scholarly journals Induction of Spreading Depression in the Ischemic Hemisphere following Experimental Middle Cerebral Artery Occlusion: Effect on Infarct Morphology

1996 ◽  
Vol 16 (2) ◽  
pp. 202-213 ◽  
Author(s):  
Tobias Back ◽  
Myron D. Ginsberg ◽  
W. Dalton Dietrich ◽  
Brant D. Watson
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Spreading Depression ◽  
Ischemic Injury ◽  
Artery Occlusion ◽  
Ischemic Penumbra ◽  
Mca Occlusion ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

This study was undertaken to test whether transient depolarizations occurring in periinfarct regions are important in contributing to infarct spread and maturation. Following middle cerebral artery (MCA) occlusion we stimulated the ischemic penumbra with recurrent waves of spreading depression (SD) and correlated the histopathological changes with the electrophysiological recordings. Halothane-anesthetized, artificially ventilated Sprague–Dawley rats underwent repetitive stimulation of SD in intact brain (Group 1; n = 8) or photothrombotic MCA occlusion coupled with ipsilateral common carotid artery occlusion (Groups 2 and 3, n = 9 each). The electroencephalogram and direct current (DC) potential were recorded for 3 h in the parietal cortex, which represented the periinfarct border zone in ischemic rats. In Group 2, only spontaneously occurring negative DC shifts occurred; in Group 3, the (nonischemic) frontal pole of the ischemic hemisphere was electrically stimulated to increase the frequency of periinfarct DC shifts. Animals underwent perfusion-fixation 24 h later, and volumes of complete infarction and scattered neuronal injury (“incomplete infarction”) were assessed on stained coronal sections by quantitative planimetry. Electrical induction of SD in Group 1 did not cause morphological injury. During the initial 3 h following MCA occlusion, the number of spontaneous periinfarct depolarizations in Group 2 (7.0 ±1.5 DC shifts) was doubled in Group 3 by frontal current application (13.4 ± 2.7 DC shifts; p < 0.001). The duration as well as the integrated negative amplitude of DC shifts over time were significantly greater in Group 3 than in Group 2 rats (duration, 5.7 ± 3.8 vs. 4.1 ± 2.5 min; p < 0.05). Histopathological examination disclosed well-defined areas of pannecrosis surrounded by a cortical rim exhibiting selectively damaged acidophilic neurons and astrocytic swelling in otherwise normal-appearing brain. Induction of SD in the ischemic hemisphere led to a significant increase in the volume of incomplete infarction (19.0 ± 6.1 mm3 in Group 3 vs. 10.3 ± 5.1 mm3 in Group 2; p < 0.01) and of total ischemic injury (100.7 ± 41.0 mm3 in Group 3 vs. 66.5 ± 24.7 mm3 in Group 2; p < 0.05). The integrated magnitude of DC negativity per experiment correlated significantly with the volume of total ischemic injury ( r = 0.780, p < 0.0001). Thus, induction of SD in the ischemic hemisphere accentuated the development of scattered neuronal injury and increased the volume of total ischemic injury. This observation may be explained by the fact that, with limited perfusion reserve, periinfarct depolarizations are associated with episodic energy failure in the acute ischemic penumbra.

scholarly journals Evaluation of fetal condition in uncomplicated pregnancies at 40 weeks and beyond by calculation of amniotic fluid indexes and Doppler in the middle cerebral artery.

