Brain tissue pressure in focal cerebral ischemia

1985 ◽  
Vol 62 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Fausto Iannotti ◽  
Julian T. Hoff ◽  
Gerald P. Schielke
Keyword(s):  
Blood Flow ◽  
Pressure Gradient ◽  
Brain Tissue ◽  
Focal Cerebral Ischemia ◽  
Fluid Pressure ◽  
Artery Occlusion ◽  
Tissue Pressure ◽  
Edema Formation ◽  
Content Type ◽  
Ischemic Brain Edema

✓ Twenty-three anesthetized cats underwent permanent middle cerebral artery occlusion in a study of the relationships of regional cerebral blood flow, ventricular fluid pressure, brain tissue pressure, and ischemic edema formation. A pressure gradient of 8 mm Hg developed between ischemic tissue and normally perfused tissue during a 4-hour observation period after occlusion. Brain water accumulated as tissue pressure rose, while blood flow in the same area fell. The data suggest, but do not prove, that ischemic brain edema causes tissue pressure to rise focally, and that blood flow to the ischemic zone is compromised further by the resultant hydrostatic pressure gradient.

scholarly journals Cortical Tissue Pressure Gradients in Early Ischemic Brain Edema

1986 ◽  
Vol 6 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Shizuo Hatashita ◽  
Julian T. Hoff
Keyword(s):  
Pressure Gradient ◽  
Brain Edema ◽  
Fluid Pressure ◽  
Pressure Gradients ◽  
Tissue Pressure ◽  
Ischemic Brain ◽  
Ischemic Brain Edema ◽  
Ventricular Fluid Pressure ◽  
Severe Degree

We examined the role of ischemic brain edema, tissue pressure gradients, and regional CBF (rCBF) in adjacent regions of cerebral cortex in cats with middle cerebral artery (MCA) occlusion (MCAO). Tissue pressure, rCBF, and water content were measured from gray matter in the central core and the peripheral margin of the MCA territory over 6 h after MCAO. Ventricular fluid pressure and CSF pressure were recorded. Tissue pressure in the ischemic core, with a flow of ∼5 ml/100 g/min, increased more than that in the periphery where flow was ∼19 ml/100 g/min. Tissue pressure rose progressively to 14.8 ± 1.0 mm Hg in the core over 6 h after MCAO, establishing a significant pressure gradient between that tissue and the lateral ventricle nearby or the subarachnoid space in the middle fossa within the first 3 h. The increase in tissue pressure was linearly related to the amount of edema fluid that developed until the edema reached a severe degree. This study shows that a hydrostatic tissue pressure gradient within ischemic cortex is associated with ischemic brain edema. The magnitude of the gradient that develops is related to the severity of ischemic edema in that tissue.

Regional brain tissue pressure gradients created by expanding extradural temporal mass lesion

1997 ◽  
Vol 86 (3) ◽  
pp. 505-510 ◽  
Author(s):  
Christopher E. Wolfla ◽  
Thomas G. Luerssen ◽  
Robin M. Bowman
Keyword(s):  
Intracranial Pressure ◽  
Frontal Lobe ◽  
Brain Tissue ◽  
Temporal Lobe ◽  
Mass Lesion ◽  
Pressure Monitor ◽  
Tissue Pressure ◽  
Content Type ◽  
Regional Brain ◽  
The Right

✓ A porcine model of regional intracranial pressure was used to compare regional brain tissue pressure (RBTP) changes during expansion of an extradural temporal mass lesion. Measurements of RBTP were obtained by placing fiberoptic intraparenchymal pressure monitors in the right and left frontal lobes (RF and LF), right and left temporal lobes (RT and LT), midbrain (MB), and cerebellum (CB). During expansion of the right temporal mass, significant RBTP gradients developed in a reproducible pattern: RT > LF = LT > RF > MB > CB. These gradients appeared early, widened as the volume of the mass increased, and persisted for the entire duration of the experiment. The study indicates that RBTP gradients develop in the presence of an extradural temporal mass lesion. The highest RBTP was recorded in the ipsilateral temporal lobe, whereas the next highest was recorded in the contralateral frontal lobe. The RBTP that was measured in either frontal lobe underestimated the temporal RBTP. These results indicated that if a frontal intraparenchymal pressure monitor is used in a patient with temporal lobe pathology, the monitor should be placed on the contralateral side and a lower threshold for therapy of increased intracranial pressure should be adopted. Furthermore, this study provides further evidence that reliance on a single frontal intraparenchymal pressure monitor may not detect all areas of elevated RBTP.

