Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of an anaesthetic dose of chlormethiazole (Hemineurin) on blood flow (CBF) and oxygen consumption (CMRO2) in the rat brain was investigated. In spontaneously breathing animals a dose of 160 mg . kg-1 of chlormethiazole, infused i.v., induced a state close to surgical anaesthesia. In paralyzed animals, the same dose decreased CBF and CMRO2 to about 60% of control, an effect similar to that observed after an anaesthetic dose of phenobarbitone. Neither a protective nor a detrimental effect of chlormethiazole could be demonstrated when the drug was given during reversible and pronounced, incomplete ischaemia, as evaluated from the postischaemic tissue concentrations of labile phosphates (PCr, ATP, ADP, AMP) and of lactate and pyruvate. It is concluded that protection in this situation (as earlier shown with phenobarbitone) must, at least partly, be related to other mechanisms than a depression of metabolism.
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PMID:Influence of chlormethiazole on cerebral blood flow and oxygen consumption in the rat, and its effect on the recovery of cortical energy metabolism after pronounced, incomplete ischaemia. 3 16

Eighty-five studies of regional cerebral blood flow (rCBF) were performed on 49 patients with ruptured intracranial aneurysms. The changes in rCBF were analyzed under various pathophysiological conditions, The degree of flow abnormalities correlated well with the clinical severity of neurological deficits. All of the patients with diffuse vasospasm of severe grade, to less than half of their control value, showed focal areas of decreased flow below 30 ml/100 gm/min, in addition to a reduction in mean CBF. The relief or disappearance of vasospasm in angiograms was followed by the increase of rCBF in the ischemic focus and mean CBF. Marked reduction in rCBF was found in patients with intracerebral hematoma and ventricular dilatation. Impaired CO2 response and autoregulation were found in patients with severe neurological deficits, a severe degree of vasospasm and marked depression of CBF. In this series direct operation was delayed in patients with impaired vascular reactivity as well as marked decrease of mean CBF below 30 ml/100 gm/min; good clinical results were obtained in thses patients.
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PMID:Regional cerebral blood flow in patients with ruptured intracranial aneurysms. 43 Jan 52

CBF was studied in 15 cases of vascular headache by the 135Xe intra-arterial injection method. The mean CBF was found to be increased during the headache phase of the migraine attacks in half the cases, mainly due to an increase in the rapid component (CBFg). After the attack there could be an increase or a decrease of the slow component (CBFw). Reactivity to anaesthetic depression was studied in 8 migraine cases and on the whole it was found not to be much altered in most cases. Finally, no modifications of CBF were found in any of 3 cases of cluster headache who were studied during attacks of severe pain.
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PMID:Cerebral blood flow in migraine and cluster headache. Compartmental analysis and reactivity to anaesthetic depression. 72 60

Forty-five studies of regional cerebral blood volume (rCBV), regional cerebral blood flow (rCBF), and regional cerebral oxygen utilization (rCMRO2) were performed in 30 patients undergoing diagnostic cerebral angiography for evaluation of a subarachnoid hemorrhage due to a ruptured intracranial aneurysm. Tracer methods employing radioactive oxygen-15 were used to measure rCBV, rCBF, and rCMRO2. The patient studies were divided into groups based on their neurological status and the presence or absence of cerebral vasospasm. Subarachnoid hemorrhage, with and without vasospasm, produced significant decreases in CBF and CMRO2. In general, patients with more severe neurological deficits, and patients with more severe degrees of vasospasm, had a more marked depression of CBF and CMRO2. The most striking finding was a significant (p less than 0.001) increase in CBV (to 58% above normal) in patients with severe neurological deficits associated with severe cerebral vasospasm. This large increase suggests that cerebral vasospasm consists of constriction of the large, radiographically visible extraparenchymal vessels accompained by a massive dilation of intraparenchymal vessels.
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PMID:Effects of subarachnoid hemorrhage on cerebral blood volume, blood flow, and oxygen utilization in humans. 84 30

The effects of diazepam, clomipramine, and chlorpromazine upon cerebral metabolism and blood flow were examined separately in 18 dogs. After the administration of diazepam or clomipramine, cerebral cortical oxygen consumption (CMRO2) decreased significantly by a maximum of 17% and 13% of control within 10 minutes and 15 minutes, and returned to control at 120 minutes and 90 minutes, respectively. Chlorpromazine, however, decreased by a maximum of 10% of control, a level which continued throughout the period of observation. It was observed that reduction in CMRglucose was followed by the reduction in CMRO2 at an interval during the early stages of CMRO2 depression. Diazepam produced a significant decrease in CBF accompanied by reduction in CMRO2, but neither clomipramine nor chlorpromazine had any effect on CBF in spite of reduction in CMRO2. Reduction in CMRO2 both with diazepam and clomipramine was accompanied by slow wave activities of EEG, but with chlorpromazine reduction in CMRO2 was accompanied with less pronounced slow wave activities. It was concluded that the three drugs examined were cerebral metabolic depressants.
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PMID:Effects of psychotropic drugs on canine cerebral metabolism and circulation related to EEG--diazepam, clomipramine, and chlorpromazine. 118 21

