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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effect of a gamma-aminobutyric acid (GABA)-A receptor-induced postsynaptic inhibition on regional CBF (rCBF) in awake humans. For this purpose we used a new specific GABA-A agonist, 4,5,6,7-tetrahydroisoxazolo(5,4)-pyridin-3-ol (THIP). As part of a new diagnostic procedure for the determination of which hemisphere subserved language, THIP was infused into the internal carotid artery 20 s before measurement of the rCBF. Administered by this route the THIP is distributed to the neocortex and neostriatum. THIP induced a dosage-dependent decrease of the rCBF. The rCBF decrease was not due to any direct effect on the cerebral vessels. The efficiency of the THIP-induced postsynaptic inhibition was tested by having the subjects voluntarily activate the inhibited cortex. During submaximal inhibition the subjects were able voluntarily to counteract decreases of rCBF in superior frontal cortex and motor cortex. Larger doses of THIP abolished this response and depressed the rCBF to baseline levels (20 ml/100 g/min). This was associated with 10-min total depression of function of the anterior two-thirds of the injected hemisphere. An analysis of the changes of rCBF in activated and nonactivated cortex--with and without THIP-induced inhibition--showed that it would be very unlikely that average increases in synaptic inhibition would increase rCBF in neocortical areas. Intracarotid injection of the water-soluble, nonirritative THIP is a very useful alternative to sodium amytal injection for determination of hemispheric dominance.
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PMID:The effect of the GABA-A agonist THIP on regional cortical blood flow in humans. A new test of hemispheric dominance. 336 94

Focal cerebral ischemia was induced in rats by occlusion of the middle cerebral artery. By a triple-tracer technique, cerebral glucose utilization, glucose content, and blood flow were simultaneously determined. Computer-assisted autoradiography revealed a core of dense ischemia in the lateral two-thirds of the striatum. A border zone of increased 2-deoxy-D-glucose (DG) uptake surrounded the ischemic insult in the acute stage. The lumped constant was increased only moderately in the border zone. Therefore, the enhanced DG uptake reflected increased glucose consumption. CBF was reduced to 20-30% in the cortical border, while minor depression and in some animals hyperemia were evident in the striate border. Six hours after the insult, the border zones of increased glucose consumption had disappeared in half the animals. In no animals examined after 20 h was glucose consumption enhanced. The study indicated a stable metabolic response to a reproducible focal insult. We conclude that continued enhancement of glucose consumption in marginally perfused areas indicates neuronal damage.
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PMID:Focal ischemia of the rat brain: autoradiographic determination of cerebral glucose utilization, glucose content, and blood flow. 373 1

A review and a reappraisal are presented of earlier data on cerebral circulatory and metabolic studies in normal active elderly men (Group I) of mean age 71 years, compared with normal young subjects of mean age 21 years, conducted at the National Institutes of Health, Bethesda, MD, U.S.A., during 1956-1958. There was no significant difference in the mean CBF and cerebral metabolic rate for oxygen (CMRO2) values between the two populations; i.e., these important parameters did not fall with chronological aging per se. There was significant depression in the mean cerebral metabolic rate for glucose (CMRG) value (by approximately 23%) in the aged compared with the young. Newer methods using positron emission tomography and appropriate isotopes have confirmed these findings in normal aging in human subjects and experimental animals. As expected, MABP and cerebral vascular resistance (CVR) were significantly elevated in the normal aged. MABP was even more elevated in elderly hypertensive subjects, and the CVR more elevated in the subjects with arteriosclerosis (Group II), who also showed a small but significant fall in CBF and in internal jugular venous PO2. The CBF showed a more pronounced fall in senile aged patients with chronic brain syndrome (Group III), in whom the CMRO2 also showed a marked drop (by approximately 22%); the CMRG fell still further (approximately 40% of that in the young). Of the few aged subjects followed up after a lapse of 11 years by a repeat estimation of the same physiological and psychological parameters and of the EEG, most showed clear worsening, together with a fall in overall physical and intellectual performance, probably related to a rise in CVR and an increase in atherosclerosis with aging.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral blood flow and metabolism in normal human aging, pathological aging, and senile dementia. 397 14

