Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In baboons the right cerebral hemisphere was embolised by a shower of microemboli, immediately followed by one large embolus designed to occlude the middle cerebral artery (MCA). One hour after embolism a significant, though small, reduction in blood flow and oxygen consumption of the embolised hemisphere was recorded, at which time the animals were killed and brain monoamines measured. Dopamine was reduced in the ipsilateral caudate nucleus, the reported site of maximal ischaemic damage in this model. Dopamine levels were increased in frontal and occipital grey matter sampled from areas surrounding the occluded MCA territory and in similar brain areas of the opposite non-embolised hemisphere. Noradrenaline was increased in grey matter from both cerebral hemispheres, as well as subcortical structures bilaterally. Brain 5-hydroxytryptamine levels were unaltered, but increased 5-hydroxyindoleacetic acid in cisternal cerebrospinal fluid suggested transient alteration in 5-hydroxytryptamine metabolism after embolism. The effects of cerebral embolism on brain monoamine metabolism appear to be different from the effects of permanent surgical occlusion of major cerebral vessels. The bilaterality of effects after unilateral hemispheric embolism might be related to diaschisis. The mechanisms of the observed changes, as well as their relevance to the progression of cerebral ischaemia and the complications associated with cerebral embolism, still require to be established.
 ...
PMID:Influence of cerebral embolism on brain monoamines. 4 Oct 29

Local cerebral ischemia was produced in rats by internal carotid artery injection of 35 mu carbon microspheres, and brain norepinephrine (NE), dopamine, and cyclic adenosine 3, 5-monophosphate (cAMP) were measured in embolized and intact hemispheres at intervals up to four hours. Sham-operated animals were controls. There was an instantaneous increase of cAMP. Norepinephrine was reduced within two minutes after embolization and remained low for four hours. Dopamine increased by five minutes after embolization and returned to normal after four hours. Results were qualitatively similar, but less, in the nonembolized hemisphere. Accumulation of cAMP is thought to be due to a direct effect of ischemic hypoxia and may be the initiating factor in increased glycolysis that occurs in ischemia. Decrease in NE may be secondary to its generalized release from presynaptic terminals throughout the brain and could be a factor in cortical vasocontriction that follows embolization. Dopamine changes are a reflection of alterations in energy metabolism.
 ...
PMID:Catecholamines in experimental brain ischemia. 23 32

Using specific anesthetic agents, permanent segmental occlusion of the proximal middle cerebral artery (MCA) causes ischemic infarction limited to the putamen and other deep hemispheral structures in primates. Using this model, 25 rhesus monkeys were subjected to acute arterial hypertension before, during and up to 5 days after onset of MCA occlusion in order to reevaluate the possible role of the ischemic process in pathogenesis of cerebral hemorrhage. Norepinephrine infusion induced prompt rapid rise in mean arterial pressure (MAP) and intracranial pressure (ICP) limited to the duration of infusion. This procedure produced acute ischemic lesions which were totally bland but topographically more extensive than untreated controls; in chronic lesions, however, deep nuclear masses showed hemorrhagic infarction. Animals given 5% CO2 air had slowly progressive elevation in ICP and MAP. Acute specimens showed intact, widely-dilan hypercarbia was induced 5 days after MCA occlusion, animals developed intracerebral hematoma involving putamen, external capsule and claustrum, occasionally dissecting through to ipsilateral ventricle. In acute cerebral ischemia, elevated MAP produced only quantiative changes in lesion size. In the vasoproliferative stages of mature infarction, MAP elevation induced by a cerebral vasoconstrictor caused hemorrhagic infarctions while cerebral vasodilation caused intracerebral hematomas.
 ...
PMID:Primate model of cerebral hematoma. 82 36

The changes in acetylcholine (ACh), monoamine and monoamine metabolite levels following cerebral ischemia in Mongolian gerbils were examined. In addition, the effects of Sho-saiko-to-go-keishi-ka-shakuyaku-to (TJ-960), which is a spray-dried mixture of 9 herbal drugs, on these changes were also examined. The dramatic decrement of ACh levels in ischemic gerbils was significantly inhibited by p.o. administration of TJ-960 at a daily dose of 3.5 g/kg or 700 mg/kg for one month. Norepinephrine (NE) was also reduced in all ischemic brain regions, and TJ-960 also recovered the level of NE. In ischemic gerbil brains, the dopamine (DA) levels decreased and its metabolites increased in the striatum, but DA and its metabolites in the thalamus + midbrain region increased. The serotonin (5HT) level was reduced in the cerebral cortex and hippocampus. TJ-960 inhibited these monoaminergic changes in ischemic gerbils. This suggests that TJ-960 may provide anti-ischemic action and beneficial effects on various symptoms induced by ischemia.
 ...
PMID:The effects of sho-saiko-to-go-keishi-ka-shakuyaku-to (TJ-960) on ischemia-induced changes of brain acetylcholine and monoamine levels in gerbils. 237 Sep 41

