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)

Clinical bleeding in uremia is a frequent problem and seems to correlate with a prolonged bleeding time. The vasopressin analog deamino-8-D-arginine vasopressin has been shown to shorten the bleeding time and to decrease clinical bleeding when administered intravenously to uremic patients. In the present study we administered the readily available intranasal deamino-8-D-arginine vasopressin to 2 uremic patients and demonstrated a decreased bleeding time and improvement in clinical bleeding.
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PMID:Intranasal deamino-8-D-arginine vasopressin shortens the bleeding time in uremia. 633 34

In a randomized double-blind cross-over trial we gave either 1-deamino-8-D-arginine vasopressin or placebo to 12 patients with uremia, hemorrhagic tendencies, and prolonged bleeding times. After vasopressin infusion, all patients had shortened bleeding times, with the effect lasting for at least four hours in most cases. Platelet count, platelet cyclic AMP levels, platelet retention on glass beads, plasma fibronectin, serum thromboxane B2 and residual prothrombin, hematocrit, and plasma osmolarity were unchanged after vasopressin. A consistent post-infusion increase in factor VIII coagulant activity and, to a lesser extent, in factor VIII-related antigen and ristocetin cofactor accompanied the shortening of bleeding time. In addition, vasopressin induced the appearance in plasma of larger von Willebrand-factor multimers than those present in the resting state. The compound was given to nine additional patients with acute or chronic renal failure and prolonged bleeding times, before major surgery or renal biopsy. In these patients, shortening of the bleeding time was associated with normal hemostasis. Our findings indicate that 1-deamino-8-D-arginine vasopressin can be used for temporary correction of bleeding time and may prevent surgical bleeding in patients with uremia.
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PMID:Deamino-8-D-arginine vasopressin shortens the bleeding time in uremia. 640 Nov 93

Gelfoam (gelatin foam) powder was used for embolization therapy of massive gastric bleeding from small vessels in 14 patients with severe underlying medical problems. Bleeding was controlled in 10 patients with lesions localized in areas supplied by the embolized left gastric artery. In four patients with concurrent lesions in other portions of the stomach, bleeding decreased only (3 patients) or did not respond to embolization (1 patient). Complications developed in 2 patients with compromised vascular supply of the stomach: superficial ischemic ulcers that healed, and a large ulcer that perforated and required surgery. Microscopic studies demonstrated Gelfoam powder penetration mostly into vessels 100 to 200 microns in diameter and only occasionally into smaller vessels 50 to 60 microns, with occlusion of approximately 10 to 15% of the vasculature. It is concluded that Gelfoam fragments are the primary embolic material to be used for occlusion of the left gastric artery. Use of Gelfoam powder should be limited to occasional patients who have only little chance of responding to Gelfoam fragment embolization. Potential candidates for Gelfoam powder embolization include patients with major coagulopathies and/or uremia who massively hemorrhage from small-vessel lesions localized in upper portions of the stomach, exhibit significant mucosal hypervascularity, and do not respond to selective vasopressin treatment. An uncompromised vascular supply of the stomach is a precondition of a safe left gastric artery embolization.
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PMID:Gelfoam powder embolization of the left gastric artery in treatment of massive small-vessel gastric bleeding. 660 49