The regional flow-metabolism couple was studied during the recovery period after 1 h of left middle cerebral artery (MCA) occlusion in cats. Local CBF (LCBF) was assessed at the end of ischemia as well as at the end of 4 h of recirculation by the microsphere technique. Local CMRgl (LCMRgl) was measured at the end of the recirculation period with [14C]2-deoxyglucose. Histology was evaluated by light microscopy from coronal brain blocks adjacent to those used for the determination of LCBF and LCMRgl. When LCBF in the central and peripheral MCA territories during the recovery period was between 40 and 115% of the value in sham occlusion studies, LCMRgl was greater than the control level found in the sham studies, and was accompanied by slight histological damage. This finding suggests that anaerobic glycolysis may persist after transient ischemia in spite of the recovery of LCBF to a level that is normally greater than the threshold for the activation of anaerobic glycolysis (less than 40% of the control). Persistent anaerobic glycolysis in the reperfusion period following an ischemic insult may be a sign of early tissue damage. Some of the regions in the peripheral MCA territory with LCBF between 40 and 110% of the levels during the recovery period in the sham studies showed a mild to moderate depression in LCMRgl so that the flow-metabolism ratio remained normal. These regions did not exhibit histological damage. This possible protective mechanism of the tissue in response to ischemia is discussed from the standpoint of the relationship between flow and metabolism.
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PMID:Regional flow-metabolism couple following middle cerebral artery occlusion in cats. 398 23

The effect of iodoacetate (IAA), an inhibitor of glycolysis, on local CBF (LCBF) and local CMRglu (LCMRglu) was studied in cats by means of a double-radionuclide autoradiographic method. Artificial CSF containing 5 mM IAA was superfused on the left parietal cortex under a cranial window for 30 min. [14C]2-Deoxyglucose and [123I]iodoantipyrine were injected for the determination of LCMRglu and LCBF, respectively. A marked increase in LCBF, accompanied by a moderate to severe depression of LCMRglu, was observed in the IAA-superfused cortex. This result suggests that LCBF may be closely regulated by the cellular energy state associated with glycolytic activity in brain tissue.
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PMID:Effect of iodoacetate on local cerebral blood flow and glucose metabolism in cats: a double-radionuclide autoradiographic study. 398 28

The purpose of the present study was to examine the cerebral perfusion after spreading depression with special emphasis on its relation to the perfusion changes in migraine. The cerebrovascular reactivity to changes of arterial PCO2 tension in the range of 24-70 mm Hg and to changes of MABP in the range of 55-150 mm Hg was studied in the rat brain after one episode of cortical spreading depression. Regional CBF (rCBF) was measured in the frontal, parietal, and occipital cortex, the basal ganglia, and the cerebellum of both hemispheres after the intravenous bolus injection of [14C]iodoantipyrine. rCBF decreased in the cortical regions to 69-73% of control values for 1 h after spreading depression in every single rat, but remained unchanged in the basal ganglia and cerebellum. CBF changed with alterations of arterial carbon dioxide tension in all brain regions. In control regions, CBF changed by 2.8-3.9% per mm Hg PaCO2 change, whereas in the spreading depression cortex, CBF changed by only 1.3-1.5%. The difference between control and spreading depression cortex was significant at p less than 0.001, indicating a reduced CO2 sensitivity of the cortical regions invaded by spreading depression. rCBF remained unchanged in all brain regions in the MABP range of 80-150 mm Hg, reflecting the intact autoregulatory function of the two sides, and at a MABP of less than 80 mm Hg, rCBF decreased in parallel in symmetrical regions. It is concluded that the hypoperfusion after spreading depression is due to a vasoconstrictor stimulus overriding the vasodilatory effect of acid pH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-lasting reduction of cortical blood flow of the brain after spreading depression with preserved autoregulation and impaired CO2 response. 643 24

With the use of positron emission tomography (PET) and the 15O steady-state-[18F]fluorodeoxyglucose combined method, the local interrelationships between the cerebral metabolic rate for oxygen (CMRO2) and the cerebral metabolic rate for glucose ( CMRGlc ) were investigated in control subjects and in stroke patients. In addition to the classic in vivo autoradiographic approach, a kinetic method was used to measure CMRGlc because it was expected to be more reliable in cerebral ischemia. In control subjects local coupling between CBF, CMRO2, and CMRGlc was confirmed, and acceptable values for the CMRO2/ CMRGlc ratio were found; the latter, however, was lower in white matter than in gray. Uncoupling between CMRO2 and CMRGlc was observed in all stroke patients, suggesting that (1) enhanced anaerobic glycolysis occurred both in reperfused recent infarcts and in chronically ischemic tissue, and (2) substrates other than blood-borne glucose were being oxidized at the borders of recent infarcts. However, methodological uncertainties presently make such observations only tentative. Finally, a coupled depression of CMRO2 and CMRGlc was found in the contralateral cerebellum.
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PMID:Local interrelationships of cerebral oxygen consumption and glucose utilization in normal subjects and in ischemic stroke patients: a positron tomography study. 660 28