Nonhyperemic blood flow restoration and brain edema in experimental focal cerebral ischemia

1989 ◽  
Vol 70 (1) ◽  
pp. 73-80 ◽  
Author(s):  
Toshihiko Kuroiwa ◽  
Makoto Shibutani ◽  
Riki Okeda
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Brain Edema ◽  
Focal Cerebral Ischemia ◽  
Reactive Hyperemia ◽  
Diffusion Method ◽  
Left Middle Cerebral Artery ◽  
Content Type ◽  
Bbb Opening ◽  
Fine Print

✓ The effect of suppression of postischemic reactive hyperemia on the blood-brain barrier (BBB) and ischemic brain edema after temporary focal cerebral ischemia was studied in cats under ketamine and alpha-chloralose anesthesia. Regional cerebral blood flow (rCBF) was measured by a thermal diffusion method and a hydrogen clearance method. The animals were separated into three groups. In Group A, the left middle cerebral artery (MCA) was occluded for 6 hours. In Group B, the MCA was occluded for 3 hours and then reperfused for 3 hours; postischemic hyperemia was suppressed to the preischemic level by regulating the degree of MCA constriction. In Group C, the MCA was occluded for 3 hours and reperfused for 3 hours without suppressing the postischemic reactive hyperemia. The brain was removed and cut coronally at the site of rCBF measurement. The degree of ischemic edema was assessed by gravimetry in samples taken from the coronal section and correlated with the degree of BBB disruption at the corresponding sites, evaluated by densitometric determination of Evans blue discoloration. The findings showed that 1) ischemic edema was significantly exacerbated by postischemic hyperemia during reperfusion in parallel with the degree of BBB opening to serum proteins, and 2) suppression of postischemic hyperemia significantly reduced the exacerbation of ischemic edema and BBB opening. These findings indicate that blood flow may be restored without significant exacerbation of postischemic edema by the suppression of postischemic hyperemia in focal cerebral ischemia.

Regional blood flow and capillary permeability in the ethylnitrosourea-induced rat glioma

1981 ◽  
Vol 55 (6) ◽  
pp. 922-928 ◽  
Author(s):  
Kazuo Yamada ◽  
Toru Hayakawa ◽  
Yukitaka Ushio ◽  
Norio Arita ◽  
Amami Kato ◽  
...  
Keyword(s):  
Blood Flow ◽  
Brain Tissue ◽  
Evans Blue ◽  
Capillary Permeability ◽  
Regional Blood Flow ◽  
Blue Staining ◽  
Content Type ◽  
Rat Glioma ◽  
Blood Flows ◽  
Diameter Reduction

✓ Regional cerebral blood flow and capillary permeability of rat brains bearing ethylnitrosourea-induced gliomas of various size were investigated with 14C-antipyrine autoradiography and Evans blue staining. In the small tumors (<2 mm in diameter), blood flow was uniformly reduced when compared to the adjacent brain. Even in tiny tumors (0.3 to 0.4 mm in diameter), reduction in blood flow was evident. In the medium (2 to 4 mm in diameter) and large (> 4 mm in diameter) tumors, the blood flow increased or decreased depending on the part of the tumor examined. The necrotic center and peripheral edge had low blood flows, whereas the viable portion adjacent to the necrotic center had high blood flows. Blood flow in the brain tissue adjacent to medium and large tumors was lower than control brain tissue, probably due to local edema. Leakage of intravenous Evans blue in the tissue was only evident in the large tumors with central necrosis. The present findings suggest that neovascularization of the tumor may occur when the tumor reaches a certain size, and leaky new vessels may be the cause of brain edema associated with tumor.

Brain Tissue Pressure in Focal Cerebral Ischemia with and without Reperfusion

1986 ◽  
pp. 566-569 ◽  
Author(s):  
F. Iannotti ◽  
G. P. Schielke ◽  
V. Albanese ◽  
P. Picozzi ◽  
M. Rotondo ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Brain Tissue ◽  
Focal Cerebral Ischemia ◽  
Tissue Pressure

scholarly journals Brain Tissue Concentrations of ATP, Phosphocreatine, Lactate, and Tissue pH in Relation to Reduced Cerebral Blood Flow following Experimental Acute Middle Cerebral Artery Occlusion

1988 ◽  
Vol 8 (6) ◽  
pp. 866-874 ◽  
Author(s):  
T. P. Obrenovitch ◽  
O. Garofalo ◽  
R. J. Harris ◽  
L. Bordi ◽  
M. Ono ◽  
...  
Keyword(s):  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Brain Tissue ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Tissue Samples ◽  
Tissue Ph ◽  
Focal Ischaemia ◽  
Cerebral Artery Occlusion

