Experimentelle Untersuchungen über die Abhängigkeit der Nierenfunktion vom Nervensystem

Jungmann, Paul; Meyer, Erich

doi:10.1007/bf01865338

Cited by 117 publications

(4 citation statements)

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“…This observation has been confirmed many times (Eckhard (12), Klecki (13) Grek (14), Rohde and Ellinger (15), Asher and Pearce (16), Jungmann and Meyer (17)). It also increases markedly the elimination of chlorides and carbonates and to a less extent that of urea, phosphates and sulfates.…”

Section: Ph Ysiologicalsupporting

confidence: 60%

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The Effect of Renal Denervation on Patients Suffering From Nephritis 1

Page¹,

Heuer²

1935

J. Clin. Invest.

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Jaboulay(1) appears to have been the first to perform the operation of periarterial neurectomy in man. The procedure, however, did not achieve popularity until after the appearance of a series of papers by Leriche and his associates (2, 3). The effect on patients suffering from peripheral vascular disease has been especially extensively investigated. Denervation of the kidneys more recently has been performed on patients suffering from nephralgia and hydronephrosis, success being achieved in the relief of pain. ANATO M ICALThe renal nervre supply is derived mainly from the celiac ganglia with small branches from the plexuses around the adrenal gland and the aorta.Usually one branch comes from the splanchnic nerves direct. Through the celiac ganglion the renal nerves are brought into connection with the splanchnic nerves and with the vagus. The vagus nerve also sometimes-sends a direct branch to the kidneys. A few branches are received from the superior mesenteric ganglion.It has long been recognized that the splanchnic nerves form the chief vasomotor supply of the kidneys. Bradford (4) found that stimulation of the anterior roots of the cord from the sixth thoracic to the second lumbar segment caused the kidneys to constrict. Of these roots the tenth to twelfth dorsal were most effective. Vasodilator fibers were also present but were weak in comparison with the constrictors.Langley and Anderson (5), Jost (6), and Hirt (7) have clearly demonstrated fibers coursing from the third, fourth, and fifth lumbar ganglia to join the renal plexus. Most of the nerves are non-medullated, but some in the plexus are myelinated (Renner (8)). Ganglion cells which are

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Section: Ph Ysiologicalsupporting

confidence: 60%

“…Denervation caused neither increased urine flow nor diminished ability to concentrate, although animal experiments in the literature (11,12,13,14,15,16,17,18) led us to expect these changes. On the contrary, two patients (Cases 1 and 4) exhibited a significant increase in concentrating power during the months after operation.…”

Section: LImentioning

confidence: 90%

The Effect of Renal Denervation on Patients Suffering From Nephritis 1

Page¹,

Heuer²

1935

J. Clin. Invest.

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“…Disordered sodium balance may be provoked in animals by stimulation or destruction of the hypothalamus or of areas in the brain-stem. Thus unilateral lesions in the floor of the fourth ventricle of rabbits provoked a diuresis with increased excretion of chloride ions (Jungmann and Meyer, 1913); bipolar stimulation of the caudal portion of the floor of the fourth ventricle in dogs resulted in an increased excretion of sodium (Wise, 1956); cerebral hypoxia increased the tubular reabsorption of sodium in the dog (Foldi, Korach, and Takacs, 1955); unilateral lesions in the hypothalamus of cats caused hyperchloraemia and hypochloruria, with maximal blood levels at three to six hours (Lewy and Gassmann, 1935). In this last experiment the changes were too acute to be attributed to factors such as water deficiency.…”

Section: Discussionmentioning

confidence: 96%

Hypernatraemia in cerebral disorders

Taylor

1962

Journal of Clinical Pathology

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SYNOPSIS Six patients are described in whom cerebral damage was associated with raised plasma sodium and chloride concentrations and with extremely low urinary outputs of sodium and chloride. The patients were not clinically dehydrated and direct determinations showed that the blood and plasma volumes, the endogenous creatinine clearance, and the urinary output of antidiuretic hormone were normal. For these and other reasons it is concluded that the metabolic picture results not from diminished circulatory volume, water deficiency, sodium deficiency, undetected diabetes insipidus or osmotic diuresis, but from the cerebral damage itself.In these and other cited cases, the cerebral damage was localized chiefly in the frontal lobes, hypothalamus or lower brain-stem, thus suggesting a descending pathway, the relationship of which to the pineal area controlling aldosterone secretion requires clarification.Allott (1939) first reported the occurrence of hypernatraemia and hyperchloraemia, associated with an abnormally low urinary excretion of sodium and chloride, in patients suffering from cerebral disease in whom there was no renal disease, and Higgins, Lewin, O'Brien, andTaylor (1951, 1954) described a total of 14 patients in coma after severe head injury in whom the same features were found. Cooper and MacCarty (1951) also described this syndrome in three patients suffering from different intracranial disorders. Subsequently, there have been reports of essentially similar cases (Persson, 1953;Anthonisen, Hilden, and Thomsen, 1954;Elliot, 1955; Allott, 1957; Petit-Dutaillis and BernardWeil, 1958). These authors have, in general, taken the view that the hypernatraemia that they have observed could not be adequately explained without postulating a direct and primary connexion, other than diabetes insipidus, between the cerebral disorder and the metabolic effect.Hypernatraemia

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“…A variety of lesions of the central nervous system may be associated with disturbances of renal function characterized by either the increased urinary loss of sodium and chloride (1)(2)(3) or the retention of salt (3)(4)(5)(6)(7)(8). It has also been postulated that changes in the excretion of salt, secondary to alterations in the volume of blood or extracellular fluid, are mediated by a "volume receptor" located in the cranial cavity (9)(10)(11)(12).…”

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confidence: 99%

The Failure of Intracranial Pressure-Volume Change to Influence Renal Function 1

Fishman¹,

Halla²

1953

J. Clin. Invest.

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A variety of lesions of the central nervous system may be associated with disturbances of renal function characterized by either the increased urinary loss of sodium and chloride (1-3) or the retention of salt (3-8). It has also been postulated that changes in the excretion of salt, secondary to alterations in the volume of blood or extracellular fluid, are mediated by a "volume receptor" located in the cranial cavity (9-12). The following experiments were therefore undertaken in order to investigate the influence of alterations in intracranial venous volume and pressure, and cerebrospinal fluid (CSF) volume and pressure on renal function. METHODSFemale dogs were anesthetized with sodium pentobarbital (30 mg. per Kg.) except for two experiments in which chloralose (75 mg. per Kg.) was used. Urine was collected through an indwelling catheter. The bladder was washed out with distilled water after each collection and emptied completely by blowing out with air. Glomerular filtration rate was measured by the clearance of exogenous creatinine (Ccr) (13) and renal plasma flow was estimated from the clearance of paraminohippurate

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Experimentelle Untersuchungen über die Abhängigkeit der Nierenfunktion vom Nervensystem

Cited by 117 publications

References 4 publications

The Effect of Renal Denervation on Patients Suffering From Nephritis 1

The Effect of Renal Denervation on Patients Suffering From Nephritis 1

Hypernatraemia in cerebral disorders

The Failure of Intracranial Pressure-Volume Change to Influence Renal Function 1

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