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)

The effects of hypothyroidism duration on several factors implicated in GH secretion control were studied in the male rat at different maturity stages, ranging from the peripuberal period to adulthood. Thyroid ablation was performed on 22-day-old Wistar male rats maintained on a low iodine diet (T group). Age-paired controls (C group) were fed with the same diet, supplemented with potassium iodide. Subgroups of T and C animals (aged 32, 42, 52, 82 and 112 days) were studied 10, 20, 30, 60 and 90 days after surgery. After pentobarbital anesthesia, jugular blood was withdrawn before and 5 min after an intravenous TRH stimulus, for GH assay. Hypothalamic and pituitary tissues were obtained in order to measure GH, immunoreactive somatostatin (IR-SRIF) and growth hormone-releasing factor (IR-GRF). Growth rate and serum testosterone confirmed that C rats reached sexual maturity by day 30 of the study. Mean +/- SE serum GH (ng/ml) increased (p less than 0.05) in C animals from day 10 (38.5 +/- 5) to day 30 (67.4 +/- 7.3), with no significant variations thereafter. The same time sequence pattern was observed in pituitary GH concentrations. In T rats, both serum and pituitary GH decreased progressively from day 10 to 90, being significantly lower than in C at all times of the study. No GH response to TRH could be found in C groups. In contrast, GH increased significantly (p less than 0.05) in T animals after TRH at days 20 and 30.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of hypothyroidism duration on developmental changes in the hypothalamic factors implicated in growth hormone secretion in the male rat. 168 42

The effect of brain temperature and anesthesia on ischemic neuronal damage was studied in the hippocampal formation using the four vessel occlusion model in awake and anesthetized rats. Neuronal damage was assessed by immunocytochemistry and silver impregnation of tissue sections. The degree of ischemia was monitored by recording spontaneous and evoked electrical activity from the hippocampus and dentate gyrus in all animals. In addition, the hippocampal temperature and oxygen tension were also recorded using a chamber-type thin-film microelectrode in the anesthetized animals. Fifteen minutes ischemia in the awake animals caused greater neuronal damage and mortality of animals than 30 min ischemia in anesthetized rats. The temperature of the brain was found to drop by 4-6 degrees C during complete forebrain ischemia in the latter group. Neuronal damage was observed infrequently in the hippocampus of these animals. When the brain temperature was kept constant at the preischemic level during 30 min occlusion, all animals died within a day, while after 15 min occlusion the majority showed an almost complete degeneration of CA1 pyramidal cells and hilar somatostatin immunoreactive neurons. Following 15 min ischemia, the awake animals showed a similar cell loss in the CA1 region and the hilus. It is concluded that, in the anesthetized animals prepared for acute recording, the decreased temperature of the brain during ischemia is a major factor in protecting neurons from damage, but that Equithesin anesthesia also has a significant protective effect. Consistent ischemic degeneration occurs in awake animals by four vessel occlusion, if the brain temperature is controlled and the completeness of ischemia is monitored by recording spontaneous and evoked electrical activity with chronic electrodes.
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PMID:Hippocampal cell death following ischemia: effects of brain temperature and anesthesia. 169 78

To assess the effect of chemical stimulation of the central nervous system (CNS) on ketogenesis, we injected neostigmine (5 x 10(-8)mol) into the third cerebral ventricle in normal rats fasted for 48 h and fed rats with diabetes induced by streptozotocin (STZ, 80 mg/kg). The hepatic venous plasma levels of ketone bodies (3-hydroxybutyrate and acetoacetate), free fatty acids (FFA), and glucose were measured for 120 min after the injection of neostigmine under pentobarbital anesthesia. In the normal rats, plasma glucose levels were significantly increased but neither ketone bodies nor FFA were affected by CNS stimulation with neostigmine. In contrast the plasma levels of ketone bodies and FFA were significantly increased in STZ-diabetic rats, while glucose levels remained unchanged. The intravenous infusion of somatostatin (1.0 microgram/kg/min) suppressed the increase in plasma ketone bodies following CNS stimulation in STZ-diabetic rats. These findings suggest that CNS stimulation with neostigmine may accelerate ketogenesis by promoting the lipolysis, which may be induced by glucagon, in fed diabetic rats but not in normal fasted rats.
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PMID:Reciprocal changes of plasma glucose and ketone bodies in fasted and acutely diabetic rats after CNS stimulation. 189 76

