Influence of the corticotropin releasing hormone (CRH) on the brain-blood barrier permeability in cerebral ischemia in rats.
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The increase in the blood-brain barrier (BBB) permeability and a developing cerebral oedema due to the ischemic infarction appear a few hours, and intensify during a few days, after closing the carotid arteries. It fails to be clear, however, what causes the increase in the microvessels damage, and whether the damage is a secondary result of the vasoactive substances released by the neurones and glia cells damaged by the ischemia. CRH, which plays an essential role in integrative the nervous, endocrine, and immunological systems, has a positive effect on the decrease in the permeability of the BBB damaged by various physical and chemical factors. Therefore, the examination of the CRH role in the cerebral ischemia may prove useful for explaining the processes taking place in the foci of the cerebral infarction and their environment. The experiment was carried out on rats which, 20 minutes before closing of both internal carotid arteries, was administered 10 microg CRH to cerebrospinal fluid via cisterna magna of the brain. The BBB permeability was measured 30 minutes, 3 hours, 3 days, and 7 days after closing the arteries. The experiment has shown the CRH protective effect on the BBB and its consequent effect on the decrease in the BBB permeability which appears in the 3 hours after closing the arteries (p<0.05), and is high significant during the chronic phase of the cerebral ischemia (p<0.03). It can be thus concluded that CRH, by affecting directly the endothelium of the cerebral vessels, decreases the endothelial damage in the acute phase of the ischemia. The decrease is noted to be more significant in the chronic phase of the ischemia; such an effect can be attributed to CRH stimulating the hypothalamic-adrenal axis, and to the secondary activation of the mechanisms decreasing the BBB permeability. (+info)
Production of cerebrospinal fluid leak artifact by residual 99mTc-pertechnetate.
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Residual oropharyngeal 99mTc activity was detected on an 111In-DTPA cisternogram creating the appearance of a CSF leak. This can be prevented by employing a spectrometer setting that encompasses only the higher principal photopeak of 111In. (+info)
Intracisternal urocortin inhibits vagally stimulated gastric motility in rats: role of CRF(2).
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1. Corticotropin-releasing factor (CRF) acts in the brain to inhibit thyrotropin-releasing hormone (TRH) analogue, RX-77368-induced vagal stimulation of gastric motility. We investigated CRF receptor-mediated actions of rat urocortin (rUcn) injected intracisternally (ic) on gastric motor function. 2. Urethane-anaesthetized rats with strain gauges on the gastric corpus were injected i.c. with rUcn and 20 min later, with i.c. RX-77368. CRF antagonists were injected i.c. 10 min before rUcn. 3. RX-77368 (1.5, 3, 10, 30 and 100 ng, i.c.) dose-dependently increased corpus contractions, expressed as total area under the curve (AUC, mV min(-1)) to 2.6+/-2.5, 6.1+/-5.9, 9.8+/-2.6, 69.7+/-21.7 and 74.9+/-28.7 respectively vs 0.2+/-0.1 after i.c. saline. Ucn (1, 3 or 10 microg) inhibited RX-77368 (30 ng)-induced increase in total AUC by 28, 62 and 93% respectively vs i.c. saline+RX-77368. 4. The CRF(1)/CRF(2) antagonist, astressin-B (60 microg, i.c.) completely blocked i.c. rUcn (3 microg, i.c.)-induced inhibition of gastric motility stimulated by RX-77368 (30 ng). 5. The selective CRF(2) antagonist, astressin(2)-B (30, 60 or 100 microg, i.c. ) dose-dependently prevented i.c. rUCn action while the CRF(1) antagonist, NBI-27914 did not. 6. In conscious rats, rUcn (0.6 or 1 microg, i.c.) inhibited gastric emptying of an ingested chow meal by 61 and 92% respectively. rUcn action was antagonized by astressin(2)-B. 7. These data show that i.c. rUcn acts through CRF(2) receptors to inhibit central vagal gastric contractile response and postoprandial emptying. (+info)
Hereditary subependymal heterotopia associated with mega cisterna magna: antenatal diagnosis with magnetic resonance imaging.
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Bilateral nodular subependymal heterotopia has recently been identified as a hereditary disease linked to the X-chromosome. The sonographic findings are very subtle and difficult to observe during the second trimester when the germinal matrix is at its largest. Fetal magnetic resonance imaging facilitates visualization of the periventricular area. We report a case of bilateral nodular heterotopia associated with mega cisterna magna diagnosed by ultrasound and magnetic resonance imaging at 29 weeks' gestation. Magnetic resonance imaging of the brain of the mother revealed similar findings to those observed in the fetus and neonate. This case confirms the association between mega cisterna magna and bilateral periventricular nodular heterotopia and demonstrates that neuroimaging studies of the mother can contribute to the fetal diagnosis. (+info)
A dissociation between fever and prostaglandin concentration in cerebrospinal fluid.
