Stimulation Of Autonomic Nervous System Research Articles

Pressor hormones regulate atrial-stretch-induced release of atrial natriuretic peptide in the pithed rat.

Atrial wall stretching is a known stimulus for atrial natriuretic peptide (ANP) secretion. The effects of the stimulation of autonomic nervous system, hemodynamic factors, and humoral factors (epinephrine, angiotensin, vasopressin, and brain extracts) on the release of ANP under basal conditions and during increased atrial pressure produced by acute volume loading in pithed rats were examined. In conscious rats, acute volume expansion by 0.9% of saline (4 ml) increased the plasma immunoreactive ANP (IR-ANP) concentrations by a factor of 4 (140 +/- 30 pg/ml vs. 521 +/- 140 pg/ml, p less than 0.001, n = 8), whereas volume-induced ANP release was blocked in pithed rats (75 +/- 9 pg/ml vs. 99 +/- 13 pg/ml, NS, n = 7). The ANP versus right atrial pressure curve shifted to the right, indicating that much smaller amounts of IR-ANP were released in pithed than in conscious rats for each given increase in right atrial pressure. Electrical vagal and sympathetic nerve stimulation or changes in heart rate had no effect on plasma IR-ANP concentrations and failed to restore the volume-load-induced release of ANP in pithed rats. When extracts of anterior pituitary lobe, brain cortex, or hypothalamus were infused, no effect on volume-expansion-induced plasma IR-ANP levels was seen. In contrast, acute volume expansion caused a fourfold increase in levels of circulating IR-ANP in pithed rats that received posterior pituitary extracts, and the ANP versus right atrial pressure curve shifted markedly to the left. Infusion of a V1 antagonist blocked the volume-expansion-induced ANP release produced by the posterior pituitary extract. When [Arg8]-vasopressin (0.025 or 0.05 micrograms/kg/min) was infused to pithed rats, mean arterial pressure increased but basal plasma IR-ANP did not change significantly. However, acute volume expansion in the presence of vasopressin infusion (0.05 micrograms/kg/min) increased the amount of circulating IR-ANP by a factor of 4 (113 +/- 14 pg/ml vs. 414 +/- 43 pg/ml, p less than 0.001, n = 8). Thus, for a given increase in right atrial pressure, a similar amount of IR-ANP was released in the pithed rat during the vasopressin infusion as in the normal conscious animal. V1 antagonist blocked the increase in mean aterial pressure as well as the increase of plasma IR-ANP produced by [Arg8]-vasopressin. In addition, volume expansion during intravenous epinephrine (1.75 micrograms/kg/min) and angiotensin (1.0 micrograms/kg/min) doubled plasma IR-ANP levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of electrical stimulation of autonomic nervous system on degranulation of von Ebner's gland acini

In a series of studies to understand interactions between taste sensation and salivary gland function, we are pursuing experiments to determine the autonomic nervous system control of von Ebner's lingual salivary glands. Electrical stimulation of the glossopharyngeal nerve, which contains the parasympathetic nerve supply to von Ebner's glands, caused a reduction in secretory granules of the glands in the rat. This depletion of granules could be blocked by prior administration of the parasympathetic antagonist, atropine. In contrast, electrical stimulation of the sympathetic nerve supply was ineffective in causing granule depletion in von Ebner's gland, but produced almost total degranulation in the parotid gland of the same animals. It is concluded that parasympathetic nerves exert the principal control over von Ebner's gland, acinar degranulation in the rat; this is compared with autonomic control of other salivary glands that have a dual peripheral control by parasympathetic and sympathetic innervation.

