Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A perioperative anesthetic management of a 69 year old woman with acromegaly whose clinical course was characterized by severe heart failure is described. The patient showed symptoms of massive cardiomegaly. Endocrine studies indicated that her pituitary tumor was active with hyperproduction of growth hormone. There was no demonstrable evidence for other known causes of heart disease. Following hormonal therapy using continuous subcutaneous infusion of somatostatin for about two months, there was improvement in daily activity and reduction in heart size. After the improvement of cardiac function, transsphenoidal hypophysectomy was performed under general anesthesia and its perioperative course was quite uneventful. We conclude that because cardiac involvement such as left ventricular dilatation in acromegaly might be reversible with proper treatment, any surgical procedure, as long as the case is elective, should be considered after hormone therapy.
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PMID:[A patient with acromegalic heart disease--a case report]. 925 11

The involvement of somatostatin in urethane-anesthesia-evoked suppression of gastric acid secretion has been described. The present study has examined the role of endogenous somatostatin in diminished pancreatic enzyme secretion during anesthesia, while monitoring acid secretion concurrently. Rats were anesthetized with either urethane or sodium pentobarbital. An indwelling catheter was placed into the right jugular vein. The esophagus and the pylorus were ligated, and the stomach was perfused with saline. The common bile duct was ligated at the hepatic hilum, and cannulated at the duodenal end of the duct for collecting pure pancreatic juice. Purified somatostatin monoclonal antibody (CURE.S6) or control antibody (keyhole limpet hemacyanin, KLH) was injected iv in increasing doses (0.05; 0.15; 0.5; and 1.5 mg) every 30 min (n = 6). Gastric acid and pancreatic amylase secretions were measured. The effect of the antibodies on CCK-8-stimulated (0.25-2.50 nmol/kg/h) pancreatic amylase secretion was also tested. During urethane anesthesia somatostatin antibody induced a dose-dependent increase in acid output, while control antibody did not change it. Basal pancreatic amylase secretion was not affected by either somatostatin or by control antibody. Pancreatic secretory responses to high but not to low doses CCK-8 were found to be significantly increased following immunoneutralization of somatostatin. In sodium pentobarbital-anesthetized rats somatostatin antibody stimulated basal acid secretion but did not affect basal pancreatic amylase secretion. Our data indicate that in anesthetized rats endogenous somatostatin mediates suppression of basal gastric acid secretion but not that of basal pancreatic amylase secretion, and this action does not depend on the type of anesthesia. Furthermore, endogenous somatostatin may play a physiological role in modulating stimulated pancreatic enzyme secretion in this species.
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PMID:Effect of somatostatin immunoneutralization on gastric acid and pancreatic enzyme secretion in anesthetized rats. 940 99

Insulin-like growth factor-binding protein-1 (IGFBP-1) production is increased by somatostatin and its analogues. In order to determine the time course and identify possible mechanisms of this increase in vivo we administered octreotide to rats and determined IGFBP-1 concentrations by RIA. After 60 min of anaesthesia, the mean baseline IGFBP-1 concentrations were 166 (95% confidence interval 123 to 225) ng/ml and increased in saline-infused animals to 729 (488 to 1086) ng/ml after 180 min. IGFBP-1 was stimulated transiently in response to octreotide, with circulating IGFBP-1 concentrations peaking at 1605 (1220 to 2111) ng/ml at 105 min during a continuous infusion of octreotide (100 micrograms/kg per h). In conscious chronically cannulated rats, baseline IGFBP-1 concentrations were 22 (18 to 28) ng/ml, 8-fold less than in the anaesthetised state, and were stimulated in the short term after administration of an octreotide bolus (100 micrograms/kg s.c.) to reach 88 (62 to 126) ng/ml at 60 min. A similar response was seen after i.v. administration to conscious rats. Intravenous bolus of octreotide (100 micrograms/kg) in rats anaesthetised for 3 h resulted in an increase in IGFBP-1 to peak at 1556 (1268 to 1910) ng/ml at 60 min. The IGFBP-1 response to octreotide was diminished in high-fat fed hyperinsulinaemic rats. The pattern of disappearance of iodinated IGFBP-1 from the circulation was not influenced by octreotide. The changes in GH, insulin and glucose concentrations alone did not sufficiently account for the patterns of response observed. We conclude that, in rats, octreotide stimulates IGFBP-1 acutely and this response is potentiated by factors related to anaesthesia.
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PMID:Factors regulating the rat insulin-like growth factor-binding protein-1 response to octreotide. 971 27