We examined the effects of 20 minutes' cerebral ischemia on cerebral microcirculatory responses to topical norepinephrine and systemic hypotension in three groups (sham-operated control, 2-3 hours postischemia, and 24 hours postischemia) of anesthetized newborn pigs equipped with closed cranial windows. Cerebral ischemia may eliminate the prostanoid vasodilator system from the cerebral circulation. Norepinephrine (10(-4) M) decreased pial arteriolar diameters similarly in all three groups (27%, 28%, and 21%, respectively), but only the sham-operated group exhibited pial arteriolar dilation in response to hypotension (28% at 33 mm Hg). Two-three and 24 hours after cerebral ischemia, hypotension decreased pial arteriolar diameters (21% and 17%, respectively). In sham-operated piglets, norepinephrine and hypotension increased cortical periarachnoid cerebrospinal fluid prostanoid concentrations. However, neither norepinephrine nor hypotension altered cerebral prostanoid production 2-3 or 24 hours after cerebral ischemia. Therefore, we conclude that after cerebral ischemia, autoregulatory pial arteriolar dilation in response to hypotension is absent, while vasoconstriction in response to norepinephrine is intact.
 ...
PMID:Postischemic cerebral microvascular responses to norepinephrine and hypotension in newborn pigs. 292 31

Changes in cerebral free amino acids, catecholamines and uric acid levels were explored for up to 7 days after cerebral ischemia in the rat. Fifty male Sprague-Dawley rats were subjected to occlusion of the middle cerebral artery on the olfactory tract, under halothane anesthesia. The animals were decapitated at 2, 4, 6, 12, 24 hours and 2, 3, 5, 7 days after the surgery, respectively. The brains were rapidly removed. The cerebral hemispheres were divided into right and left halves, and homogenized in sulfosalicylic acid solution. Free amino acids were analyzed by colormetric method. Cathecholamines and uric acid were analyzed by high-performance liquid chromatography. Each parameters were measured both on the ischemic and contralateral hemispheres. The time course of changes in each parameters were observed by means of the ratio, which is the value of ischemic side divided by that of contralateral side. Free amino acids Dicarboxylic group; Decreases in glutamate and increases in glutamine suggest one aspect of detoxication of ammonia within the ischemia tissue. Monocarboxylic group; GABA, glycine, alanine were increased in early ischemic state, and gradually lowered to the normal values. These suggest the impairment of tricarboxylic acid (TCA) cycle in the ischemic tissues, since these amino acids are closely related to TCA cycle. Essential amino acids, except for tryptophan, were increased until the end of study. These increases suggest the utilization of essential amino acids for protein synthesis might be disturbed in the ischemic tissues. Catecholamines and precursors; Norepinephrine and dopamine were lowered gradually. On the other hand, phenylalanine and tyrosine were increased during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Biochemical studies of the cerebral ischemia in the rat--changes in cerebral free amino acids, catecholamines and uric acid]. 370 75

Ischemic brain injury affects the content and metabolism of brain monomines. Our aim was to know the time course of changes in regional cerebral catecholamines during focal cerebral ischemia, and whether focal cerebral ischemia may affect the metabolism of catecholamines in distant area of the brain. Methods Fifty-five rats were subjected to occlusion of the middle cerebral artery (MCA) on the olfactory tract, under halothane anesthesia. Fourteen animals were sham-operated group. Animals were decapitated at 1/2, 1,2,3,6,12 and 24 hours post-occlusion (PO), respectively. The brains were removed, and the brain structures dissected out include bilateral corpus striatum, cerebral cortex (MCA territory) and cerebellar hemisphere. Catecholamines were extracted by alumina procedure, and determined by high-performance liquid chromatography with electrochemical detection. Results Dopamine (DA) contents, in ipsilateral corpus striatum and cerebral cortex to the ischemia, decreased at 1 hour PO, and reached, at 6 hours PO, to 40% of control value in corpus striatum and 30% in cerebral cortex, respectively. After 6 hours PO, DA remained low. Norepinephrine (NE) content in the ipsilateral corpus striatum gradually reduced and reached to 60% of control value at 24 hours PO. NE in the ipsilateral cerebral cortex decreased to 50% of control at 1 hour PO, and thereafter remained reduced. In the contralateral corpus striatum and cerebral cortex, either DA or NE showed no significant changes, except 1/2 hour PO. NE contents in bilateral cerebral cortex showed a transient increase at 1/2 hour PO. Cerebellar NE content, bilaterally, reduced slowly to 70% of control at 24 hours PO.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Changes in regional cerebral catecholamines following middle cerebral artery occlusion in the rat]. 407 79

Norepinephrine (NE) depletion of the cerebral cortex after lesion of the ipsilateral locus ceruleus (LC) causes abnormalities of cerebral oxidative metabolism when the cortex is stimulated to increased energy demand (Harik, S. I., J. C. LaManna, A. I. Light, and M. Rosenthal (1979) Science 206: 69-71; LaManna, J. C., S. I. Harik, A. I. Light, and M. Rosenthal (1981) Brain Res. 204: 87-101). These abnormalities were exhibited as decreased mitochondrial reducing equivalent flow. One possible cause of this would be the decreased availability of oxidative metabolic substrates in the NE-depleted cortex. We therefore investigated the effect of unilateral LC lesion and the resultant depletion of ipsilateral endogenous NE on glycogen and other energy metabolites in the cerebral cortex of rats under three conditions: (1) at "rest," (2) when energy demand is inncreased markedly by seizures, and (3) during total cerebral ischemia. We report no differences in cerebral metabolites between NE-depleted and control hemispheres at "rest." In seizures and ischemia, however, the increase in the level of adenosine 3':5'-monophosphate (cyclic AMP) and the breakdown of glycogen were impaired considerably in the NE-depleted cortex. The data suggest that depletion of central NE impairs cerebral glycogenolysis in response to increased energy demands and ischemia. Such impairment may be mediated via a cyclic AMP-related mechanism.
 ...
PMID:Norepinephrine regulation of cerebral glycogen utilization during seizures and ischemia. 627 95