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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Based on studies in animals and humans, it has been suggested that nausea activates the hypothalamo-neurohypophyseal system with resultant increases in circulating concentrations of oxytocin or vasopressin. The purpose of these studies was to determine in humans whether nausea is associated with increases in circulating concentrations of neurohypophyseal hormones or various enteropancreatic peptides (vasoactive intestinal polypeptide, substance P, or pancreatic polypeptide). Nausea, induced by intravenous infusion of apomorphine, was associated with fivefold to 75-fold increases in plasma vasopressin concentrations in 7 subjects (mean increase, 41-fold), with no change in plasma oxytocin levels. Furthermore, nausea was associated with sevenfold to 16-fold increases in plasma pancreatic polypeptide concentrations (mean increase, ninefold), with no change in plasma levels of vasoactive intestinal polypeptide or substance P. In 1 subject refractory to nausea, there was no increase in plasma vasopressin or pancreatic polypeptide concentrations with apomorphine. These studies indicate that nausea in humans is associated with vasopressin and pancreatic polypeptide release.
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PMID:Apomorphine-induced nausea in humans: release of vasopressin and pancreatic polypeptide. 245 45

With the development of sensitive and specific radio-immunoassays to measure the low circulating concentrations of vasopressin there has been a quantum leap in our understanding of the physiological processes involved in the regulation of its secretion. The results of Verney's pioneering studies in dogs led to the concept of 'osmoreceptors'. It is now appreciated that osmoregulation of vasopressin release is of principal importance in the maintenance of water balance. Functional characteristics of the osmoregulatory system have been defined clearly by independent laboratories, and more recently the physiological influences that can subtly alter this very finely controlled system have been described. Non-osmotic factors that release vasopressin have been recognized for many years. Secretion of vasopressin in response to haemodynamic influences has been characterized, and significant hypotension and/or hypovolaemia are potent stimuli to hormone release. Other non-osmotic factors--nausea/emesis, hypoglycaemia--may play important roles in disturbances of water balance. Vasopressin should not, however, be regarded as a stress hormone, since recent careful studies in a variety of species indicate that secretion is not enhanced following a series of different noxious stimuli.
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PMID:Regulation of vasopressin secretion. 269 40

Metoclopramide was orally administered (10 or 20 mg) to 22 subjects, 75 min before parabolic flight. Serum levels of ACTH, EPI, NE, and vasopressin (AVP) were unaltered by metoclopramide. AVP and ACTH (1.2 and 36 pg.ml-1) were elevated 77 and 3.8-fold (92.3 and 135 pg.ml-1) following emesis, after 40 parabolas (68.7 and 140 pg.ml-1) and landing (8.7 and 79 pg.ml-1). Seven subjects displaying no nausea and no emesis demonstrated smaller elevations (8.2 and 2.2-fold). Of 15 vomiting subjects, 7 reported no nausea and had lower elevations of AVP with faster recoveries. These findings are consistent with Rowe's suggestion (1979) that nausea may correlate with AVP release. Inhibition of AVP release by fluid shifts during microgravity might account for our findings and astronaut-reported episodes of vomiting without nausea. Elevations in EPI followed emesis or exposure to 40 parabolas whether emesis occurred or not. Only emesis elevated NE (578 to 840 pg.ml-1).
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PMID:Hormonal responses of metoclopramide-treated subjects experiencing nausea or emesis during parabolic flight. 282 88

We have investigated the role of the area postrema (AP) in mediating the neurohypophyseal hormone response to peripheral administration of nausea-producing agents in rats. In control animals, lithium chloride (LiCl) and apomorphine (APO) caused a rise in plasma levels of immunoreactive oxytocin (OT) and arginine-vasopressin (AVP), whereas sulphated cholecystokinin octapeptide (CCK-8s) stimulated OT secretion only. Rats with AP lesions exhibited a similar OT and AVP response to LiCl and APO but the OT response to CCK-8s was significantly diminished. The results indicate that the selective stimulation of OT secretion by CCK-8s is partly mediated via the AP. Although the nausea-producing effects of LiCl and APO may involve the AP, the neuroendocrine effects of these agents may well be mediated via actions outside the AP.
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PMID:A role for the area postrema in mediating cholecystokinin-stimulated oxytocin secretion. 282 55

