The Influence of the Calcium Antagonist Nimodipine and Induced Hypertension on the Behavior of the Cerebral Pial Arteries, the Blood-Brain Barrier, Cerebral Edema, and Cerebral Infarction in Cats with One-Hour Occlusion of the Middle Cerebral Artery

Neurosurgery ◽  
1991 ◽  
Vol 28 (2) ◽  
pp. 267-272 ◽  
Author(s):  
Toshisuke Sakaki ◽  
Shigeru Tsunoda ◽  
Tetsuya Morimoto
Keyword(s):  
Middle Cerebral Artery ◽  
Blood Brain Barrier ◽  
Cerebral Artery ◽  
Cerebral Edema ◽  
Evans Blue ◽  
Control Group ◽  
Blue Dye ◽  
Pial Arteries ◽  
Evans Blue Dye ◽  
Induced Hypertension

Abstract Thirty anesthetized cats were randomly assigned to one of three groups of 10 cats each: nimodipine treatment, nimodipine treatment combined with induced hypertension, or a control group. The behavior of the cerebral pial arteries was measured by means of microscopic observation through a cranial window. The middle cerebral artery of each cat was clipped for 1 hour via the transorbital approach. Five hours after circulation was reestablished in the middle cerebral artery. Evans blue dye was injected intravenously: 30 minutes later, the animal was killed. Administration of nimodipine or saline in the treated or control group was started 5 minutes before the middle cerebral artery was clipped and maintained until the end of the experiment. Induced hypertension was produced by administration of dopamine during the occlusion. Damage to the blood-brain barrier (BBB) was judged by extravasation of Evans blue dye. Cerebral edema and infarction were evaluated from histological findings. They were most prominent in the control group; the extent of the hemisphere affected was as follows (mean ± standard error): extravasation. 40.5 ± 8.8%: edema, 43.2 ± 5.7%: infarction, 35.5 ± 9.6%. On the other hand, the extravasation of Evans blue dye and cerebral edema were significantly more extensive in the group treated with nimodipine and induced hypertension (extravasation, 28.2 ± 9.6% of the hemisphere; edema, 30.3 ± 7.1%) than in the group treated with nimodipine alone (extravasation. 18.5 ± 8.7% of the hemisphere; edema, 19.4 ± 6.3%). but the infarction size was similar in both groups (16.6 ± 4.9% of the hemisphere in the former; 17.0 ± 6.2 in the latter). Based on these results, we arc cautious in combining calcium entry blocking agents such as nimodipine with induced hypertension in patients with acute cerebral ischemia.

The influence of nimodipine on cerebral blood flow autoregulation and blood-brain barrier

1988 ◽  
Vol 69 (6) ◽  
pp. 919-922 ◽  
Author(s):  
Hans-Georg Höllerhage ◽  
Michael R. Gaab ◽  
Matthias Zumkeller ◽  
Gerhard F. Walter
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Brain Barrier ◽  
Evans Blue ◽  
Brain Barrier ◽  
Control Group ◽  
Blue Dye ◽  
Evans Blue Dye ◽  
Blood Brain ◽  
Anesthetized Rats

✓ Twenty anesthetized rats were randomly assigned to a nimodipine-treated group or a control group of 10 rats each. Local cerebral blood flow (lCBF) was measured by means of a surface electrode using the hydrogen clearance technique. Systemic arterial pressure (SAP) was varied with administration of norfenefrine or by hemorrhage in order to obtain SAP/cerebral blood flow (CBF) curves under different conditions. In the control group, a typical autoregulation curve was obtained with an lCBF plateau between 70 and 120 mm Hg SAP. The nimodipine-treated animals, however, showed only a slight diminution in the slope of the curve but no real plateau, indicating impairment of CBF autoregulation. In another series, 20 anesthetized rats were randomly assigned to a treatment group or a control group of 10 animals each. Intravenous Evans blue dye was used as a tracer for blood-brain barrier (BBB) function. In both groups, SAP was raised to a level of 180 mm Hg with administration of norfenefrine for 6 minutes. Extravasation of significantly more Evans blue dye was observed in the nimodipine group than in the control group, indicating impairment of the BBB. It is concluded that nimodipine may impair CBF autoregulation, allowing damage to the BBB under hypertensive conditions.