Fatal coronary artery tumor metastasis

occupying lesions, suggested that stimulation of autonomic nervous system, primarily sympathetic, was a major factor in their genesis. Large P waves were also found in 2.4% of normal individuals and in 4% of patients with lobar pneumonia.* Since the ECG changes are more frequently observed in patients with subarachnoid hemorrhage than in other intracranial catastrophes, Cropp and Manning4 postulated that ECG abnormalities were related to irritation of cortical area 13. CT scanning has made it possible to identify accurately the site of intracerebral hemorrhage. In a recent publication5 describing ECG changes in 186 patients with CT scan documented cerebral hemorrhage, left atria1 abnormality was noted in 20%) but there was no mention of tall P waves. No tall P waves were described in another recent study6 of subarachnoid hemorrhage. Our study suggests that tall P waves may not be uncommon in patients with ventricular bleeding, and appears to be the first attempt at correlating tall P waves with echocardiography and CT scanning.

Influence of autonomic nervous system stimulation on the protective zone.

The effect of sympathetic and parasympathetic stimulation on the vulnerable period threshold and the protective zone was studied in chloralose-anaesthetised dogs. Sympathetic stimulation substantially decreased the repetitive extrasystole threshold and shifted the timing of the protective zone earlier into diastole. Vagus nerve excitation exerted the opposite effect on both electrophysiological properties. During concurrent sympathetic nerve stimulation, the changes produced by vagal activation were accentuated. These findings suggest that parasympathetic influences on the protective zone are due, in part, to an antagonism of adrenergic effects on ventricular electrical properties.

Pharmacological Effects from Drugs Injected Intracerebrally in Unanesthetized Animals

The intracerebral injection of cardiac glycosides, quinidine sulfate, procainamide, chlorpromazine, reserpine, and lysergic acid diethylamide in unanesthetized dogs produced symptoms of a profound autonomic nervous system stimulation. Many common effects were produced by several structurally unrelated drugs. However, certain drugs had rather specific actions, which seemed to be localized in discrete areas in the brain. Studies with such preparations allow an estimate to be made of central activity without the complicating factors of general anesthesia or diffusion across the blood brain-barrier.

