Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a series of 602 consecutive sclerotherapies, two cirrhotic patients who had received successful sclerotherapy for control of variceal bleeding while on vasopressin infusions developed mesenteric thrombosis. We found no other cases (in our institution or in literature review) where sclerotherapy or vasopressin infusion alone precipitated mesenteric thrombosis. During vasopressin infusion, there is portal stasis and an increased caudad flow of sclerosant. We suggest that mesenteric thrombosis is a consequence of the combination of these two effects. Direct injection of gastric varices is difficult because of increased postsclerotherapy bleeding, but sclerosis of esophageal varices often leads to their obliteration by the caudad flow of sclerosant. We propose, therefore, that vasopressin infusion during esophageal sclerotherapy may be beneficial in the obliteration of gastric varices. We conclude that (a) in patients without gastric varices, vasopressin infusion increases the incidence of mesenteric thrombosis, and (b) vasopressin infusion during sclerotherapy may enhance the sclerosis of gastric varices.
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PMID:Mesenteric thrombosis following sclerotherapy during vasopressin infusion: mechanism and therapeutic implications. 278 37

We addressed in this study, with immunocytochemical methods, the following questions: are immunoreactive enkephalins in the rat neurohypophysis stored in nerves distinct from neurosecretory nerves; where is [Met]enkephalin immunoreaction localized; does immunoreactive [Leu]enkephalin coexist with pro-enkephalin or with pro-dynorphin fragments; and are the interpretations of localization studies influenced by the choice of pre-embedding or post-embedding immunocytochemical techniques? We compared immunoreactions due to antibodies which had been used by others in previous studies, examined both lyophilized and conventionally fixed specimens, and applied pre- and post-embedding protocols. Both pre- and post-embedding stainings confirmed co-storage of immunoreactive dynorphin(1-8)-like materials with vasopressin. Immunoreactive [Met]enkephalin-like material always coexisted with oxytocin. Most of the immunoreactive [Leu]enkephalin-like material appeared to occur in oxytocin nerves; only in larger vasopressin varicosities was there some dot-like [Leu]enkephalin immunoreaction. This indicates that neural lobe [Leu]enkephalin predominantly is cleaved from a precursor which also contains [Met]enkephalin. When pre-embedding methods were modified in order to block diffusion and to enhance penetration of antibodies, enkephalin immunoreactivity was always found in typical neurosecretory varicosities with large granules. Structures previously interpreted as enkephalinergic nerve terminals contacting pituicytes most likely are neurosecretory varicosities.
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PMID:A re-examination of the localization of immunoreactive dynorphin(1-8), [Leu]enkephalin and [Met]enkephalin in the rat neurohypophysis. 288 79

Different types of release site were studied ultrastructurally with tannic acid and immunohistochemical techniques in the central nervous system (CNS) of the invertebrate pond snail Lymnaea stagnalis and in two neuromediator rich core regions in the CNS of the rat, viz., the median eminence (ME) and the mesencephalic central grey substance (MCG). In the CNS of the snail, release of the contents of the secretory granules could be clearly demonstrated in (1) neurohaemal axonterminals, (2) synapses and (3) in nonsynaptic release sites: neuronal processes without morphological synaptic specializations. In the ME, release of secretory products by exocytosis was found in neurohaemal axonterminals in the external part of the palisade layer and in nonsynaptic release sites in all other layers of the median eminence. It was found that oxytocine and vasopressin were released by exocytosis into the extracellular space from such (preterminal) nonsynaptic release sites. Serial section analysis revealed three types of fibre in the MCG, viz. (1) varicose fibres that made synaptic contacts with MCG dendrites on every varicosity, (2) fibres with two types of varicosity, viz. synapse-bearing varicosities and varicosities without synaptic specializations, and (3) varicose fibres without any synaptic specializations. It has been discussed that the nonsynaptic release sites in the CNS of the snail Lymnaea stagnalis, and the nonsynaptic varicosities in the rat brain are the morphological correlates of nonsynaptic communication in the CNS. The results further indicate that particular peptidergic neuromediators are released from such nonsynaptic varicosities, and may reach via the extracellular space receptors located at some distance.
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PMID:Synaptic and nonsynaptic release of neuromediators in the central nervous system. 290 65