1. Anaesthesia caused marked decreases in the plasma concentrations of triiodothyronine (T3) and thyroxine (T4) and in the body temperature of young fowl. 2. Exogenous T4 or a thyroid hormone secretagogue (somatostatin antiserum), increased endogenous T3 and T4 concentrations and body temperature in conscious birds and prevented the body temperature decline in anaesthetized fowl. 3. These results provide further evidence for a role of T3 and T4 in temperature regulation in birds, particularly during anaesthesia.
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PMID:Thyroid regulation of body temperature in anaesthetized chickens. 197 May 31

The role of endogenous somatostatin in mediating urethane anesthesia-induced inhibition of gastric acid secretion was investigated using measurement of somatostatin messenger RNA concentrations in the antrum and the influence of somatostatin monoclonal antibody CURE.S6 on acid secretion in rats anesthetized with urethane and acutely implanted with gastric fistulas. Fifteen minutes after injection of urethane, somatostatin messenger RNA concentrations were increased by 128% compared with those in nontreated rats. The significant elevation of somatostatin messenger RNA was maintained for 2 hours after injection. Somatostatin monoclonal antibody injected intravenously (2 mg) completely reversed the inhibitory effect of somatostatin (20 micrograms/kg.h) on pentagastrin (24 micrograms/kg.h)-stimulated gastric acid secretion. The somatostatin monoclonal antibody dose dependently increased basal gastric acid secretion in urethane-anesthetized rats. Peak acid response to the somatostatin monoclonal antibody (2 mg) was observed 20 minutes after antibody injection (preinjection, 1.4 +/- 1.2 mumol/10 min; postinjection, 10.6 +/- 0.6 mumol/10 min); meanwhile, levels of plasma gastrin increased from 27 +/- 6 pg/mL to 75 +/- 8 pg/mL and were maintained elevated for the 2-hour experimental period. When gastrin monoclonal antibody 28.2 was injected together with somatostatin monoclonal antibody, the stimulatory effect of the somatostatin antibody was inhibited by 82%. A control monoclonal antibody 109-21 directed against the biologically inactive glycine-extended fragment 66-72 of progastrin did not alter basal gastric acid secretion or the inhibitory effect of somatostatin. These results indicate that one mechanism by which urethane induced low basal gastric acid secretion involved increased synthesis and release of endogenous somatostatin and associated inhibition of gastrin secretion.
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PMID:Somatostatin monoclonal antibody immunoneutralization increases gastrin and gastric acid secretion in urethane-anesthetized rats. 197 17

Our study has been made on a retrospective basis in order to evaluate the efficacy of somatostatin (SST) in the treatment of acute haemorrhage caused by gastroduodenal ulcer. Sixty patients were allocated in 2 groups: those who received SST (n = 30), and those who did not received it (n = 30), and were treated only with conventional measures (nasogastric catheter, H2 blockers, blood or derivatives, etc.). Both groups were monitored and controlled at the Anesthesia-Intensive Care Unit. The patients in the SST group received a continuous intravenous infusion of 250 micrograms/h. These patients showed better hemodynamic parameters, and only seven needed surgery. The patients in the conventional treatment group showed worse hemodynamics, needed higher volumes of hemoderivatives, and 25 of them needed surgery. The statistical analysis of our data supports the efficacy of SST in the treatment of uncontrollable upper gastrointestinal bleeding due to gastroduodenal ulcer.
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PMID:[Effectiveness of somatostatin in the treatment of acute upper digestive hemorrhage]. 197 14