We have developed the multiprobe assembly (MPA) by which metabolic, ionic and electrical activities can be monitored from the surface of the brain. In the present study we included optical fibers for the monitoring of intracapillary hemoglobin oxygenation by use of the Erlangen Microlight Guide Spectrophotometer (EMPHO-I) from the surface of the gerbil brain. The newly developed MPA provides simultaneous information about oxygen delivery (oxydeoxy Hb), tissue pO2 level, as well as the intracellular oxygen balance (intramitochondrial redox state). The ionic homeostasis was evaluated by monitoring extracellular K+ and Ca2+ activities reflecting the permeability changes of cation channels as well as the activities of Na+,K(+)-ATPase and other ion linked transport processes. The electrical activities were monitored by a bipolar electrocortical surface probe and DC steady potential. The subjects of the present study were Mongolian gerbils (Meriones unguiculatus) anesthetized and operated according to our routine techniques. After 30 min of recovery from the operation each gerbil was exposed to a short anoxia, graded hypoxia, ischemia as well as spreading depression. The results can be summarized as follows: 1. A clear correlation was recorded between the changes in oxydeoxy Hb spectra, tissue pO2 level and oxidation-reduction state of intramitochondrial NADH under oxygen deficiency situations (hypoxia, ischemia). 2. Blood volume changes under various perturbations monitored by various probes (366 reflectance and EMPHO-I) correlated very well with each other. 3. The degree of inhibition of Na+,K(+)-ATPase induced by oxygen deficiency could be interpreted by changes in extracellular levels of K+ measured by the surface mini-electrode. 4. Brain stimulation induced by spreading depression mechanism led to transient changes in ionic homeostasis and increase in energy requirements. The major HbO2 response was an increase in oxygenation due to the large CBF increase as monitored by the laser Doppler flowmeter. 5. Changes in oxy-deoxy Hb under fast scanning of 500-600 nm during 2-3 seconds of bilateral carotid arterial occlusion provided an indirect index for tissue O2 consumption.
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PMID:Multiparametric evaluation of brain functions in the Mongolian gerbil in vivo. 133 23

Cerebral blood flow was measured by the H2 clearance method 30 and 60 min after the implantation of 300, 250, 125, or 50 microns diameter platinum-iridium electrodes 2 mm deep into the right parietal cortex of normothermic, normocarbic halothane-anesthetized rats. Another group of animals had 50 microns electrodes inserted 1 mm. In all animals, the presence or absence of a wave of spreading depression (SD) was noted at the time of implantation, with recordings made with glass micropipettes. H2 flow values were compared with those measured in gray matter from the same anatomical region (but from different rats), using [3H]nicotine. The incidence of SD ranged from 60% following insertion of 300 microns electrodes to 0% with 50 microns electrodes. H2 clearance flows also varied with electrode size, from 77 +/- 21 ml 100 g-1 min-1 (mean +/- standard deviation) with 300 microns electrodes to 110 +/- 31 and 111 +/- 16 ml 100 g-1 min-1 with 125 and 50 microns electrodes, respectively (insertion depth of 2 mm). A CBF value of 155 +/- 60 ml 100 g-1 min-1 was obtained with 50 micron electrodes inserted only 1 mm. Cortical gray matter blood flow measured with [3H]nicotine was 154 +/- 35 ml 100 g-1 min-1. When the role of SD in subsequent flow measurements was examined, there was a gradual increase in CBF between 30 and 60 min after electrode insertion in those animals with SD, while no such change was seen in rats without SD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of electrode size on the incidence of spreading depression and on cortical cerebral blood flow as measured by H2 clearance. 154 95