Immunohistochemical and axonal transport methods were used to chart the distribution of somatostatin-immunoreactive (SS-IR) fibres in the paraventricular (PVH) and supraoptic (SO) nuclei of the rat hypothalamus and to identify the cell group(s) from which they originate. Fibres and varicosities immunoreactive for SS-28 and/or SS-281-12 are found primarily in the parvocellular division of the PVH, though aspects of the magnocellular division, and of the SO, in which oxytocinergic neurons are clustered also receive moderate inputs. Combined retrograde transport-immunohistochemical studies indicated that these arise principally from non-catecholaminergic neurons in the lateral aspect of the commissural part of the nucleus of the solitary tract (NTS). SS-28 has been shown to act within the central nervous system to elicit both oxytocin and vasopressin secretory responses, and may be involved in mediating vasopressin secretory responses to haemorrhage. Direct SS-28-IR inputs to the magnocellular cell groups from the NTS, which receives primary visceral sensory inputs, are in a position to play a role in mediating oxytocin secretory responses to interoceptive stimuli; the pathway(s) and mechanism(s) which allow SS-28 to interact with vasopressinergic neurons are not clear.
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PMID:Somatostatin 28-immunoreactive inputs to the paraventricular and supraoptic nuclei: principal origin from non-aminergic neurons in the nucleus of the solitary tract. 290 91

Dual antigen immunocytochemical staining procedures were used in the same tissue section to determine the distribution of ACTH immunostained fibers and varicosities within the magnocellular and parvocellular divisions in the paraventricular nucleus (PVN) of rat hypothalamus and elucidate its anatomical relationship to vasopressin (VP) and oxytocin (OXY)-containing neurons. Double immunostained preparations using glucose oxidase-antiglucose oxidase complex combined with PAP complex to visualize two antigens with contrasting colors in the same tissue section were employed. ACTH-immunoreactive (ir) fibers were distributed throughout the periventricular stratum and the parvocellular component of the PVN; in the latter area fibers were particularly dense in the ventral medial portion of the medial parvocellular division. Dual immunostained sections revealed a close anatomical association between opiocortin fibers and oxytocin and vasopressin parvocellular neurons. ACTH immunostained fibers were present in the anterior and medial magnocellular component of PVN and in the ventral medial portion of the posterior magnocellular division; these immunoreactive fibers were in intimate proximity to oxytocin-ir perikarya. The very close approximation between the ACTH-ir fibers and oxytocin-containing cell bodies suggests potential cell to cell communication between the two peptidergic systems in PVN. Few ACTH immunostained fibers were seen in the dorsal lateral portion of the posterior magnocellular division in which vasopressinergic neurons predominate. The present anatomical study supports pharmacological and physiological studies which indicate that opioids can influence the activity of magnocellular PV neurons. This study also elucidates an anatomical relationship between opiocortins (ACTH1-39) and parvocellular PV neurons which suggests that the opiocortin system may play a role in the regulation of both the neuroendocrine and autonomic activities of specific PV neurons.
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PMID:Relationship of ACTH1-39-immunostained fibers and magnocellular neurons in the paraventricular nucleus of rat hypothalamus. 300 68

Figure 2 is the algorithm followed in our institution for management of acute variceal hemorrhage. A small percentage of patients who present with active variceal hemorrhage will stop bleeding after gastric lavage alone. However, most patients require an intravenous vasopressin infusion at a dose of 0.4 units per minute, preferably combined with intravenous administration of nitroglycerin. Although glypressin and somatostatin may be associated with fewer side effects than vasopressin, the superiority of these drugs remains to be determined. Whether pharmacologic therapy succeeds or fails, most patients then proceed to endoscopic sclerotherapy. Sclerotherapy may be used as a temporizing measure in preparation for elective surgery or as a long-term, definitive treatment for prevention of recurrent hemorrhage. Balloon tamponade is reserved for patients who are bleeding too rapidly for effective sclerotherapy and for sclerotherapy failures in preparation for emergency surgery. Because recurrent hemorrhage frequently occurs after balloon deflation, a more definitive treatment (surgery or endoscopic sclerotherapy) should be planned for all patients who undergo balloon tamponade. Because operative risk is unacceptably high for patients with hepatic functional decompensation secondary to variceal hemorrhage, we believe that a policy of routine emergency surgery is unwise. Rather, emergency surgical intervention is reserved for the relatively small number of patients (15 to 25 per cent) who continue to bleed after nonoperative options have failed. Shunt surgery should be considered early in the course of patients with bleeding secondary to gastric varices and portal hypertensive gastropathy, both of which respond poorly to nonoperative measures.
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PMID:Variceal hemorrhage. 304 46

The variceal bleeding episode represents several days of high risk of bleeding, thus therapy should be evaluated not only in terms of immediate cessation of bleeding but also in terms of providing a bleed-free interval of a few days. As the risk of continued bleeding or very early rebleeding from varices diminishes rapidly following admission, time is an important confounding variable when comparing therapies within and between trials. Cirrhotics with better liver function are more likely to stop bleeding with simple measures than those with worse liver function. Vasopressin, glypressin, vasopressin combined with nitroglycerin and somatostatin have all been used as splanchnic arteriolar vasoconstrictors thus reducing portal pressure. No trial has demonstrated increased survival with use of these agents. The efficacy of vasopressin is now disputed. Vasopressin combined with nitroglycerin and somatostatin have the fewest side-effects and may be more effective than vasopressin alone. Balloon tamponade arrests bleeding and prevents exsanguination, but should be used solely as a temporizing measure before the use of emergency sclerotherapy or surgery. Sclerotherapy is the only non-operative emergency technique which has been shown not only to stop variceal bleeding, but to reduce the frequency of very early rebleeding. Emergency oesophageal transection is equally if not more effective in arresting bleeding than sclerotherapy and has a lower early rebleeding rate and a similar mortality. Choice of treatment depends on expertise available. Further studies in the management of variceal bleeding should evaluate 3 main areas. Firstly improvement of existing therapies or new therapies. Secondly, investigation of therapies not related to bleeding, eg prophylaxis against infection, improvement in renal support. Lastly evaluation of predictive factors which may a priori determine a high risk of continued bleeding or early rebleeding thus justifying immediate sclerotherapy or surgery in a sub-group of patients.
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PMID:Randomised controlled trials for variceal bleeding. 305 15

