction in the neurological deficit.

scholarly journals Ischemic Thresholds of Cerebral Protein Synthesis and Energy State following Middle Cerebral Artery Occlusion in Rat

1991 ◽  
Vol 11 (5) ◽  
pp. 753-761 ◽  
Author(s):  
G. Mies ◽  
S. Ishimaru ◽  
Y. Xie ◽  
K. Seo ◽  
K.-A. Hossmann
Keyword(s):  
Blood Flow ◽  
Protein Synthesis ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Energy State ◽  
High Threshold ◽  
Atp Content ◽  
Mca Occlusion ◽  
Cerebral Protein Synthesis ◽  
Energy Failure

The ischemic threshold of protein synthesis and energy state was determined 1, 6, and 12 h after middle cerebral artery (MCA) occlusion in rats. Local blood flow and amino acid incorporation were measured by double tracer autoradiography, and local ATP content by substrate-induced bioluminescence. The various images were evaluated at the striatal level in cerebral cortex by scanning with a microdensitometer with 75 μm resolution. Each 75 × 75 μm digitized image pixel was then converted into the appropriate units of either protein synthesis, ATP content, or blood flow. The ischemic threshold was defined as the flow rate at which 50% of pixels exhibited complete metabolic suppression. One hour after MCA occlusion, the threshold of protein synthesis was 55.3 ± 12.0 ml 100 g−1 min−1 and that of energy failure was 18.5 ± 9.8 ml 100 g−1 min−1. After 6 and 12 h of MCA occlusion, the threshold of protein synthesis did not change (52.0 ± 9.6 and 56.0 ± 6.5 ml 100 g−1 min−1, respectively) but the threshold of energy failure increased significantly at 12 h following MCA occlusion to 31.9 ± 9.7 ml 100 g−1 min−1 ( p < 0.05 compared to 1 h ATP threshold value; all values are mean ± SD). In focal cerebral ischemia, therefore, the threshold of energy failure gradually approached that of protein synthesis. Our results suggest that with increasing duration of ischemia, survival of brain tissue is determined by the high threshold of persisting inhibition of protein synthesis and not by the much lower one of acute energy failure. If the ischemic penumbra is considered to comprise the region in which cerebral protein synthesis is suppressed and energy state is preserved, it follows that the size of the penumbra decreases with the duration of ischemia.

scholarly journals Periinfarct and Remote Excitability Changes after Transient Middle Cerebral Artery Occlusion

2000 ◽  
Vol 20 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Tobias Neumann-Haefelin ◽  
Otto W. Witte
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Field Potential ◽  
Extracellular Recording ◽  
Artery Occlusion ◽  
Early Reperfusion ◽  
Paired Pulse ◽  
Mca Occlusion ◽  
Cortical Regions

Transient middle cerebral artery (MCA) occlusion results in substantially smaller cortical infarcts than permanent MCA occlusion if reperfusion is initiated within the first few hours. Only little information is available on the long-term functional outcome of the cortical regions “salvaged” by early reperfusion. To address this issue we examined basic electrophysiologic parameters in vitro using standard extracellular recording techniques at 7 and 28 days after transient MCA occlusion (1- and 2-hour ischemia) in rats. Both neocortical areas ipsi- and contralateral to MCA occlusion were systematically mapped to delineate the extent of periinfarct and remote alterations. In the periinfarct region we found a significant reduction of field potential amplitudes up to 3 mm when measuring from the infarct border at 7 days and up to 7 mm at 28 days. Paired-pulse inhibition, an indicator of GABAergic transmission, was only moderately impaired in this region at 7 days and not significantly different from control at 28 days. Remote effects were observed both ipsi- and contralaterally. Ipsilaterally they were restricted to a region close to the midline (presumably motor cortex) and were most likely attributable to the degeneration of corticostriatal connections. The extent of the contralateral excitability changes was clearly related to the size of the neocortical infarcts with large infarcts resulting in the widespread reduction of field potential amplitudes and an impairment of paired-pulse inhibition. The results show that there is a relatively large periinfarct region with decreased overall excitability after transient MCA occlusion which is likely to have a profound effect on perilesional processes involved in functional recovery. Remote excitability changes may contribute to the functional deficit and are probably related to deafferentation.

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