2021 ◽  
Author(s):  
elvira semenova ◽  
Nikolai Rukhliada ◽  
Olga Klicenko
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Inclusion Criteria ◽  
Trigger Level ◽  
Hypoxic Brain Damage ◽  
Emergency Cesarean ◽  
Hypoxic Brain ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Objective. The aim of our data is to reveal the method of prognosis abnormal perinatal outcome, using combination US and Doppler results in uncomplicated pregnancies at 40 weeks and beyond. Design.1020 uncomplicated pregnant women at 40 weeks and beyond were examined 48 hours before delivery. We analyzed fetus’s condition during labor and just after. Setting. According these dates all women were divided into 3 groups after amniotic index(AI)and pulsatility indices(PI) in the middle cerebral artery(MCA). Population.260 women were included in the study because they met the inclusion criteria. Methods.All women were divided into 3 groups (group 1 - PI>0.835, any value of AI, group 2-AI >85, PI ≤ 0.835, group 3- AI ≤ 85 and PI ≤ 0.835).We analyzed fetus’s condition during labor and just after delivery (Apgar score <=7 and >7 on the 1st minute). Result. We’ve got trigger level for pulsatility index (PI) as 0.835, if we had PI less than that threshold cases of emergency cesarean section increases in 2,12 times, if PI less than 0,835 in combination with Amniotic Index(AI) 85 and less in 5,28 times. If PI =<0,835 risk of newborns having Apgar 7 and less increases in 1,18, but in combination with AI =<85 in 4,72 times. Conclusion. In results we found out the following data: low PI in the MCA may be parameter which cans prognoses fetus distress. Combination of PI reduce with low AI increases its specific and can use in practical ways to avoid hypoxic brain damage during labor.

Effect of hyperthermia on glutamate release in ischemic penumbra after middle cerebral artery occlusion in rats

1994 ◽  
Vol 267 (5) ◽  
pp. H1770-H1776 ◽  
Author(s):  
K. Takagi ◽  
M. D. Ginsberg ◽  
M. Y. Globus ◽  
E. Martinez ◽  
R. Busto
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Glutamate Release ◽  
Threshold Value ◽  
Artery Occlusion ◽  
Ischemic Penumbra ◽  
Doppler Flowmetry ◽  
Mca Occlusion ◽  
Normothermic Group ◽  
Cerebral Artery Occlusion

Using microdialysis, we investigated the effect of hyperthermia on glutamate release in penumbral cortex of rats with 2 h of either normothermic (37 degrees C) or hyperthermic (39 degrees C) middle cerebral artery (MCA) occlusion. Penumbral blood flow (CBF) was measured by laser-Doppler flowmetry. CBF values (expressed as % preischemic values) in normothermic and hyperthermic groups were 24 +/- 11 (SD) and 24 +/- 16%, respectively, during ischemia and 102 +/- 81 and 147 +/- 79% during recirculation. Average extracellular glutamate in the hyperthermic group increased from a baseline of 7 +/- 2 microM to a peak of 217 +/- 184 microM at 10-20 min after onset of ischemia but returned to near baseline after 60 min. Glutamate in the normothermic group increased from 4 +/- 2 microM to a peak of 26 +/- 17 microM at 10-20 min after MCA occlusion but fell to near-baseline before recirculation. Thus reuptake systems appeared to remain functional in ischemic penumbra, even during hyperthermia. Ischemic glutamate release was significantly higher in hyperthermic than in normothermic rats: average values of individual rats' peak levels were 251 +/- 221 microM and 37 +/- 34 microM, respectively. The ischemic CBF threshold value for glutamate release was 33% of control in the normothermic group but 61% in the hyperthermic group.

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 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.

Effects of Sufentanil on Cerebral Hemodynamics and Intracranial Pressure in Patients with Brain Injury

1995 ◽  
Vol 83 (4) ◽  
pp. 721-726. ◽  
Author(s):  
Christian Werner ◽  
Eberhard Kochs ◽  
Hanswerner Bause ◽  
William E. Hoffman ◽  
Jochen Schulte am Esch
Keyword(s):  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
Artery Blood Flow ◽  
Arterial Blood ◽  
Norepinephrine Infusion ◽  
Group 2 ◽  
Group 1