Thirty-nine patients admitted during a 16-month period for acute bleeding from varices confirmed by emergency endoscopy were randomized to receive either continuous intravenous infusions of vasopressin alone (0.66 units per min) (Group I: 19 patients) or vasopressin plus sublingual nitroglycerin (0.6 mg every 30 min for 6 hr) (Group II: 20 patients). The two groups of patients were similar in the type and severity of their cirrhosis. Bleeding was controlled initially in 47% (9/19) of the patients in Group I and 55% (11/20) of the patients in Group II after 6 hr of infusion (not statistically significant). Complete control of bleeding during 24 hr of infusion was achieved in only 4 of 19 patients in Group I (21%) but in 9 of 20 in Group II (45%). This difference is not statistically significant. The total number of patients with complications during infusions were significantly different statistically in the vasopressin and vasopressin-nitroglycerin groups, respectively (17/19 vs. 7/20, p less than 0.001). Major complications requiring immediate cessation of infusions were observed in 6 of 19 of the patients in Group I (32%) and in 2 of 20 in Group II (10%) (p less than 0.05). Mortality (58% in Group I, 55% in Group II) and transfusion requirements were similar in the two groups. This study shows that the addition of sublingual nitroglycerin to intravenous vasopressin does not alter the efficacy of vasopressin alone in controlling hemorrhage from esophageal varices, but it does significantly reduce the complications.
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PMID:Controlled trial of vasopressin plus nitroglycerin vs. vasopressin alone in the treatment of bleeding esophageal varices. 308 3

Endoscopic injection sclerotherapy of oesophageal varices was performed in 71 patients: 50 with intrahepatic and 21 with extrahepatic block. In summary 330 procedures were done: 220 under general anaesthesia using the Negus rigid oesophagoscope and 110 with diazepam as premedication using a flexible, fibreoptic endoscope. Definitive control of variceal haemorrhage was achieved in 30 of 34 emergency admissions (88%). The hospital mortality in acute variceal bleeding was 26.5%. Elective, repeated sclerotherapy was performed in 60 patients. In 43 patients complete obliteration of varices or their marked reduction were observed. Rebleeding occurred in 23% and major complications in 17% of patients. The overall one year survival rate was 82%. We consider sclerotherapy as a method of choice in bleeding oesophageal varices uncontrollable by vasopressin and balloon tamponade. It also represents a valuable method of preventing rebleeding particularly in patients with a high operative risk.
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PMID:Emergency and elective sclerotherapy of oesophageal varices. 326 65

In a prospective controlled trial of conservative therapy (vasopressin/balloon tamponade (control group] versus endoscopic sclerotherapy (ST) for the acute bleeding and at rebleeding, 107 cirrhotic patients with major variceal haemorrhage were studied from 1979 to 1983. The prospective follow-up study is now presented of the 51 patients surviving for more than 1 year. The present ST group (30 patients) was followed for a median of 5 years (range, 1-7.5 years), and the controls for 4 years (3-5.5 years). Variceal eradication was obtained in 22 ST patients in the 1st year after a median of 6 months and 5 ST sessions, and in 7 ST patients after 21 months and 9 ST sessions. The delay was due to alcoholic abuse. Eleven ST patients and 11 controls (NS) rebled on 30 and 45 occasions during a total follow-up time of 1364 and 696 months and 0.0220 and 0.0647 bleeds per patient-month, respectively (p = 0.098). Eight ST patients experienced 12 variceal bleeds, 11 controls had 39 haemorrhages with variceal aetiology, 0.0088 and 0.0560 bleeds per patient-month (p = 0.016), respectively. Five ST patients had recurrent varices on nine occasions with five episodes of bleeding a median of 13 months after completion of the initial serial ST. Reelimination was achieved with a median of three ST sessions during 3 months, but three patients had a second variceal recurrence 14-24 months later, successfully treated with one ST session in two of them. There was no difference in survival.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term survivors after variceal haemorrhage. Follow-up of a controlled study of endoscopic sclerotherapy versus conservative management. 331 Jan 96


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