DISTURBANCES OF THE ENDOCRINE BALANCE AND THEIR RELATION TO DISEASES OF METABOLISM

Article1 June 1936DISTURBANCES OF THE ENDOCRINE BALANCE AND THEIR RELATION TO DISEASES OF METABOLISMC. N. H. LONG, M.D., D.SC.C. N. H. LONG, M.D., D.SC.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-9-12-1619 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptLast year it was my privilege to address the College upon the subject of carbohydrate metabolism and the implications that recent work in this field had upon our knowledge of diabetes mellitus.Since this address appeared to meet with a certain measure of approval from you, I have ventured this evening to speak again upon certain pieces of work that to my mind are significant to those of us whose interest is concerned with the so-called diseases of metabolism.It appears to me that it is becoming more and more apparent that the clinical condition that follows hypo- or hyperfunction...Bibliography1. CROOKERUSSELL ACDS: The pituitary gland in Addison's disease, Jr. Path. and Bact., 1935, xl, 255. CrossrefGoogle Scholar2. GROLLMANFIROR AWM: Rôle of the hypophysis in experimental chronic adrenal insufficiency, Am. Jr. Physiol., 1935, cxii, 310. CrossrefGoogle Scholar3. ZECKWERDAVISONKELLERLIVINGOOD ILWTBBS: The pituitary in experimental cretinism. I. Structural changes in the pituitaries of thyroidectomized rats, Am. Jr. Med. Sci., 1935, cxc, 145. CrossrefGoogle Scholar4. FRY HJ: The pituitary gland in diabetes mellitus and disorders of the glands of internal secretion, Quart. Jr. Med., 1915, viii, 277-299. CrossrefGoogle Scholar5. KRAUS EJ: Hypophyse und Diabetes mellitus, Virchow's Arch. f. path. Anat., 1920, ccxxviii, 68-133. CrossrefGoogle Scholar6. HOUSSAYBIASOTTI BAH: Hypophysis, carbohydrate metabolism and diabetes, Endocrinology, 1931, xv, 511. CrossrefGoogle Scholar7. MANNMAGATH FCTB: The effect of removal of the liver after pancreatectomy on the blood sugar level, Arch. Int. Med., 1923, xxxi, 797. CrossrefGoogle Scholar8. YATERMARKOWITZCAHOON WMJRF: Consumption of sugar by muscle in the non-diabetic and diabetic state, Arch. Int. Med., 1933, li, 800. CrossrefGoogle Scholar9. CAMPOSCURUTCHETLANARI CAJLA: Rôle du foie dans l'action diabétogène du lobe glandulaire de l'hypophyse de crapaud, Compt.-rend. Soc. de biol., 1933, cxiii, 467. Google Scholar10. LONGLUKENS CNFD: The effect of adrenalectomy and hypophysectomy upon experimental diabetes in the cat, Jr. Exper. Med., 1936, lxiii, 465. CrossrefGoogle Scholar11. BESTFERGUSONHERSHEY CHGCJM: Choline and liver fat in diabetic dogs, Jr. Physiol., 1933, lxxix, 94. CrossrefGoogle Scholar12. ALLEN FM: Glycosuria and diabetes, 1913, Harvard University Press. CrossrefGoogle Scholar13. DAVISCLEVELANDINGRAM LDWR: Effect of hypothalamic lesions and stimulation of autonomic nervous system upon carbohydrate metabolism, Arch. Neurol. and Psychiat., 1935, xxxiii, 592. CrossrefGoogle Scholar14. CROOKE AC: A change in the basophile cells of the pituitary common to conditions which exhibit the syndrome attributed to basophile adenoma, Jr. Path. and Bact., 1935, xli, 339. CrossrefGoogle Scholar15. HIMSWORTH HP: (a) Physiological activation of insulin, Clin. Sci., 1933, i, 1. (b) Dietetic factors influencing glucose tolerance and activity of insulin, Jr. Physiol., 1934, lxxxi, 29. (c) Influence of diet on sugar tolerance of healthy men and its reference to certain extrinsic factors, Clin. Sci., 1934, i, 251. (d) Dietetic factor determining glucose tolerance and sensitivity to insulin of healthy men, Clin. Sci., 1935, ii, 67. (e) Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive types, Lancet, 1936, ccxxx, 127. Google Scholar16. SOSKINALLWEISSCOHN SMDDJ: Influence of the pancreas and the liver upon the dextrose tolerance curve, Am. Jr. Physiol., 1934, cix, 155. CrossrefGoogle Scholar17. ZUNTZLABARRE EJ: Sur l'augmentation de la teneur en insuline du sang veineux pancréatique après l'hyperglycémie provoquée par injection de glucose, Compt.-rend. Soc. d. biol., 1927, xcvi, 421. Sur la sensibilité des centres nerveux supérieurs à l'hyperglycémie provoquée par l'injection de dextrose, Compt.-rend. Soc. d. biol., 1927, xcvi, 1400. Google Scholar18. CANNON WB: Stresses and strains of homeostasis, Am. Jr. Med. Sci., 1935, clxxxix, 1. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Philadelphia, Pennsylvania*Presented at the Detroit meeting of the American College of Physicians, March 2, 1936.From the George S. Cox Medical Research Institute, University of Pennsylvania, Philadelphia. Nextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDiseases of the Adrenal Glands**Some of this material has appeared previously in “The Fundamentals of Internal Medicine” by W. B. Yater, New York, D. Appleton-Century Company, Inc., 1938, pp. 451–509.Disturbances of carbohydrate metabolism observed in association with tumors of the adrenal cortex1Disorders of internal gland secretion in childrenThe unknown liver 1 June 1936Volume 9, Issue 12Page: 1619-1627KeywordsCarbohydrate metabolismDiabetes mellitus ePublished: 1 December 2008 Issue Published: 1 June 1936 PDF downloadLoading ...