Time course of the local cortical blood flow in experimental cerebral ischemia

1982 ◽  
Vol 93 (5) ◽  
pp. 573-577
Author(s):  
L. N. Dorokhova ◽  
V. A. Sorokoumov ◽  
V. A. Tsyrlin
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Time Course ◽  
Cortical Blood Flow ◽  
Local Cortical Blood Flow ◽  
Experimental Cerebral Ischemia

Vascular pressures and cortical blood flow in cavernous angioma of the brain

1990 ◽  
Vol 73 (4) ◽  
pp. 555-559 ◽  
Author(s):  
John R. Little ◽  
Issam A. Awad ◽  
Stephen C. Jones ◽  
Zeyd Y. Ebrahim
Keyword(s):  
Blood Flow ◽  
Cavernous Angioma ◽  
Sitting Position ◽  
Cortical Blood Flow ◽  
Content Type ◽  
Cavernous Angiomas ◽  
Arterial Blood ◽  
Mean Pressure ◽  
Local Cortical Blood Flow ◽  
The Brain

✓ This study was designed to investigate the hemodynamic characteristics of cavernous angiomas of the brain. Five adult patients with a cavernous angioma underwent local cortical blood flow studies and vascular pressure measurements during surgery for the excision of the cavernous angioma. Clinical presentation included headache in four patients, seizures in four patients, and recurring diplopia in one patient. Magnetic resonance imaging demonstrated the cavernous angiomas in all patients and revealed an associated small hematoma in two. Four patients with a cerebral cavernous angioma were operated on in the supine position and the remaining patient, whose lesion involved the brain stem, was operated on in the sitting position. Mean local cortical blood flow (± standard error of the mean) in the cerebral cortex adjacent to the lesion was 60.5 ± 8.3 ml/100 gm/min at a mean PaCO2 of 35.0 ± 0.6 torr. Mean CO2 reactivity was 1.1 ± 0.2 ml/100 gm/min/torr. The local cortical blood flow results were similar to established normal control findings. Mean pressure within the lesion in the patients undergoing surgery while supine was 38.2 ± 0.5 mm Hg; a slight decline in cavernous angioma pressure occurred with a drop in mean systemic arterial blood pressure and PaCO2. Mean pressure in the cavernous angioma in the patient operated on in the sitting position was 7 mm Hg. Jugular compression resulted in a 9-mm Hg rise in cavernous angioma pressure in one supine patient but no change in the patient in the sitting position. Direct microscopic observation revealed slow circulation within the lesions. The hemodynamic features demonstrated in this study indicate that cavernous angiomas are relatively passive vascular anomalies that are unlikely to produce ischemia in adjacent brain. Frank hemorrhage would be expected to be self-limiting because of relatively low driving pressures.

Characteristics of reactive hyperemia in the cerebral circulation

1984 ◽  
Vol 246 (1) ◽  
pp. H52-H58 ◽  
Author(s):  
J. K. Gourley ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
White Matter ◽  
Cerebral Ischemia ◽  
Gray Matter ◽  
Cerebral Circulation ◽  
Time Course ◽  
Reactive Hyperemia ◽  
Arterial Occlusion ◽  
Maximal Peak ◽  
Minimal Resistance

Reactive hyperemia has been characterized in many vascular beds, but little is known about quantitative characteristics of reactive hyperemia in the cerebral circulation. We measured velocity of blood flow and pial artery diameter to characterize the time course of reactive hyperemia and used microspheres to study regional blood flow in the brain. Cerebral ischemia was produced by raising intracranial pressure or by arterial occlusion with a cuff around the neck. Five seconds of ischemia produced virtually maximal peak reactive hyperemia, and 30 s of ischemia produced maximal peak reactive hyperemia. During reactive hyperemia after 30 s of cerebral ischemia, there was a three- to fourfold increase in cerebral blood flow. The magnitude of reactive hyperemia was greater in gray matter than in white matter. Minimal resistance during reactive hyperemia, after ischemia produced by arterial occlusion, is similar to minimal resistance during seizures or hypercapnia, which suggests that reactive hyperemia produces maximal vasodilatation. Oxygen saturation of cerebral venous blood increased almost twofold during reactive hyperemia, which indicates that factors in addition to venous (and presumably tissue) oxygen are important determinants of reactive hyperemia. In summary, 1) we have characterized the time course of reactive hyperemia in the cerebral circulation; 2) reactive hyperemia after arterial occlusion produces maximal cerebral vasodilatation; and 3) there is marked heterogeneity of the response, with much larger increases in flow in cortical gray matter than white matter.

Correlation between local cerebral blood flow and electroencephalography in experimental cerebral ischemia and following recirculataion

Nosotchu ◽  
1986 ◽  
Vol 8 (5) ◽  
pp. 370-378 ◽  
Author(s):  
Kenji Kusuda ◽  
Seizo Sadoshima ◽  
Kenichiro Fujii ◽  
Setsuro Ibayashi ◽  
Masatoshi Fujishima
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Local Cerebral Blood Flow ◽  
Experimental Cerebral Ischemia

Effect of nimodipine on intracellular brain pH, cortical blood flow, and EEG in experimental focal cerebral ischemia

1986 ◽  
Vol 64 (4) ◽  
pp. 617-626 ◽  
Author(s):  
Fredric B. Meyer ◽  
Robert E. Anderson ◽  
Tony L. Yaksh ◽  
Thoralf M. Sundt
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Adjunctive Treatment ◽  
Control Group ◽  
Cortical Blood Flow ◽  
Content Type ◽  
Mca Occlusion ◽  
Brain Ph ◽  
Major Branch

✓ Intracellular brain pH, cortical blood flow, and electroencephalograms (EEG's) were recorded in severely and moderately ischemic regions in 10 control and 10 nimodipine-treated rabbits prior to and following major branch occlusion of the middle cerebral artery (MCA). Preocclusion cortical blood flow was 51 ml/100 gm/min and intracellular brain pH was 7.01 in both the control and the treated animals. After MCA occlusion, the severely ischemic regions in the control group showed initial and 4-hour postocclusion flows of 12.7 and 5.2 ml/100 gm/min with a brain pH of 6.64 and 6.08, respectively. In animals given nimodipine after MCA occlusion, blood flow increased from 10.5 to 18.8 ml/100 gm/min, with an associated elevation in intracellular brain pH from 6.57 to 6.91. Comparable findings were observed in areas of moderate ischemia. Improvements in cortical blood flow, intracellular brain pH, and EEG attenuations produced by nimodipine were all statistically significant. Inspection of the cortex revealed reversal of cortical pallor and small-vessel spasm following treatment with nimodipine. It is hypothesized that nimodipine exerts its effects through reversal of ischemia-induced secondary vasoconstriction, and that this drug may be an important adjunctive treatment for patients with focal cerebral ischemia.

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