Background The current study investigates the effects of sufentanil on cerebral blood flow velocity and intracranial pressure (ICP) in 30 patients with intracranial hypertension after severe brain trauma (Glasgow coma scale &lt; 6). Methods Mechanical ventilation (FIO2 0.25-0.4) was adjusted to maintain arterial carbon dioxide tensions of 28-30 mmHg. Continuous infusion of midazolam (200 micrograms/kg/h intravenous) and fentanyl (2 micrograms/kg/h intravenous) was used for sedation. Mean arterial blood pressure (MAP, mmHg) was adjusted using norepinephrine infusion (1-5 micrograms/min). Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a 2-MHz transcranial Doppler sonography system. ICP (mmHg) was measured using an epidural probe. After baseline measurements, a bolus of 3 micrograms/kg sufentanil was injected, and all parameters were continuously recorded for 30 min. The patients were assigned retrospectively to the following groups according to their blood pressure responses to sufentanil: group 1, MAP decrease of less than 10 mmHg, and group 2, MAP decrease of more than 10 mmHg. Results Heart rate, arterial blood gases, and esophageal temperature did not change over time in all patients. In 18 patients, MAP did not decrease after sufentanil (group 1). In 12 patients, sufentanil decreased MAP &gt; 10 mmHg from baseline despite norepinephrine infusion (group 2). ICP was constant in patients with maintained MAP (group 1) but was significantly increased in patients with decreased MAP. Vmean did not change with sufentanil injection regardless of changes in MAP. Conclusions The current data show that sufentanil (3 micrograms/kg intravenous) has no significant effect on middle cerebral artery blood flow velocity and ICP in patients with brain injury, intracranial hypertension, and controlled MAP. However, transient increases in ICP without changes in middle cerebral artery blood flow velocity may occur concomitant with decreases in MAP. This suggests that increases in ICP seen with sufentanil may be due to autoregulatory decreases in cerebral vascular resistance secondary to systemic hypotension.

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.

Neuroprotective effects of erythropoietin pretreatment in a rodent model of transient middle cerebral artery occlusion

2014 ◽  
Vol 121 (1) ◽  
pp. 55-62 ◽  
Author(s):  
Bernardo Oliveira Ratilal ◽  
Mariana Moreira Coutinho Arroja ◽  
Joao Pedro Fidalgo Rocha ◽  
Adelaide Maria Afonso Fernandes ◽  
Andreia Pereira Barateiro ◽  
...  
Keyword(s):  
Treatment Group ◽  
Middle Cerebral Artery ◽  
Brain Edema ◽  
Cerebral Artery ◽  
Plasma Levels ◽  
Infarct Volume ◽  
Neuron Specific Enolase ◽  
Artery Occlusion ◽  
Mca Occlusion ◽  
Cerebral Artery Occlusion

Object There is an unmet clinical need to develop neuroprotective agents for neurosurgical and endovascular procedures that require transient cerebral artery occlusion. The aim in this study was to explore the effects of a single dose of recombinant human erythropoietin (rhEPO) before middle cerebral artery (MCA) occlusion in a focal cerebral ischemia/reperfusion model. Methods Twenty-eight adult male Wistar rats were subjected to right MCA occlusion via the intraluminal thread technique for 60 minutes under continuous cortical perfusion monitoring by laser Doppler flowmetry. Rats were divided into 2 groups: control and treatment. In the treated group, rhEPO (1000 IU/kg intravenously) was administered 10 minutes before the onset of the MCA ischemia. At 24-hour reperfusion, animals were examined for neurological deficits, blood samples were collected, and animals were killed. The following parameters were evaluated: brain infarct volume, ipsilateral hemispheric edema, neuron-specific enolase plasma levels, parenchyma histological features (H & E staining), Fluoro-Jade–positive neurons, p-Akt and total Akt expression by Western blot analysis, and p-Akt–positive nuclei by immunohistochemical investigation. Results Infarct volume and Fluoro-Jade staining of degenerating neurons in the infarct area did not vary between groups. The severity of neurological deficit (p < 0.001), amount of brain edema (78% reduction in treatment group, p < 0.001), and neuron-specific enolase plasma levels (p < 0.001) were reduced in the treatment group. Perivascular edema was histologically less marked in the treatment group. No variations in the expression or localization of p-Akt were seen. Conclusions Administration of rhEPO before the onset of 60-minute transient MCA ischemia protected the brain from this insult. It is unlikely that rhEPO pretreatment leads to direct neuronal antiapoptotic effects, as supported by the lack of Akt activation, and its benefits are most probably related to an indirect effect on brain edema as a consequence of blood-brain barrier preservation. Although research on EPO derivatives is increasing, rhEPO acts through distinct neuroprotective pathways and its clinical safety profile is well known. Clinically available rhEPO is a potential therapy for prevention of neuronal injury induced by transitory artery occlusion during neurovascular procedures.