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1. Sustained fever has been induced in conscious rabbits by I.V. injection and infusion of endogenous pyrogen. 2. Cerebrospinal fluid (e.s.f.) was sampled from the cisterna magna at hourly intervals. The concentration of prostaglandin increased in parallel with rectal temperature. The prostaglandin was identified as one of the E series. 3. When sodium salicylate (1-5 m-mole followed by a continuous infusion of 9 mumole/min) was started 1 hr before endogenous pyrogen, the febrile response to the pyrogen was not significantly diminished but no rise of prostaglandin concentration was detected in c.s.f. 4. This dissociation between fever and prostaglandin concentration means that changes in cisternal prostaglandin concentration cannot be accepted as evidence that prostaglandin mediates the febrile response. (+info)
Intracranial administration of transforming growth factor-beta3 increases fat oxidation in rats.
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The effects of intracranial transforming growth factor (TGF)-beta3 on spontaneous motor activity and energy metabolism were examined in rats. After injection of TGF-beta3 into the cisterna magna of the rat, spontaneous motor activity decreased significantly for 1 h. The intracranial injection of TGF-beta3 produced an immediate decrease in respiratory exchange ratio (RER). No significant changes were observed in energy expenditure. TGF-beta3 induced a significant increase in total fat oxidation and a decrease in total carbohydrate oxidation. Furthermore, the serum substrates associated with fat metabolism were significantly altered in rats injected with TGF-beta3. Both lipoprotein lipase activity in skeletal muscle and the concentration of serum ketone bodies increased, suggesting that the increase in fat oxidation caused by TGF-beta3 may have occurred in the liver and muscle. Intracranial injection of TGF-beta3 appeared to evoke a switch in the energy substrates accessed in energy expenditure. These results suggest that the release of TGF-beta3 in the brain by exercise is a signal for regulating energy consumption. (+info)
The diagnosis of acoustic neuroma is usually evoked in a patient presenting with a long history of hearing disturbance in whom an enhancing lesion within the internal auditory canal and/or the cerebellopontine angle is found on MRI. Hypervascularity with arteriovenous shunting and early filling of enlarged veins is a common feature of malignancy and has been reported very rarely in benign acoustic neuroma. We present the case of a patient without hearing disturbance, who showed a highly vascular lesion with no component in the internal auditory canal, making the preoperative diagnosis of acoustic neuroma very challenging. We discuss here the intracisternal site of origin and hypervascularity of acoustic neuroma, and also the differential diagnoses and management of such tumors. (+info)
Vasopressin release by nicotine: the site of action.
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1. In cats anaesthetized with chloralose the release of neurohypophysial hormones was examined after injection of nicotine into the cerebral ventricles or cisterna magna or its topical application through perspex rings to the ventral surface of the brain stem. The release was measured by assaying the hormones in samples of venous blood. 2. Injected into a lateral or the third cerebral ventricle, nicotine (0.5 to 1 mg) produced release of vasopressin without oxytocin. When the aqueduct was cannulated, preventing access to the fourth ventricle and to the subarachnoid space, this release did not occur. 3. Vasopressin was also released without oxytocin when nicotine (0.25 to 2 mg) was injected into the subarachnoid space through the cisterna magna. With this route of administration the nicotine did not enter any part of the ventricular system. 4. Applied through paired perspex rings placed across the ventral surface of the brain stem, nicotine again produced release of vasopressin without ocytocin. The amount of nicotine placed in each ring was usually 80 mug, but a release was obtained with 10 mug and in one experiment with as little as 5 mug. 5. The bilateral region on the ventral surface of the brain stem where nicotine acts when producing release of vasopressin lies lateral to the pyramids and in a longitudinal direction, 6 to 9 mm caudal to the trapezoid bodies. 6. The vasopressin release by nicotine injected intraventricularly or intracisternally, or applied topically to the ventral surface of the brain stem was not due to absorption of nicotine into the blood stream, nor to blood pressure effects. 7. It is concluded that nicotine acts on the ventral surface of the brain stem probably by activating the central projection to the supra-optic and possibly also the paraventricular nuclei of afferent pathways in the sinus and vagus nerves which control the release of vasopressin in response to changes in blood volume or distribution. (+info)