A cytochemical bioassay for parathyroid hormone (PTH) was used for the characterization of the biological activity of circulating forms of the hormone. PTH-stimulated glucose-6-phosphate dehydrogenase activity in distal convoluted tubule cells was quantitated by integrating microdensitometry and the response to native bovine (b)PTH(1-84) was found to be linear between graded doses of hormone from 5 fg/ml to 5 pg/ml. Synthetic bPTH(1-34) and human (h)PTH(1-34) elicited a parallel and equimolar response; however calcitonin, ACTH, glucagon, epinephrine, vasopressin, and insulin failed to significantly stimulate the enzyme in doses up to 100,000 times greater than the lowest concentration of bPTH used. The assay was capable of distinguishing hormonal activity in normal, hypoparathyroid, and hyperparathyroid human plasma. After gel chromatography, bioactivity in plasma of hyperparathyroid patients with skeletal disease but normal kidney function coeluted mainly with bPTH(1-84), whereas bioactivity in plasma of hyperparathyroid patients with skeletal disease but severe uremia coeluted in approximately equivalent amounts with bPTH(1-84) and hPTH(1-34). Despite the abundance of small molecular-weight bioactivity in the peripheral circulation in uremia, approximately 85% of the bioactivity in the parathyroid venous effluent coeluted with bPTH(1-84). The results therefore demonstrate the sensitivity and specificity of the assay for PTH and its utility in measuring the hormone in human parathyroid disorders. The results furthermore demonstrate the importance of entities cochromatographing with bPTH(1-84) in comprising the circulating bioactive hormone in hyperparathyroidism, and support the concept of a biological role for smaller forms of PTH, at least in chronic renal failure.
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PMID:Cytochemical bioassay of parathyroid hormone: characteristics of the assay and analysis of circulating hormonal forms. 741 May 46

In previous clinical investigations on uremic patients we found a stimulatory effect of the presence of hyperparathyroidism on the Ca(2+)-induced secretion of various hormones, i.e. aldosterone and vasopressin. The present investigation, therefore, examined the possible effect of PTH on the calcium-mediated aldosterone secretion from isolated, purified zona glomerulosa cells obtained from the rat. After washing the cells and after 30 min of preincubation Ca2+ was added to the preparations at concentrations from 0.5 to 2.0 mmol and PTH(1-84) or PTH(1-34) were added at concentrations from 10(-7) to 10(-10) M. The cells were then incubated for 120 min and aldosterone measured in the supernatant. The aldosterone response to Ca2+ stimulation--without PTH added--served as baseline controls, while cell preparations with ACTH 10(-6) M added secured the viability and responsiveness of the cells. In all cell preparations with PTH(1-84) as well as PTH(1-34) added the aldosterone responses to a certain Ca2+ concentration increased significantly by up to 200% (p < 0.001) above baseline values. It is suggested that PTH may have a Ca2+ ionophore-like effect on endocrine glands, which are not normally related to PTH and thus enhance the calcium-stimulated hormone secretion. The hypothesis is raised that this phenomenon may take place in uremia during the state of secondary hyperparathyroidism.
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PMID:Enhancement of the stimulatory effect of calcium on aldosterone secretion by parathyroid hormone. 770 Feb 20

This study aimed to assess the effect of anaemia on volume related hormones in dialyzed patients with chronic uraemia. Three groups of subjects were examined. The first one comprised 34 hemodialyzed patients with severe anaemia (haematocrit value < 28%). 17 patients were treated with EPO for 1 year (EPO group) while the other 17 patients did not receive rHuEPO (no-EPO group) but were intensively monitored biochemically and clinically as patients of the EPO group. The second group (HD) consisted of 12 hemodialyzed uraemic patients with a Hct > 30% without rHuEPO treatment, while the third one comprised 15 healthy subjects. In patients of the EPO and no-EPO group plasma renin activity (PRA), plasma concentration of aldosterone (Ald) atrial natriuretic peptide (ANP and vasopressin (AVP) were assessed before (0) and after 3, 6, 9 and 12 months of clinical monitoring, while in patients of the HD group and in normals the above mentioned parameters were estimated only once. EPO treatment improved significantly the Hct value already after three months of therapy. No significant changes in PRA and plasma concentrations of Ald, ANP and AVP in the noEPO group were noticed during 12 months of monitoring. In contrast EPO treatment induced a significant, although transitory decrease of PRA, Ald and AVP, but an increase of plasma ANP. No influence of rHuEPO therapy on blood pressure was noticed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Does long-term human recombinant erythropoietin (rHuEPO) influence secretion of hormones regulating volume and pressure of arterial blood?]. 780 May 84