Exogenous administration of cholecystokinin octapeptide (CCK) is known to decrease food intake and slow gastric emptying in humans and animals. Recent studies have shown that CCK stimulates neurohypophyseal secretion of oxytocin (OT) in rats and arginine vasopressin (AVP) in monkeys, and that gastric distention also stimulates OT release in rats. We therefore studied AVP and OT secretion in 14 normal subjects in response to meal-induced gastric distention and administration of CCK, both separately and in combination, to assess whether these stimuli similarly activated central neurohypophyseal pathways in humans. Neither plasma AVP nor OT concentrations increased after gastric distention produced by ingestion of a large meal. However, a dose-related increase in plasma AVP, but not OT levels, occurred after CCK administration, the threshold CCK dose being 0.05 micrograms/kg body weight. The AVP secretion in response to CCK administration was significantly correlated with subjective aversive symptoms quantified by use of a numeric scale (r = 0.61, P less than 0.001). In 12 of the 14 subjects plasma AVP levels increased in association with symptoms of epigastric pressure and discomfort before the onset of overt nausea or emesis. The combination of CCK and meal-induced gastric distention did not stimulate increases in plasma AVP levels in excess of those produced by CCK administration alone. The results demonstrate that AVP secretion resulting from emetic center activation often is a graded response that can begin in association with milder degrees of visceral discomfort before symptoms of overt nausea or emesis. In addition, the stimulation of AVP secretion by CCK administration, but not by meal-induced gastric distention in association with physiological satiety, suggests that some component of the anorectic effects of exogenous CCK in man likely results from activation of brainstem emetic centers.
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PMID:Neurohypophyseal secretion in response to cholecystokinin but not meal-induced gastric distention in humans. 292 13

One of the important factors in outer space is the absence of gravity (OG). During longterm missions, this factor is responsible for the larger number of anatomical and physiological changes that astronauts experience. The cardiovascular system undergoes these changes with severe intensity, which is part of an adaptation process to the new environmental conditions. The modifications observed in both the anatomy of the cardiovascular system and its hemodynamics occur in two phases. The first phase begins when the astronauts enter into Earth orbit or in interplanetary trajectory and extends until the second or fourth day of the mission. It is characterized by an important shifting of fluids from the lower extremities to the cephalic regions which produces an increase of the venous return and the preload, the heart rate is increased, the blood volume in the thorax is also increased, the cardiac chambers become dilated, and by reflex action, the antidiuretic hormone diminishes, diuresis increases and leads to a virtual state of dehydration. Clinically, the first stage is manifested by headache, dizziness, space disorientation, nausea, anorexia, projectile vomiting, sweating and pallor. This constalation of data is known as "The Space Adaptation Syndrome". The second phase begins at the end of the first phase and finishes toward the fortieth or fiftieth day of the mission.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Behavior of the cardiovascular system in outer space]. 295 26

Administration of lithium chloride and copper sulfate to adult monkeys caused marked elevations in plasma vasopressin (AVP) levels without significant increases in plasma oxytocin (OT) levels. Emesis was produced in five of the seven animals given these agents, in support of nausea as the main stimulus to AVP release. A similar pattern of AVP release without OT release was found after administration of cholecystokinin (CCK). Although most monkeys vomited in response to 10 micrograms/kg of CCK, a significant increase in plasma AVP levels also was produced with a dose of 1 microgram/kg, which did not produce emesis in any animal. These findings are in marked contrast with previous results in rats, which indicated that lithium chloride, copper sulfate, and CCK each stimulated OT rather than AVP release. Despite this interspecies difference, the significant neurohypophysial hormone secretion in response to both nausea-producing agents and CCK suggests that AVP secretion in monkeys, similar to OT secretion in rats, might reflect activation of central pathways mediating nausea and/or inhibition of food intake, even when overt illness is not produced.
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PMID:Vasopressin release in response to nausea-producing agents and cholecystokinin in monkeys. 303 8