Seventy measurements of CBF were performed in 12 stroke patients by 133Xe inhalation and a rapidly rotating single photon emission computerized tomograph. CBF was measured every other day during the acute phase and at 2- and 6-month follow-up visits. A persistent contralateral cerebellar blood flow depression was evident in five patients with severe hemispheric low flow areas, which correlated with large, hypodense lesions on the computerized tomographic scan. In a sixth patient with a small, deep infarct, a transient crossed cerebellar low flow was observed, while the clinical symptoms persisted. It is concluded from this serial study that crossed cerebellar diaschisis is a common finding in completed stroke. It is probably caused by disconnection of the corticopontine pathways, a disconnection that tends to persist. The phenomenon is in fact less variable than the stroke-related CBF changes in the infarcted hemisphere, in which a period of relative hyperemia is frequently seen.
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PMID:Crossed cerebellar diaschisis in ischemic stroke: a study of regional cerebral blood flow by 133Xe inhalation and single photon emission computerized tomography. 660 30

Progressive brain damage after transient cerebral ischemia may be related to changes in postischemic cerebral blood flow and metabolism. Regional cerebral blood flow (rCBF) and cerebral glucose utilization (rCGU) were measured in adult rats prior to, during (only rCBF), and serially after transient forebrain ischemia. Animals were subjected to 30 minutes of forebrain ischemia by occluding both common carotid arteries 24 hours after cauterizing the vertebral arteries. Regional CBF was measured by the indicator-fractionation technique using 4-iodo-[14C]-antipyrine. Regional CGU was measured by the 2-[14C]deoxyglucose method. The results were correlated with the distribution and progression of ischemic neuronal damage in animals subjected to an identical ischemic insult. Cerebral blood flow to forebrain after 30 minutes of moderate to severe ischemia (less than 10% control CBF) was characterized by 5 to 15 minutes of hyperemia; rCBF then fell below normal and remained low for as long as 24 hours. Post-ischemic glucose utilization in the forebrain, except in the hippocampus, was depressed below control values at 1 hour and either remained low (neocortex, striatum) or gradually rose to normal (white matter) by 48 hours. In the hippocampus, glucose utilization equaled the control value at 1 hour and fell below control between 24 and 48 hours. The appearance of moderate to severe morphological damage in striatum and hippocampus coincided with a late rise of rCBF above normal and with a fall of rCGU; the late depression of rCGU was usually preceded by a period during which metabolism was increased relative to adjacent tissue. Further refinement of these studies may help identify salvageable brain after ischemia and define ways to manipulate CBF and metabolism in the treatment of stroke.
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PMID:Regional cerebral blood flow and glucose metabolism following transient forebrain ischemia. 710 26

CBF increases concomitantly with cortical spreading depression (CSD). We tested the hypothesis that CBF changes during CSD are mediated by nitric oxide (NO). Male Wistar rats (n = 23) were subjected to KCl-induced CSD before and after administration of nitric oxide synthase (NOS) inhibitors N-nitro-L-arginine (L-NNA) or N-nitro-L-arginine methyl ester (L-NAME) and in nontreated animals. CBF, CSD, and mean arterial blood pressure were recorded. Brain NOS activity was measured in vitro in control, L-NNA, and L-NAME-treated rats by the conversion of [3H]arginine to [3H]citrulline. Our data show that the NOS inhibitors did not significantly change regional CBF (rCBF) during CSD, even though cortical NOS activity was profoundly depressed and systemic arterial blood pressure was significantly increased. Our data suggest that rCBF during CSD in rats is not regulated by NO.
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PMID:Cerebral blood flow changes during cortical spreading depression are not altered by inhibition of nitric oxide synthesis. 752 32


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