Emergent surgical embolectomy for middle cerebral artery occlusion due to carotid plaque rupture followed by elective carotid endarterectomy

2014 ◽  
Vol 121 (3) ◽  
pp. 631-636 ◽  
Author(s):  
Satoshi Kiyofuji ◽  
Tomohiro Inoue ◽  
Hirotaka Hasegawa ◽  
Akira Tamura ◽  
Isamu Saito
Keyword(s):  
Middle Cerebral Artery ◽  
Carotid Endarterectomy ◽  
Cerebral Artery ◽  
Vulnerable Plaque ◽  
Carotid Plaque ◽  
Plaque Rupture ◽  
Artery Occlusion ◽  
Large Artery ◽  
Mca Occlusion ◽  
Surgical Embolectomy

Embolic intracranial large artery occlusion with severe neurological deficit is associated with an extremely poor prognosis. The safest and most effective treatment strategy has not yet been determined when such emboli are associated with unstable proximal carotid plaque. The authors performed emergent surgical embolectomy for left middle cerebral artery (MCA) occlusion, and the patient experienced marked neurological recovery without focal deficit and regained premorbid activity. Postoperative investigation revealed “vulnerable plaque” of the left internal carotid artery without apparent evidence of cardiac embolism, such as would be seen with atrial fibrillation. Specimens from subsequent elective carotid endarterectomy (CEA) showed ruptured vulnerable plaque that was histologically consistent as a source of the intracranial embolic specimen. Surgical embolectomy for MCA occlusion due to carotid plaque rupture followed by CEA could be a safer and more effective alternative to endovascular treatment from the standpoint of obviating the risk of secondary embolism that could otherwise occur as a result of the manipulation of devices through an extremely unstable portion of plaque. Further, this strategy is associated with a high probability of complete recanalization with direct removal of hard and large, though fragile, emboli.

scholarly journals Reduction of Infarct Volume by Magnesium after Middle Cerebral Artery Occlusion in Rats

1991 ◽  
Vol 11 (6) ◽  
pp. 1025-1030 ◽  
Author(s):  
Yoshio Izumi ◽  
Simon Roussel ◽  
Elisabeth Pinard ◽  
Jacques Seylaz
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Triphenyltetrazolium Chloride ◽  
Ischemic Brain ◽  
Mca Occlusion ◽  
Cerebral Artery Occlusion ◽  
Hyperglycemic Effect

The effects of magnesium, an endogenous inhibitor of calcium entry into neurons, upon ischemic brain damage were investigated using a well-characterized model of focal cerebral ischemia in rats. Infarct volumes were determined by 2,3,5-triphenyltetrazolium chloride transcardiac perfusion 48 h after middle cerebral artery (MCA) occlusion. The area of ischemic damage was quantified by image analysis in coronal sections taken every 0.5 mm. MgCl2 (1 mmol/kg) was injected intraperitoneally just after MCA occlusion and again 1 h later. Posttreatment with MgCl2 (16 control and 16 treated rats) significantly reduced the cortical infarct volume. Compensation for the hyperglycemic effect of MgCl2 with insulin (17 rats) further reduced the infarct volume in the neocortex. No systemic effects of either treatment could account for the observed neuroprotection.

Sign in / Sign up

Export Citation Format

Share Document