We examined whether central somatostatin prevents an inhibitory effect of central calcitonin-gene related peptide (CGRP) on pancreatic secretion in conscious male Wistar rats (330-330 g). Rats were prepared with separate cannulas for draining bile and pancreatic juice and with a duodenal cannula and an extrajugular vein cannula. In addition, another cannula was stereotactically implanted into the left lateral cerebral ventricle. Rats were placed in restraint cages and experiments were conducted 4 days after the operation without anesthesia. An injection of CGRP (0.1, 1.0 nmol/10 microl) into the left lateral cerebral ventricle (i.c.v.) inhibited pancreatic secretion dose-dependently. To confirm the inhibitory effect of CGRP (i.c.v.) was mediated via sympathetic nerves, phentolamine was injected intravenously (i.v.) bolus (0.5 mg kg(-1)) 0.5-h before CGRP (i.c.v.), followed by continuous infusion of 0.2 mg kg(-1) h(-1). Phentolamine (i.v.) reversed the inhibition produced by CGRP (i.c.v.). An injection of 4 nmol/10 microl somatostatin (i.c.v.) 5 min prior to CGRP injection diminished the inhibitory effect of CGRP (i.c.v.). It is concluded that centrally administered somatostatin diminished the inhibitory action of CGRP (i.c.v.) on pancreatic secretion, probably via inhibiting autonomic (sympathetic) nerve excitation at the central site.
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PMID:Central somatostatin diminished inhibitory action of central CGRP on pancreatic basal secretion in conscious rats. 986 89

Glomus tumors arise in the chemical receptors of vessels in the tympanic and jugular regions. Clinical signs depend on location, the structures invaded and a tumor's ability to secrete active amines and peptides. A 44-year-old woman was scheduled for excision of a serotonin-secreting tympanic glomus tumor. Urinary excretion of 5-hydroxyindolacetic acid (5-HIA) in urine over the previous 24 hours was 80 mg (normal < 10 mg). The patient received oral diazepam, ranitidine, intravenous diphenhydramine and subcutaneous octreotide (150 micrograms). Anesthesia was induced with propofol, alfentanil and vecuronium. The tumor produced an episode of bronchospasm and cutaneous rubor during surgical manipulation of the tumor. Airway pressure increased to 42 cmH2O and SpO2 decreased to 89%. Hypotension and bradycardia appeared. Once it was suspected that the symptoms stemmed from tumoral secretion of active substances, 20 micrograms of intravenous octreotide was administered. The bronchospasm decreased and hemodynamic changes were resolved in three minutes, with no recurrence of symptoms. The patient received 100 micrograms of octreotide subcutaneously every 8 hours throughout the 72 postoperative hours. Urinary excretion of 5-HIA was 12 mg on the fifth day and the patient was released without having experienced complications. Appropriate preoperative preparation is important in patients with such tumors, as are early detection of respiratory and hemodynamic changes that may occur during surgery and correct perioperative treatment. Octreotide, a longer-lasting somatostatin analogue, has facilitated the handling of such cases.
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PMID:[Octreotide and a serotonin-secreting glomus tumor]. 1037 89

The preoperative evaluation and safe anesthetic treatment of patients with endocrine gland tumors mandate an understanding of the physiologic dysfunctions attributable to these tumors. Some patients will exhibit various signs and symptoms characteristic of the MEN syndromes. In the patient with acromegaly, a fiberoptic-guided intubation of the trachea to secure the airway before induction of general anesthesia must be anticipated. Anesthetic treatment of the patient with hyperadrenocorticism requires knowledge of the physiologic effect of excess cortisol. In the patient with severe hyperparathyroidism, we attempt to correct the markedly elevated plasma calcium levels and maintain adequate hydration and urine output perioperatively. Following thyroidectomy for MCT, 2 potential problems of concern are upper airway obstruction and aspiration resulting from injury (unilateral or bilateral) to the recurrent laryngeal nerve and the superior laryngeal nerve, respectively. The major focus during excision of an insulinoma is prevention of wide swings in blood glucose concentrations. In the gastrinoma patient, the anesthesiologist not only must correct any intravascular fluid volume deficit or electrolyte imbalance but must also consider the patient to have a full stomach at the time of anesthetic induction. Correction of hypokalemia and control of hypertension may be required in the preoperative preparation of the patient with an adrenal cortex tumor. Preoperative alpha-adrenergic blockade must be initiated in the patient with a pheochromocytoma to prevent dangerous elevations in blood pressure during anesthesia and surgery for the tumor's removal. Vasodilators with rapid onset and short duration are used to treat intraoperative hypertension. After ligation of the tumor's blood supply, falls in blood pressure may require treatment with fluids and vasopressors. Carcinoid syndrome patients should be treated with somatostatin to prevent stimuli such as anxiety, abdominal scrubbing, or tumor manipulation from precipitating severe hypotension, hypertension, bronchospasm, or tachycardia. In both pheochromocytoma and carcinoid patients, a smooth anesthetic induction and tracheal intubation plus avoidance of drugs that release histamine or activate the sympathetic nervous system may also prevent intraoperative crises.
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PMID:Anesthetic implications for surgical patients with endocrine tumors. 1081 14