To date, positron emission tomography (PET) has been the only technology for the quantitative imaging of the changes of regional cerebral glucose (rCMRGl) or oxygen metabolism and blood flow (rCBF) associated with psychophysical stimulation and with the performance of mental tasks. So far, the majority of studies performed in healthy subjects demonstrated activation patterns involving not only certain limbic structures, most of all hippocampus, amygdala, parahippocampus, and cingulate, but also temporal, parietal, and occipital association cortex, depending on the applied paradigm. Indeed, the closest correlation between regional metabolism and memory test scores was found in mesiotemporal structures during the performance of memory tasks. Metabolic or CBF studies also seem to indicate that memorizing strategies may differ among individuals. PET was repeatedly used to investigate metabolic and/or blood flow abnormalities in patients with various amnestic syndromes. In cases with uni- or bilateral lesions of mesiotemporal structures, caused by surgery, herpes simplex encephalitis, or permanent ischemic, anoxic, or toxic damage, disturbances of metabolism and blood flow typically extended far beyond the morphological defects detected by computed tomography or magnetic resonance. In acute transient global amnesia, CBF and metabolism were decreased bilaterally in the mesiotemporal lobes, where hypometabolism persisted for some time, while higher values were observed in thalamus and some cortical areas. Diencephalic lesions causing Korsakoff's syndrome were associated with decreased rCMRGl in the hippocampal formation, upper brainstem, cingulate, and thalamus. Discrete thalamic infarcts caused amnesia and metabolic depression in the morphologically intact ipsilateral thalamus and in various projection areas of the infarcted nuclei. In ischemic forebrain lesions, amnestic deficits could be related to involvement of the anterior cingulate and of basal cholinergic nuclei. A large number of pathologies are diffusely spread out in the brain and affect partially or predominantly structures in memory processing. This holds true especially in the various dementias where memory disturbances are a consistent and often leading feature. Notably, Alzheimer's disease can be distinguished from other dementias by its characteristic pattern of metabolic dysfunction, with the most prominent changes occurring in parietotemporal and frontal association cortex whose residual metabolism is related to the severity of the disease. Therefore, activation studies using paradigms involving memory functions enhance that typical pattern. Only in the activated state is metabolism of mesiotemporal structures significantly correlated with the performance in memory tests. Other dementias also affect some of the distributed memory networks, with Huntington's disease suggesting a role of the striatum in memory processing.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:PET correlates of normal and impaired memory functions. 156 50

It has become increasingly clear that a stroke lesion usually consists of a densely ischemic focus and of perifocal areas with better upheld flow rates. At least in rats and cats, some of these perifocal ("penumbral") areas subsequently become recruited in the infarction process. The mechanisms may involve an aberrant cellular calcium metabolism and enhanced production of free radicals. In general, though, the metabolic perturbation in the penumbra requires better characterization. The objective of this article was to define flow distribution in a rat model of reversible middle cerebral artery (MCA) occlusion, so as to allow delineation of the metabolic aberrations responsible for the subsequent infarction. We modified the intraluminal filament occlusion model recently developed by Koizumi et al. (1986), and described in more detail by Nagasawa and Kogure (1989), adopting it for use in both spontaneously breathing and artificially ventilated rats. Successful occlusion of the MCA (achieved in about 9/10 rats) was judged by unilateral EEG depression in ventilated rats, and neurological deficits, such as circling, in spontaneously breathing ones. CBF in the ipsilateral hemisphere was reduced to nearly constant values after 20, 60, and 120 min of occlusion, flow rates in the focus being about 10% and in the perifocal ipsilateral areas about 15-20% of control (contralateral side). When the filament was left in place (permanent occlusion) 2,3,5-triphenyl tetrazolium chloride (TTC) staining and histopathology after 24 h showed a massive infarct on the occluded side, extending from caudoputamen and overlaying cortex to the occipital striate cortex. Animals recirculated after 60 min of MCA occlusion, and allowed to survive 7 days for histopathology, showed infarction of the caudoputamen (lateral part or whole nucleus) in 5/6 animals and selective neuronal necrosis in one animal. The neocortex showed either infarcts, selective neuronal necrosis, or no damage. There was some overlap between neocortical areas which were infarcted and those which were salvaged by reperfusion. In general, though, both the CBF data and the recovery studies with a histopathological endpoint define large parts of the neocortex as perifocal (penumbral) areas which lend themselves to studies of metabolic events leading to infarction.
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PMID:Ischemic penumbra in a model of reversible middle cerebral artery occlusion in the rat. 160 Nov 3

Spreading cortical depression (SCD) of EEG activity was induced in one cerebral hemisphere of conscious restrained rats by direct current stimulation of the lateral frontal cortex. Regional CBF was measured using [14C]iodoantipyrine and brain dissection. An early phase of increased CBF was not measured in conscious rats, but an early relative hyperperfusion was measured if the resting CBF was first reduced by treatment with pentobarbital or indomethacin. A long-lasting reduction in CBF was measured in conscious rats following the passage of SCD. This flow reduction resolved after 3 h. In conscious rats, CBF decreased in the striatum and thalamus ipsilateral to the SCD, paralleling the CBF changes occurring in the cortex. The CBF change in these deep structures was abolished by pentobarbital. An early transient increase in regional CBF was measured in the cerebral cortex contralateral to the hemisphere involved with SCD in conscious rats. This early contralateral hyperperfusion was also abolished by pentobarbital or indomethacin but not by atropine or propranolol. The vascular response to SCD in conscious rats differs from that which occurs in anesthetized rats.
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PMID:Regional cerebral blood flow during spreading cortical depression in conscious rats. 198 99


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