scholarly journals A Study of the Pathogenesis and Prevention of Central Pontine Myelinolysis in a Rat Model

2006 ◽  
Vol 34 (3) ◽  
pp. 264-271 ◽  
Author(s):  
Q-H Ke ◽  
T-B Liang ◽  
J Yu ◽  
S-S Zheng
Keyword(s):  
Hypertonic Saline ◽  
Blood Brain Barrier ◽  
Evans Blue ◽  
Central Pontine Myelinolysis ◽  
Brain Barrier ◽  
Blue Dye ◽  
Evans Blue Dye ◽  
Pontine Myelinolysis ◽  
Demyelinating Lesions ◽  
Central Pontine

The development of central pontine myelinolysis was studied in rats. Severe hyponatraemia was induced using vasopressin tannate and 2.5% dextrose in water and then rapidly corrected with hypertonic saline alone, hypertonic saline and dexamethasone simultaneously, or hypertonic saline plus dexamethasone 24 h later. The permeability of the blood-brain barrier was evaluated using the extravasation of Evans blue dye and the expression of inducible nitric oxide synthase (iNOS) in the brain was examined using Western blot analysis. Histological sections were examined for demyelinating lesions. In rats receiving hypertonic saline alone, Evans blue dye content and expression of iNOS began to increase 6 and 3 h, respectively, after rapid correction of hyponatraemia and demyelinating lesions were seen. When dexamethasone was given simultaneously with hypertonic saline, these increases were inhibited and demyelinating lesions were absent. These effects were lost if dexamethasone injection was delayed. Disruption of the blood-brain barrier and increased iNOS expression may be involved in the pathogenesis of central pontine myelinolysis, and early treatment with dexamethasone may help prevent the development of central pontine myelinolysis.

Effects of Repeated Temporary Clipping of the Middle Cerebral Artery on Pial Arterial Diameter, Regional Cerebral Blood Flow, and Brain Structure in Cats

Neurosurgery ◽  
1990 ◽  
Vol 27 (6) ◽  
pp. 914-920 ◽  
Author(s):  
Toshisuke Sakaki ◽  
Shigeru Tsunoda ◽  
Tetsuya Morimoto ◽  
Taiji Ishida ◽  
Yasunori Sasaoka
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cerebral Edema ◽  
Regional Cerebral Blood Flow ◽  
Regional Cerebral Blood ◽  
Arterial Diameter ◽  
Pial Arteries ◽  
Temporary Clipping

Abstract Temporary clipping of the major arterial trunk is an important maneuver to control excessive unexpected bleeding in neurosurgical operations; however, repeated temporary clipping can give rise to severe neurological deficits after surgery. The present study was performed to confirm and explain these clinical findings. Initially, a single 20-minute or 1-hour occlusion of the middle cerebral artery was performed in each of 5 cats. Pial arterial diameter was determined by video imaging, regional cerebral blood flow was measured by autoradiography, and cerebral edema and infarction were observed. In the 20-minute occlusion group, no abnormal changes were found 5 hours after recirculation. In the 1-hour occlusion group, pial arteries were dilated by 45%, and regional cerebral blood flow increased to more than twice the resting cortical values. The extent of cerebral edema was 41.2 ± 7.5% (SE) and infarction was 34.5 ± 9.5% (SE) of the hemisphere. In the second experiment, three 20-minute occlusions of the middle cerebral artery in a 1-hour interval were performed in 20 cats. In 10 of them, thiopental (40 mg/kg) was used to protect the brain. In the group without barbiturate treatment, pial arteries were dilated by 40% at the end of experiment, regional cerebral blood flow decreased to about 70% compared with single 20-minute occlusion, cerebral edema was 19.5 ± 8.1% (SE), and infarction was 8.1 ± 3.7% (SE) of the hemisphere. In the treated group, these were only trivial changes. The effect of repeated clipping may cumulatively cause brain damage, and barbiturates should be used whenever repeated clipping is necessary.