Local CBF (LCBF) was compared with the corresponding local tissue concentration of ATP, phosphocreatine (PCr), and lactate in anaesthetized baboons subjected to focal ischaemia produced by middle cerebral artery occlusion (MCAO). LCBF hydrogen electrodes were implanted in cortical regions where MCAO had been previously shown to produce severe and penumbral ischaemia and in posterior regions where blood flow is not altered. Metabolites were assayed in small tissue samples collected either by cryoprobe biopsy in the regions where LCBFs were measured (series 1) or by sampling appropriate regions of the rapidly frozen brain (series 2). Subsequent topographical study of brain tissue pH with umbelliferone was performed in this latter series. The results from these two series are compared and discussed in terms of the more appropriate way to perform simultaneous electrode measurements and analysis of tissue samples for studying focal ischaemia in the primate brain. They confirm that the concentrations of ATP and PCr decrease, and that lactate level increases, with decreasing blood flow. These metabolites tended to change more rapidly below a blood flow threshold, rather than showing a steady decrease as the blood flow was reduced, although the variability of the data precluded us from establishing this with confidence. Topographical study of tissue pH often showed sharp boundaries between zones of very low pH and regions with normal pH.

Continuous simultaneous monitoring of intraventricular and cervical subarachnoid cerebrospinal fluid pressure to indicate development of cerebral or tonsillar herniation

1970 ◽  
Vol 33 (2) ◽  
pp. 145-150 ◽  
Author(s):  
Gary E. Kaufmann ◽  
Kemp Clark
Keyword(s):  
Cerebrospinal Fluid ◽  
Pressure Gradient ◽  
Fluid Pressure ◽  
Cerebrospinal Fluid Pressure ◽  
Continuous Recording ◽  
Tonsillar Herniation ◽  
Content Type ◽  
Fine Print ◽  
Made In

✓ A simultaneous continuous recording of intraventricular and cervical subarachnoid cerebrospinal fluid pressures was made in each of 20 patients who were comatose or decerebrate. All patients with a pressure gradient greater than 10 mm Hg died and at autopsy were found to have evidence of severe transtentorial and/or tonsillar herniation.

Microregional blood flow changes in experimental cerebral ischemia

1971 ◽  
Vol 35 (2) ◽  
pp. 155-166 ◽  
Author(s):  
Y. Lucas Yamamoto ◽  
Kathryne M. Phillips ◽  
Charles P. Hodge ◽  
William Feindel
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Fluorescein Angiography ◽  
Focal Cerebral Ischemia ◽  
Gamma Activity ◽  
Collateral Flow ◽  
Silicon Detectors ◽  
Content Type ◽  
Perfusion Flow ◽  
The Brain

✓ A branch of the middle cerebral artery on the convexity of the dog brain was occluded to produce an area of focal cerebral ischemia which could then be defined by fluorescein angiography of the brain. Repeated fluorescein angiography and measurement of microregional cerebral blood flow by xenon133 injected into the carotid artery and monitored by miniature lithium-drifted silicon detectors for gamma activity demonstrated that the ischemic zone was reduced in size by better collateral flow when the animals were allowed to breathe 5% carbon dioxide and 95% oxygen. Conversely, hyperventilation reducing the pCO2 made the ischemic zone larger by reducing collateral flow. No evidence was found to indicate that hypercapnia preferentially deprived the ischemic zone of perfusion flow. Retrograde collateral flow in the surface arteries appeared effective in terms of microcirculatory perfusion.

Method for measuring brain tissue pressure

1975 ◽  
Vol 43 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Robert M. Clark ◽  
Norman F. Capra ◽  
James H. Halsey
Keyword(s):  
Blood Pressure ◽  
Brain Tissue ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Tissue Pressure ◽  
Content Type ◽  
Pressure Changes ◽  
Local Brain

✓ The authors report a method for measuring total local brain tissue pressure (BTP) using a miniature catheter transducer stereotaxically introduced into the white matter of the cat's cerebrum. Quantitative rapid phasic pressure changes were satisfactorily demonstrated. Due to some drift of baseline of the transducers and inability to perform in vivo calibration, reliable long-term quantitative pressure measurements sometimes could not be studied. The BTP from each cerebral hemisphere and the cisternal pressure (CP) were monitored during alterations of pCO2 and systemic blood pressure, and distilled H2O injection prior to and after right middle cerebral artery (MCA) ligation. The catheter transducers functioned well on chronic implantation for up to 6 weeks. Compared to the chronically implanted catheters, acutely implanted catheters responded identically except for drift. The response of intracranial pressure and CP to MCA occlusion, alterations in pCO2, and systemic blood pressure were similar. No BTP gradients appeared in response to MCA ligation, hypercapnia, hypertension, or progressive swelling of the resulting infarction.

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