Vasopressin (aVP) at low concentrations functions as an antidiuretic hormone and has vasoconstrictive effects. To investigate the possible role of aVP in the pathogenesis of migraine, six patients with a history of induced migraine were given 100 g chocolate, and blood samples for plasma aVP were taken before ingestion and every hour for 4 h. In one patient who presented with severe headache and nausea the base-line plasma aVP concentration was 15.2 pg/ml; it fell to 3.2 pg/ml at 2 h before rising to 10 pg/ml at 3 h and 4 h as the symptoms worsened. In the five patients with moderate or no headache plasma aVP concentrations remained in the normal range (less than 3 pg/ml) throughout. The results suggest that aVP does not have a role in the aetiology of migraine. The possibility exists that during severe attacks of nausea there is release of aVP, which may be responsible for the facial pallor, antidiuresis, and coagulation abnormalities occasionally observed in migraine.
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PMID:Plasma vasopressin levels in induced migraine attacks. 335 85

The development of sensitive radioimmunoassays has permitted measurement of the low concentration of vasopressin in the human cerebrospinal fluid. There is accumulating evidence to suggest that vasopressin is involved in a variety of brain functions. As an effective blood-cerebrospinal fluid barrier to vasopressin has been demonstrated, the concentration of vasopressin in the cerebrospinal fluid probably reflects the release of vasopressin within the brain. In human subjects without intracranial disease, the concentration of vasopressin in the cerebrospinal fluid is in the range 0.5-2.0 pg/ml with only little diurnal variation. Intracranial disorders associated with increased intracranial pressure may cause increased cerebrospinal fluid vasopressin concentrations, whereas degenerative brain diseases are associated with low concentrations. Only little is known about the physiologic stimuli which alter the concentration of vasopressin in cerebrospinal fluid. The concentration in cerebrospinal fluid is not influenced by a number of stimuli that cause release of vasopressin into the blood, i.e. changes in plasma osmolality, postural changes, and nausea. Elevation of the intracranial pressure, changes in the composition of the cerebrospinal fluid, electrical stimulation of the hypothalamus, and severe hemorrhage provoke an increase in cerebrospinal fluid vasopressin level.
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PMID:Studies of vasopressin in the human cerebrospinal fluid. 353 47

The development of shock initiates a cascade of responses in an effort to reestablish homeostasis. Three of the most important hormonal and neurohumoral changes are the secretion of glucocorticoids, catecholamines, and vasopressin. Regulation of adrenal function is much more complex than originally thought. Hemorrhage is a potent stimulus for cortisol release, and both ACTH and ACTH-independent mechanisms have been described. The ACTH response to its releasing hormone, corticotropin releasing hormone (CRF), is itself amplified by vasopressin, which appears to have intrinsic CRF properties. Because ACTH is synthesized as part of a large precursor molecule (pro-opiomelanocortin) containing the amino acid sequences for several important proteins, stimulation of ACTH release has far-ranging effects, the specifics of which are just being clarified. Norepinephrine and epinephrine levels increase manyfold above baseline within minutes of the onset of hemorrhagic shock. Only patients experiencing cardiac arrest or the rare patient with a very active pheochromocytoma have higher concentrations. The levels reached are far in excess of those required to cause both cardiovascular and metabolic alterations. Because of the presence of the endogenous opiates leucine and methionine enkephalin in the neurosecretory granule, it is very likely that the enkephalins are coreleased with the catecholamines, modifying their cardiovascular effects and producing analgesia. Hypovolemia is also a potent stimulus for vasopressin secretion, which overrides hypotonicity, presenting a clinical picture quite compatible with the syndrome of inappropriate antidiuretic hormone secretion, from which it must be differentiated. Vasopressin also is released by pain, nausea, and hypoxia, all of which are likely to be present in the patient with shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endocrinology of shock. 353 88


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