Desmopressin is a widely used hemostatic drug. It is a synthetic analogue of the natural hormone vasopressin, but, in contrast to vasopressin, it has no pressor activity. The effect is immediate, with two- to sixfold increases in the plasma concentrations of coagulation factor VIII, on Willebrand factor, and tissue plasminogen activator, and increases in platelet adhesiveness of comparable magnitude. Desmopressin is used in patients with mild hemophilia A, von Willebrand's disease, congenital platelet dysfunction, or acquired platelet dysfunction due to uremia or intake of such drugs as aspirin. It may also be used to reduce surgical blood loss in patients without known bleeding diathesis. Optimal hemostatic effect is achieved with a dosage of 0.3 micrograms/kg given intravenously. Other routes of administration are subcutaneous injection or intranasal spray. The latter proved to be efficient for home treatment of patients with bleeding disorders.
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PMID:Desmopressin (DDAVP) and hemostasis. 794 3

Blood loss in patients on cardiopulmonary bypass is tremendously large after surgery due to platelet dysfunction. Desmopressin acetate (a synthetic analogue of vasopressin) has been shown to improve blood coagulation in a variety of platelet disorders especially in patients with hemophilia, von Willebrand's disease and uremia. Recent years, it has been used to treat patients with severe platelet dysfunction and profuse hemorrhage after cardiopulmonary bypass. We have investigated the effect of desmopressin acetate administration in randomized trials of 48 adult patients placed on cardiopulmonary bypass during cardiac surgery. Twenty four patients received intravenous infusion 0.3 microgram/kg desmopressin acetate one hour after cardiopulmonary bypass and other patients only received a placebo. Comparing with the control group, patients receiving desmopressin had shortened bleeding time (3.4 +/- 0.6 vs 5.1 +/- 1.6 mins, 8 hrs post bypass), lessened blood loss (482 +/- 258 ml vs 1430 +/- 733 ml, 24 hrs post bypass) and received fewer blood component therapy (pack RBC 2.7 +/- 2.2 vs 6.6 +/- 3.2 units, FFP 4.3 +/- 2.4 vs 11.7 +/- 5.7 units, platelet 3.8 +/- 5.0 vs 8.4 +/- 7.2 units). We conclude that desmopressin acetate can improve blood coagulation ability with safety and in reducing blood loss in patients after cardiopulmonary bypass.
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PMID:[Clinical assessment of desmopressin to reduce blood loss in patients after cardiopulmonary bypass]. 796 27

A 35-year-old man with chronic renal failure developed toxic epidermal necrolysis due to combination antibiotic therapy for a community acquired pneumonia. During wound care for his toxic epidermal necrolysis, he developed massive bleeding, a 4 to 6 unit blood loss at each dressing change, due to uremia-associated platelet dysfunction and thrombocytopenia. After failure of standard therapy, the man was treated with intravenous triglycyl-lysine-vasopressin, a selective peripheral vasoconstrictor. Transfusion requirements stopped during treatment. This man went on to full recovery with complete wound healing. Triglycyl-lysine-vasopressin effectively reduced skin blood loss in this man with toxic epidermal necrolysis and an intrinsic hemostatic defect, and may be useful in other patients with cutaneous blood loss.
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PMID:Control of hemorrhage during renal failure with triglycyl-lysine-vasopressin. 835 24

Over the past several years, the use of 1-deamino-8-D-arginine vasopressin (DDAVP), a synthetic analogue of vasopressin, has been found to be useful in the treatment of patients with abnormal bleeding tendency. This article is a review of inherited and acquired disorders with prolonged bleeding time in which DDAVP is supposed to shorten the bleeding time. DDAVP is established as effective therapy of the abnormal haemostasis in mild or moderate haemophilia A and von Willebrand's disease. Frequently, DDAVP infusions are used to control bleeding in patients with uraemia. Bleeding time is also significantly shortened in patients with liver cirrhosis, although randomized trials of DDAVP therapy of gastrointestinal bleeding in this group of patients are still needed. Shortening or normalization of the bleeding time with DDAVP has also been observed in patients with inherited platelet dysfunctions, acquired disorders of haemostasis and abnormal haemostasis in chronic myeloproliferative diseases. In addition, preoperative treatment with DDAVP seems to reduce blood loss during surgery.
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PMID:[Desmopressin in the treatment of hemorrhagic diathesis]. 854 Jan 36


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