Effects of TA-3090, a novel 1,5-benzothiazepine calcium antagonist on cerebral energy metabolism and blood flow in bilateral carotid arterial occlusion-induced cerebral ischemia model of SHRSP

The sensitivity of cerebral energy metabolism to ischemic and hypoxic stresses following global cerebral ischemia was evaluated in a cat model using 31P nuclear magnetic resonance (NMR) spectroscopic methods. Complete global cerebral ischemia of 5 to 10 min in length was produced at 1 h intervals by reversible arterial occlusion, permitting continuous monitoring of NMR and EEG. Ischemia appeared to produce slightly more severe energy failure in animals that had previously experienced an ischemic injury. Preischemic hypoxia (5% O2 for 5 min) resulted in minor changes in the levels of phosphocreatine and intracellular inorganic phosphate, which were slightly amplified in animals that previously experienced ischemia.

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L-arginine decreases infarct size caused by middle cerebral arterial occlusion in SHR

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.263.5.h1632 ◽

1992 ◽

Vol 263 (5) ◽

pp. H1632-H1635 ◽

Cited By ~ 9

Author(s):

E. Morikawa ◽

Z. Huang ◽

M. A. Moskowitz

Keyword(s):

Cerebral Ischemia ◽

Infarct Size ◽

Focal Cerebral Ischemia ◽

Arterial Occlusion ◽

Cerebral Blood Vessels ◽

Hypertensive Rats ◽

Vessel Occlusion ◽

Spontaneously Hypertensive ◽

Cerebral Arterial Occlusion ◽

Carotid Arterial

L-Arginine, but not D-arginine, serves as a precursor for the synthesis of nitric oxide (NO), a potent dilator of cerebral blood vessels. We examined the effects of administering L-arginine (300 mg/kg ip) on the volume of infarction in two models of focal cerebral ischemia in spontaneously hypertensive rats (SHR). L-Arginine was administered before (16 and 3 h) and after (5 min and 2 h) vessel occlusion, and animals were killed 24 h later. L-Arginine treatment decreased infarct size in rats subjected to distal middle cerebral arterial (MCA) plus ipsilateral common carotid arterial (CCA) occlusion by 31% [147 +/- 12 (saline) vs. 101 +/- 9 mm3 (L-arginine), P < 0.05]. D-Arginine, administered according to the same dosage and protocol, was without effect. In the group subjected to proximal MCA occlusion, L-arginine decreased infarction size in the striatum by 28% [47 +/- 5 (saline) vs. 34 +/- 3 mm3 (L-arginine), P < 0.05] and neocortex by 11% [193 +/- 7 (saline) vs. 171 +/- 8 mm3 (L-arginine), P < 0.05]. Changes in blood pressure or other measured physiological parameters did not account for the observed differences. The possible use of L-arginine for the treatment of focal cerebral ischemia merits further investigation.

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Ascending pathways mediating somatoautonomic reflexes in exercising dogs

Journal of Applied Physiology ◽

10.1152/jappl.1987.62.3.1186 ◽

1987 ◽

Vol 62 (3) ◽

pp. 1186-1191 ◽

Cited By ~ 17

Author(s):

J. W. Kozelka ◽

G. W. Christy ◽

R. D. Wurster

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Surgical Techniques ◽

Arterial Occlusion ◽

Cardiovascular Responses ◽

Spinal Pathways ◽

Arterial Blood ◽

Bilateral Carotid ◽

Dorsolateral Funiculus ◽

Carotid Arterial

The ascending spinal pathways mediating somatocardiovascular reflexes during exercise were studied in unanesthetized dogs by placing lesions in the lumbar spinal cord. After training to run on a treadmill with hindlimbs only, 20 dogs were anesthetized and instrumented using sterile surgical techniques. To chronically record heart rate and arterial blood pressure, the aorta was cannulated via the omocervical artery. To test the intactness of descending spinal sympathetic pathways, reflex pressor responses to baroreceptor hypotension were produced by bilateral carotid arterial occlusion using pneumatic vessel occluders placed around the common carotid arteries. To generate transient ischemic exercise (120 s), a pneumatic occluder was placed around the left iliac artery. Eight to 10 days after instrumentation, blood pressure and heart rate were monitored at rest and during hindlimb running with and without simultaneous iliac arterial occlusion. The modest pressor response and tachycardia elicited by hindlimb exercise were markedly augmented by simultaneous hindlimb ischemia (i.e., iliac arterial occlusion). Lesion placement in the dorsolateral sulcus area and the dorsolateral funiculus at L2 significantly reduced the blood pressure and heart rate responses to simultaneous exercise occlusion. The cardiovascular responses to nonischemic exercise and bilateral carotid arterial occlusion were not altered by such spinal sections. It is concluded that in the dog the ascending spinal pathways mediating cardiovascular responses to ischemic exercise are located in the lateral funiculus, including the dorsolateral sulcus area and dorsolateral funiculus.

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Cerebral energy metabolism and blood flow

Caffeine and Behavior: Current Views & Research Trends ◽

10.1201/9781439822470-7 ◽

2020 ◽

pp. 95-111

Keyword(s):

Blood Flow ◽

Energy Metabolism ◽

Cerebral Energy Metabolism

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Characteristics of reactive hyperemia in the cerebral circulation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1984.246.1.h52 ◽

1984 ◽

Vol 246 (1) ◽

pp. H52-H58 ◽

Cited By ~ 7

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.

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