Brain Retractor Edema during Induced Hypotension: The Effect of the Rate of Return of Blood Pressure

Neurosurgery ◽  
1990 ◽  
Vol 27 (6) ◽  
pp. 901-906 ◽  
Author(s):  
S. Lownie ◽  
X. Wu ◽  
S. Karlik ◽  
A.W. Gelb
Keyword(s):  
Blood Pressure ◽  
Magnetic Resonance ◽  
Cerebral Edema ◽  
Evans Blue ◽  
Relaxation Times ◽  
Blue Dye ◽  
Edema Formation ◽  
Induced Hypotension ◽  
Evans Blue Dye ◽  
Significant Difference

Abstract This study evaluated the hypothesis that the postoperative formation of cerebral edema may be influenced by the rate of blood pressure return after induced hypotension in a graded brain retractor injury. Nineteen cats underwent unilateral craniotomy, isoflurane-induced hypotension to a mean of 50 mm Hg, and application of a brain retractor at 20 mm Hg of pressure for 1 hour. Blood pressure was returned to normal either within 3 minutes or over 20 minutes. The degree of cerebral edema formation was determined by Evans blue dye and coronal magnetic resonance imaging. All animals showed extravasation of Evans blue dye in the retracted hemisphere that was most marked at the periphery of the retractor. T1 relaxation times were significantly prolonged in the retracted hemispheres of both the fast return and slow return groups (18.8% and 17.8%, respectively) and more so at the Evans blue sites (42.8% and 40.8%), although not so strikingly beneath the retractor itself (6.3% and 7.8%). T2 relaxation times were similarly prolonged but to approximately half the degree of the T1 times. In the nonretracted hemisphere, drug-induced hypotension alone did not result in significant acute cerebral edema or blood-brain barrier alteration. There was no significant difference between the fast and slow groups in Evans blue extravasation or magnetic resonance changes. Thus, in a retractor-induced brain injury, restoration of arterial pressure to normal either gradually or rapidly did not influence the degree or extent of edema formation.

The influence of systemic arterial pressure and intracranial pressure on the development of cerebral vasogenic edema

1983 ◽  
Vol 59 (5) ◽  
pp. 803-809 ◽  
Author(s):  
Quentin J. Durward ◽  
Rolando F. Del Maestro ◽  
A. Loren Amacher ◽  
J. Keith Farrar
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Blood Brain Barrier ◽  
Evans Blue ◽  
Vasogenic Edema ◽  
Brain Barrier ◽  
Blue Dye ◽  
Content Type ◽  
Evans Blue Dye ◽  
Fine Print

✓ The influence of intracranial pressure (ICP), systemic arterial pressure (SAP), and cerebral perfusion pressure (CPP) upon the development of vasogenic cerebral edema is largely unknown. To study their relationship, the authors have produced an osmotic disruption of the blood-brain barrier unilaterally in rabbits by injecting 1 cc/kg of 2M NaCl into the left internal carotid artery. The amount of vasogenic edema produced was assessed by quantitation of the extravasation of Evans blue dye into the area of maximum blood-brain barrier breakdown by means of optical densitometry following formamide extraction. The ICP was measured using a cisterna magna catheter into which mock cerebrospinal fluid could be infused at a predetermined pressure. The SAP was controlled by exsanguination from a femoral artery catheter. In 18 animals in which blood pressure was not controlled, no significant relationship between the ICP and the degree of Evans blue dye extravasation was noted. In these animals, however, a direct relationship between CPP (defined as mean arterial pressure minus mean ICP) and extravasation of Evans blue dye was found (correlation coefficient 0.630; p < 0.001). When ICP was held constant at 0 to 5 mm Hg in another group of 16 animals and different levels of blood pressure were produced by exsanguination, a significant direct relationship between extravasation of Evans blue dye and the SAP was found (correlation coefficient 0.786; p < 0.001). In a third group of 20 animals, the blood pressure was held constant at 90 to 100 mm Hg and the ICP was varied between 0 and 75 mm Hg. There was a highly significant result indicating increasing Evans blue dye extravasation with lower levels of ICP (p < 0.001). Cerebral blood flow determinations by the hydrogen clearance method indicated loss of autoregulation in all animals in the areas of brain injured by intracarotid hypertonic saline. These results indicate that high SAP and low ICP (that is, a large CPP) promote Evans blue dye extravasation in this model of blood-brain barrier disruption. This finding has implications for the management of patients with vasogenic edema.

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