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The CNS Control of Glucose Metabolism (Acta Neurochirurgica Supplement, nr. 31)

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en Limba Engleză Paperback – 17 Jun 1981
In the clinic at Giessen during the last few years there has been an extensive programme of research into the various aspects of lesions of the diencephalon and brain stem and the associated autonomic and metabolic disturbances. As a continuation of this research programme Ernst Grote has investigated the central neuronal and hormonal factors acting on the peripheral regulation of glucose metabolism and their diverse inter-relationships. This research was made possible not only by the availability of well-documented clinical and experi­ mental material with primary and secondary lesions of the hypo­ thalamus and brain stem, but also by the advances in clinical endo­ crinology and the development of radio-immuno-assays. By continuous systematic investigation of the basic values and their reaction to stress-tests, as well as to trauma and operation, he has elucidated the basic facts of the central and peripheral mechanisms which are concerned in the regulation of glucose, and also their disturbances. Of particular significance are his descriptions and interpretations of the characteristic hypothalamic syndromes, as combinations of hyperglycaemia, hyperinsulinaemia and hyperglucagonaemia; dif­ ferent syndromes are produced by lesions at various levels of the brain stem and in central brain death. From this starting point it was possible to develop a rational treatment of this hormonal dys­ regulation by means of somatostatin.
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Specificații

ISBN-13: 9783211816196
ISBN-10: 3211816194
Pagini: 172
Ilustrații: VIII, 160 p.
Dimensiuni: 152 x 229 x 9 mm
Greutate: 0.33 kg
Ediția: Softcover reprint of the original 1st ed. 1981
Editura: SPRINGER VIENNA
Colecția Springer
Seria Acta Neurochirurgica Supplement

Locul publicării: Vienna, Austria

Public țintă

Research

Cuprins

1. Introduction.- 2. The Regulation of Glucose Metabolism.- 2.1. Non-Nervous Regulation.- 2.1.1. Intrinsic Cell Mechanisms.- 2.1.2. Hormonal Action.- 2.1.2.1. Insulin.- 2.1.2.2. Glucagon.- 2.1.2.3. Glucocorticoids.- 2.1.2.4. Growth Hormone.- 2.2. Central Nervous Regulation.- 2.2.1. Neural Regulation.- 2.2.1.1. Early Experimental Findings in Animals.- 2.2.1.2. “Neurotraumatic” Diabetes.- 2.2.1.3. Diencephalic Structures and Organization of the Autonomie Nervous System. Results of Stimulation and Ablation Experiments.- 2.2.1.4. Neural Influences on the Liver Cells, on Glycogenolysis and Glycogen Synthesis.- 2.2.1.5. Neural Stimulation of the Adrenal Medulla and the Role of Catecholamines.- 2.2.1.6. Nerve Supply to the Cells of the Islets of Langerhans.- 2.2.1.7. Neural Control of Glucagon Secretion.- 2.2.1.8. Neural Control of Insulin Secretion.- 2.2.2. Neurohumoral Regulation.- 2.2.2.1. The Hypothalamic-Pituitary System.- 2.2.2.2. Glucose-Sensitive Neurones in the Hypothalamus.- 2.2.2.3. Effect of the Location of Diencephalic Lesions on the Clinical and Endocrine Symptoms.- 2.3. Summary.- 3. Methods Employed.- 3.1 Standardization of the Withdrawal of Blood.- 3.2 Standardization of the Loading Tests.- 3.2.1. Intravenous Glucose Load.- 3.2.2. Insulin Hypoglycaemia.- 3.2.3. Arginine “Stress”.- 3.2.4. Somatostatin Load.- 3.3 Chemical Estimation Methods.- 3.3.1. Glucose.- 3.3.2. Free Fatty Acids.- 3.3.3. Human Growth Hormone.- 3.3.4. Insulin.- 3.3.5. Cortisol.- 3.3.6. Glucagon.- 3.3.7. Catecholamines.- 3.4 Pharmacokinetics of Glucose.- 3.5 Statistical Methods.- 4. Results.- 4.1. Survey of Material and Subdivision into Groups.- 4.2. Preliminary Studies.- 4.3. Spontaneous Behaviour.- 4.3.1. Severe Closed Craniocerebral Injury, Acute Subdural Haematoma, Secondary Coma and Midbrain Syndrome.- 4.3.2. Acute Midbrain Syndrome with Extensive Intracranial Haemorrhage.- 4.3.3. Severe Craniocerebral Injury, Acute Hypothalamic Damage.- 4.3.4. Acute Hypothalamic Damage with Transition into a Midbrain Syndrome, Bulbar Damage and Brain Death After Embolization of an A.V. Angioma.- 4.3.5. Hypothalamic Damage After Operation on a Medial Sphenoidal Wing Meningioma.- 4.4. Intravenous “Stress” with Glucose 0.33 g/kg Body Weight.- 4.4.1. Healthy Subjects.- 4.4.2. Diabetics.- 4.4.3. All Intracranial Tumours.- 4.4.3 a. Pre-Operative.- 4.4.3 b. First Post-Operative Day.- 4.4.3 c. Seventh Post-Operative Day.- 4.4.4. Endocrine Inactive Intra- and Suprasellar Pituitary Tumours.- 4.4.4 a. Pre-Operative.- 4.4.4 b. First Post-Operative Day.- 4.4.4 c. Seventh Post-Operative Day.- 4.4.5. Endocrine Active Eosinophilie Adenomas with Pathological HGH Secretion.- 4.4.5 a. Pre-Operative.- 4.4.5 b. First Post-Operative Day.- 4.4.5 c. Seventh Post-Operative Day.- 4.4.6. Patients with Complete Anterior Pituitary Failure.- 4.4.7. Para-Hypothalamic Tumours with Mechanical Changes, Displacement and Chronic Damage.- 4.4.7 a. Pre-Operative.- 4.4.7 b. First Post-Operative Day.- 4.4.8. Patients with Hemisphere Tumours Close to the Cortex.- 4.4.8 a. Pre-Operative.- 4.4.8 b. First Post-Operative Day.- 4.4.8 c. Seventh Post-Operative Day.- 4.4.9. Unconscious Patients with Acute “Midbrain Syndrome”.- 4.4.10. Unconscious Patients with Acute Mesencephalo-Ponto-Bulbar Lesions.- 4.4.11. Unconscious Patients, Regardless of the Site and Level of the Lesion, or the Cerebral Cause.- 4.4.12. Unconscious Patients with the Clinical Signs of Brain Death.- 4.4.13. Patients with Complete Lesions of the Upper Cervical Cord.- 4.5. Mean Hourly Concentrations in the Various Groups, in Response to a Glucose Load.- 4.5.1. Glucose.- 4.5.2. Insulin.- 4.5.3. Human Growth Hormone.- 4.5.4. Cortisol.- 4.5.5. Glucagon.- 4.5.6. Mean Concentrations of the Catecholamines in 24 Hour Urine.- 4.6. The Molar Insulin-Glucagon Quotient in the Various Groups.- 4.7. Pharmacokinetic Investigation of the Concentration Pattern and of the Assimilation of the Blood Glucose After an Intravenous Glucose Load.- 4.7.1. Glucose Assimilation.- 4.7.2. Glucose Transfer.- 4.8. Inhibition Tests with Somatostatin.- 5. Consideration of the Results and Discussion.- 6. Summary.- References.