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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasopressin and oxytocin are nonapeptides secreted from the neurohypophysis; increases in vasopressin are associated with nausea and vomiting in some, but not all, species. Our aim was to determine whether plasma vasopressin and oxytocin levels were altered in healthy volunteers who did or did not develop nausea during vection, an optokinetic stimulus which produces the illusion of self-motion. Vection was produced by rotating a drum with an inner surface of black and white vertical stripes around the seated stationary subject. Gastric myoelectrical activity was recorded continuously throughout the experiment with electrodes positioned on the abdominal surface. Plasma samples were obtained before vection and after drum rotation stopped when nausea and tachygastria were present. Vasopressin and oxytocin were extracted from plasma and quantified by RIA. During vection six subjects reported nausea and developed gastric dysrhythmias; six other subjects had no nausea and remained in normal 3-cpm myoelectrical rhythms. Vasopressin and oxytocin values before vection were similar in each group of subjects. One minute after vection stopped, plasma vasopressin levels were significantly greater (P less than 0.05) in subjects experiencing nausea and tachygastrias (35.4 +/- 26.7 pmol/L) than in those without symptoms (2.7 +/- 0.47 pmol/L). Oxytocin levels were unchanged by either vection or nausea. It is concluded that 1) vasopressin, not oxytocin, neurons in the magnocellular-neurohypophyseal system are activated during vection-induced nausea and gastric dysrhythmias; and 2) illusory self-motion may be used safely to study the neuroendocrine responses to brain-gut interactions and nausea in man.
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PMID:Vasopressin and oxytocin responses to illusory self-motion and nausea in man. 222 84

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

This paper addresses the different aspects of diagnosis and management of advanced abdominal pregnancy in developing countries. Advanced abdominal pregnancies typically implant at the endosalpinx area where maternal hemorrhage cannot disrupt pregnancy. Unless a diagnosis is made, pregnancy may progress to term in this fashion. Most commonly observed signs of this condition are non-specific, and the patient is typically diagnosed as having false labor. Ease of palpitations of the fetal parts, though useful, is not a reliable diagnostic tool. More sophisticated diagnostic procedures include oxytocin stimulation, abdominal x-ray, hysterosalpingogram and ultrasound. Once diagnosis is made, prompt surgery is recommended with the removal of the placenta when possible. Without surgery, the prognosis is very poor for both the mother and the infant. Most infants are stillborn and out of those that survive 40% are malformed. In very rare situations both the mother and infant are alive and healthy as presented in the following examples. Case 1 presents a 30-year-old mother who presented with an oblique breech and an uneffaced closed cervix. On operating, the placenta was found to be attached on the right side of the anterior leaf of the utero ovarian and infundibulopelvic ligaments and the right tube. Case 2 presented with a transverse lie, recurrent attacks of abdominal pregnancy and persistent nausea. A laparotomy was performed and a live female infant was delivered from the ruptured amniotic sac. The placenta originated from the right tube and nesosalpinx.
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PMID:Advanced abdominal pregnancy: diagnosis and management. 273 43

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

Apomorphine, a centrally-acting emetic, was administered subcutaneously (50 micrograms/kg) to nine normal subjects (four male, five female; aged 22-36 years) and four patients with idiopathic diabetes insipidus (DI) (one male, three female; aged 24-49 years). In the normal subjects this stimulus caused nausea (and vomiting in seven of nine) with a latency of 9.5 +/- 0.9 min which was followed by a large increase in plasma arginine vasopressin (AVP) concentration (from 0.9 +/- 0.2 pmol/l to 249 +/- 104 pmol/l at 15 min after the onset of symptoms; mean +/- SEM, P less than 0.01). There was a small but significant increase in plasma oxytocin (OXT) concentration (from 1.6 +/- 0.4 pmol/l to 6.2 +/- 3.4 pmol/l; P less than 0.05). Mean arterial pressure (MAP) fell slightly (from 87 +/- 1.9 mm Hg to 71 +/- 4.4 mm Hg; P less than 0.05) 15 min after the onset of nausea; there was no change in blood haematocrit or plasma osmolality and sodium concentration. In the DI patients apomorphine produced nausea (with vomiting in three of four) with a latency of 10.0 +/- 1.4 min but failed to cause an increase in either plasma AVP or OXT. In the DI patients the fall in MAP did not reach statistical significance (83 +/- 4 mm Hg to 71 +/- 11 mm Hg); there was also no change in haematocrit, osmolality or sodium concentration. Ipecacuanha, an emetic with both peripheral and central actions, was administered orally to seven normal subjects (three male, four female; aged 22-36 years) six of whom also underwent apomorphine tests.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responses of plasma oxytocin and arginine vasopressin to nausea induced by apomorphine and ipecacuanha. 290 23