Carcinoids are rare tumors of enterochromaffin cells. The carcinoid-syndrome most often occurs with hepatic metastases of carcinoids and is evoked by release of serotonin and other vasoactive substances, leading to typical symptoms such as hyper- or hypotension, bronchospasm, tachycardia, diarrhoe, and flushing. A lethal perioperative "carcinoid-crisis" may occur. We report on a patient with carcinoid-syndrome due to liver metastases undergoing hemihepatectomy. For prophylaxis, the patient preoperatively received H 1- and H 2-histamine-receptor antagonists, corticosteroids, and a continuous somatostatin infusion. Besides monitoring cardiovascular variables we intermittently measured serotonin- and catecholamine concentrations. Initially increased serotonin concentration decreased during the course of anaesthesia. However, it increased again during liver resection despite Pringle's manoeuvre and was associated with a decrease in arterial pressure, systemic vascular resistance, and central venous pressure. Hypotension was treated by volume and noradrenaline infusion. Thus, despite somatostatin infusion serotonin release is still possible, especially during surgical manipulation.
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PMID:[Anaesthetic management for hemihepatectomy in a patient with carcinoid-syndrome]. 1174 74

We here report a pharmacological characterization of two new somatostatin (SS) receptor subtype-2 (sst2) selective antagonists by evaluating their GH-releasing activity when administered, by different routes, in anesthetized adult rats and in freely moving 10-d-old rats. Moreover, we describe the effect of these SS antagonists on the GH response to GHRH after short-term high-dose dexamethasone (DEX) treatment in young male rats. BIM-23454 and BIM-23627, given iv, were able to counteract the SS-induced inhibition of GH secretion occurring after urethane anesthesia in a dose-dependent manner. In DEX-treated animals, the GH response to GHRH was partially blunted (5-min peak values, 270 +/- 50 ng/ml in saline-treated vs. 160 +/- 10 ng/ml in DEX-treated, P < 0.05); however, the simultaneous administration of BIM-23627 (0.2 mg/kg, iv) restored higher amplitude GH pulse, leading to a significantly higher overall mean GH response (area under the curve, 4200 +/- 120 ng/ml/30 min vs. 2800 +/- 100 ng/ml/30 min after GHRH alone; P < 0.05). The SS antagonists showed a reduced GH-releasing effect when administered sc or ip, likely attributable to decreased bioavailability, as compared with the iv route. SS antagonist administration also increased plasma glucagon, insulin, and glucose levels. Based on prior reports that sst2 tonically suppresses glucagon secretion, the antagonist most likely increased glucagon secretion from the pancreatic alpha-cells, with resultant increases in plasma glucose and then insulin.
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PMID:Characterization of new selective somatostatin receptor subtype-2 (sst2) antagonists, BIM-23627 and BIM-23454. Effects of BIM-23627 on GH release in anesthetized male rats after short-term high-dose dexamethasone treatment. 1189 76

This immunohistochemical study sought to determine whether there are any differences in the peptidergic innervation of these pulps and whether dental caries is associated with changes in neuropeptide expression. Mandibular first permanent molars and second primary molars (n=120) were obtained from children requiring dental extractions under general anaesthesia. Extracted teeth were split longitudinally, placed in fixative, and categorized as intact, moderately carious or grossly carious. The coronal pulps were removed and 10-microm frozen sections were processed for indirect immunofluorescence. Double labelling employed combinations of the following antisera: (1) protein gene product 9.5, a general neuronal marker; (2) one of the neuropeptides calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), galanin (GAL), enkephalin (ENK) and somatostatin (SOM). Image analysis was then used to determine the percentage area of immunostaining for each label within different anatomical regions of the coronal pulp. Sparse or absent immunoreactivity for GAL, ENK and SOM made analysis impossible. Analysis of CGRP, SP and VIP revealed significant interdentition differences, with their expression being significantly greater in permanent teeth, but this was not the case for NPY, with primary and permanent teeth demonstrating a similar amount of label for this peptide. Both dentitions showed significant increases in CGRP, SP, VIP and NPY expression with caries progression. These findings could have biological and clinical importance in connection with nociception, inflammation and healing.
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PMID:Comparative immunohistochemical analysis of the peptidergic innervation of human primary and permanent tooth pulp. 1201 18

The local thermal trauma activates a number of systemic mediator cascades, e.g. a complement activation, cytokine production, resulting in a generalized sequestration and a priming of local and systemic neutrophils and macrophages. We aimed to determine the possible protective effect of octreotide (OCT), a synthetic somatostatin analogue, against burn-induced intestinal tissue damage possibly by inhibiting neutrophil infiltration. Under brief ether anaesthesia, shaved dorsum of the rats was exposed to 90 degrees C bath for 10s to induce burn injury. Rats were decapitated either 3, 24 or 72 h after burn injury. Octreotide (10 microg/kg) or saline was administered subcutaneously (s.c.) immediately after the burn injury. In the 24- and 72-h burn groups, OCT injections were repeated three times daily. In the sham group the same protocol was applied except that the dorsum was dipped in a 25 degrees C water bath for 10 s Malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) activity were determined in the intestinal tissue. The results demonstrate that burn injury results in significant neutrophil accumulation, as evidenced by increases in MPO activity. The increase in MDA and the concomitant decrease in GSH levels demonstrate the role of oxidative mechanisms in burn injury. OCT may have some beneficial therapeutic effects by reducing neutrophil-dependent injury and related lipid peroxidation following burn trauma.
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PMID:Octreotide improves burn-induced intestinal injury in the rat. 1257 93


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