To determine the time onset of the growth hormone (GH) alteration in the genetically obese rat, we studied the in vivo and in vitro rat growth hormone releasing factor (rGRF(1-29)NH2)-induced GH secretion in 6- and 8-week-old lean and obese male Zucker rats. Under sodium pentobarbital anesthesia, rGRF(1-29)NH2 (GRF) was injected intravenously at two doses: 0.8 and 4.0 micrograms/kg b.w. Basal serum GH concentrations were similar in lean and obese age-matched animals. The GH response to both GRF doses tested was unchanged in 6-week-old obese rats as compared to their lean litter mates. In contrast, a significant decrease of the GH secretion in response to 4.0 micrograms/kg b.w. GRF was observed in the 8-week-old obese rats. The effect of GRF (1.56, 6.25 and 12.5 pM) was further studied in vitro, in a perifusion system of freshly dispersed anterior pituitary cells of lean and obese Zucker rats. Basal GH release was similar in the 6-week-old animal group. In contrast, it was significantly decreased in 8-week-old obese rats as compared to their lean litter mates. Stimulated GH response to 1.56 and 6.25 pM GRF was significantly greater in the 6-week-old obese group than in the age-matched control group. In contrast, the GH response to all GRF concentrations tested was significantly decreased in the 8-week-old obese rats as compared to their respective lean siblings. In 8-week-old obese rats, a decrease of GH pituitary content and an increase of hypothalamic somatostatin (SRIF) concentration were observed. Insulin and free fatty acid serum were significantly increased in 8-week-old obese rats. In contrast, lower insulin-like growth factor I serum levels were observed in the obese animals as compared to their lean litter mates. Finally, to further clarify the role of the periphery in the inhibition of GH secretion observed in the 8-week-old fatty rats, we exposed cultured pituitary cells of 8-week-old lean animals to 17% serum of their obese litter mates. A significant decrease of GRF-stimulated GH secretion of lean rat pituitary cells exposed to the obese serum was noted (P less than 0.05). This study demonstrates that, in the obese Zucker rat, an alteration of the GH response to GRF is evident by the 8th week of life. This defective GH secretion could be related to peripheral and central abnormalities.
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PMID:Dynamic of the GRF-induced GH response in genetically obese Zucker rats: influence of central and peripheral factors. 213 33

This case report describes the use of octreotide, a long-acting somatostatin analogue, in the management of a patient with an ovarian carcinoid tumour and severe cardiac valvular disease. This patient underwent laparotomy and tumour resection without complication. Anaesthesia was induced with midazolam, fentanyl, and vecuronium, and maintained with isoflurane as well as additional fentanyl and vecuronium. However, we feel that it was the use of octreotide that prevented a life-threatening crisis intraoperatively, and recommend its use in patients with carcinoid syndrome undergoing anaesthesia and surgery.
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PMID:The prophylactic use of octreotide in a patient with ovarian carcinoid and valvular heart disease. 222 98

The anaesthetic management of a 63-year-old patient with carcinoid syndrome presenting for transurethral resection of the prostate (TURP) is described. Before surgery antibradykinin, antiserotonin and antihistamine drugs were used in addition to SMS 201-995, a long-acting somatostatin analogue, to prevent the intraoperative release of hormones associated with this syndrome. Several techniques of general anaesthesia have achieved successful patient outcomes. Monitoring included pulse oximetry and radial artery cannulation. After infusion of Ringer's lactate, 750 ml, and 25 per cent albumin, 150 ml, an incremental epidural block with xylocaine two per cent without adrenaline was administered to achieve ideal operating conditions without any change in haemodynamic variables or oxygen haemoglobin saturation. Epidural anaesthesia seems to be a safe alternative to general anaesthesia in patients with carcinoid syndrome presenting for TURP.
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PMID:Epidural anaesthesia for transurethral resection of the prostate in a patient with carcinoid syndrome. 232 71

Peripheral nerve section or local capsaicin application produces depletion of substance P and an enzymatic marker, fluoride-resistant acid phosphatase (FRAP), from circumscribed regions of the terminal areas in the spinal cord. We have made use of this phenomenon to map the extent of central termination of subpopulations of primary afferent neurons containing substance P (SP), somatostatin (SOM), cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP) and FRAP in the rat lumbar spinal cord following sciatic nerve section at midthigh level under ether anaesthesia. Between 2 days and 1 year postoperatively, the animals were perfused transcardially and SP, CCK, VIP and SOM were localised in frozen transverse sections of spinal cord segments L1 to S2 and their corresponding ganglia using unlabelled antibody immunohistochemistry. FRAP was localised using a modified Gomori method. SP, SOM, CCK and FRAP were maximally depleted from identical restricted areas of the dorsal horn of the third, fourth and fifth lumbar segments fifteen days after nerve section and remained so for a year. In contrast, VIP staining increased dramatically in the areas from which the other markers were depleted and showed the same time course. Moreover, a large number of neurons in the corresponding ganglia showed positive VIP immunoreactivity after axotomy but were absent from the unoperated side.
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PMID:Vasoactive intestinal polypeptide increases in areas of the dorsal horn of the spinal cord from which other neuropeptides are depleted following peripheral axotomy. 242 58


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