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

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

Because of a hydrocephalic fetus, the 27 year old mother opted for abortion. This was done in the 21st week of pregnancy by ordinary intracervical application of 0.25 mg prostaglandin e2 gel. 30 minutes later the patient began to complain of nausea and dyspnea. Laboratory analysis revealed leukocytosis of 20800/ml and thrombocytopenia of 22000/ml, down from 150,000 ml before the procedure. There were no clinical indications of bleeding. The leukocytosis lasted 2 days and thrombocytopenia roughly 6 days. Treatment included administration of acetylsalicylic acid 3 x 0.5 g and dipyrimadol tablets 3 x 25 mg/day. After thrombocyte count was normalized, abortion was induced by means of spasmolysis and oxytocin i.v. In this case partial resorption of the prostaglandin indicates a systemic effect. Since the half life of E and F group prostaglandins is usually 1-3 minutes, and it is almost completely eliminated after passing through the liver and lungs, a direct prostaglandin effect leading to thrombocyte aggregation lasting several days is unlikely. Absence of thrombocyte antibodies point to a drug induced immune process in which the prostaglandin molecule could appear as a hapten. Ultimately the thrombocyte aggregation described here and normochromic anemia are of unclear origin. Changes in the patients' coagulation system are probably of no functional relevance. The initial leukocytosis must be considered a nonspecific immediate reaction.
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PMID:[Thrombocytopenia following intracervical prostaglandin priming]. 346 25

In a clinical trial carried out in 34 pregnancy women Enzaprost F 4 (prostaglandin F2-alpha) was administered into the uterus to cause uterine contractions in the 2nd and 3rd trimesters. The indications for the treatment were: 1. membrane rupture in 20 cases between the 21st and 26th weeks of pregnancy; 2. fetal death in 12 cases between the 24th and 34th weeks of pregnancy, and 3. induced abortion for medical reasons in 2 cases of primiparae in the 2nd trimester. Enzaprost was administered in physiological salt solution in doses of 2-5 mg with a total dose of 9-22 mg (average 18.5 mg). Contractions appeared within 15-30 minutes in groups 1 and within 20-30 minutes in groups 2 and 3. Abortions in the three different groups began 10.2, 11.5, and 6.0 hours after administration in primiparae and 7.3 and 8.2 hours, respectively, after treatment in groups 1 and 2 in women other than primiparae. Oxytocin had to be administered additionally in 3 cases in groups 1 and 2. The method proved to be safe and effective, side effects occurred in 6 cases (17.6%) consisting of cardiac pain, nausea, tachycardia, and increased systolic pressure.
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PMID:[Induction of uterine contractions using Enzaprost F administered into the uterine cavity]. 346 46

Administration of cholecystokinin (CCK) to rats caused a dose-dependent increase in plasma levels of the neurohypophyseal hormone oxytocin (OT). The OT secretion was comparable to that found in response to nausea-producing chemical agents that cause learned taste aversions. The effect of CCK on OT secretion was blunted after gastric vagotomy, as was the inhibition of food intake induced by CCK. Food ingestion also led to elevated plasma OT in rats, but CCK and aversive agents caused even greater OT stimulation. Thus, after administration of large doses of CCK, vagally mediated activation of central nausea pathways seems to be predominantly responsible for the subsequent decrease in food intake. Despite their dissimilar affective states, both nausea and satiety may activate a common hypothalamic oxytocinergic pathway that controls the inhibition of ingestion.
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PMID:Oxytocin secretion in response to cholecystokinin and food: differentiation of nausea from satiety. 371 53


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