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

Intrathecal morphine has been shown to be reliable in producing analgesia in patients with intractable cancer pain. Recently, we have demonstrated that intrathecal somatostatin is as effective in the treatment of cancer pain as intrathecal morphine. This report presents 2 cases in whom analgesia could be maintained for 60 and 25 days, respectively, under continuous intrathecal infusion of somatostatin by means of infusion devices.
Pain 1985 Sep
PMID:Intrathecal somatostatin in terminally ill patients. A report of two cases. 286 13

This review is a presentation of the various effects of somatostatin within the central nervous system and the gastrointestinal tract. Attention is focused on the analgesic effect of somatostatin, which can be induced by intrathecal or intraventricular, or by epidural administration. Chronic, morphine-responsive pain in terminal cancer patients or acute postoperative pain can be effectively treated by spinal administration of somatostatin. Intraoperative application of somatostatin saves on using anesthetics. However, further investigations are necessary to determine the limitations of spinal administration of somatostatin.
 ...
PMID:[Somatostatin. A review]. 286 26

The aetiology of acute pancreatitis may be alcoholic, dyslipidaemic, post-operative, traumatic, cryptogenic or biliary and only the biliary form is considered here. Fifteen patients with biliary pancreatitis and blood amylase above 250 mg (n.v. less than 100) were encountered in 1984-85. Six patients were given traditional medical treatment and 9 somatostatin alone. Despite the limited number treated the results obtained in the second group appear to confirm the validity and efficacy of somatostatin. In fact given the rapid disappearance of pain and the normalisation of the altered blood parameters it was never necessary to administer somatostatin for more than 24-36 hours.
 ...
PMID:[Use of somatostatin in acute pancreatitis of biliary origin]. 288 8

The effect of a long-acting somatostatin analogue SMS 201-995 on GH secretion was investigated. Eleven acromegalic patients received a single dose of 50 micrograms SMS 201-995 administered subcutaneously, and plasma GH, IGF-I, GRF, TSH, IRI and blood glucose were determined at regular intervals. Nine of 11 patients had elevated basal plasma GH levels above 5 ng/ml. In all patients, plasma GH levels fell immediately from 39.5 +/- 17.3 ng/ml (mean +/- SEM) to 4.3 +/- 1.6 ng/ml (P less than 0.05) with a maximal inhibition of 82.9 +/- 3.3% of the basal levels and the suppression persisted for about 6 h of the observation period. IGF-I and GRF levels were not apparently altered. TSH and IRI levels also rapidly fell. Blood glucose levels fell slightly by 0.5 h. Ten of 11 patients had pain at injection sites. Except for this, no side effects were observed. Our results show that the new somatostatin analogue SMS 201-995 may inhibit GH hypersecretion in acromegalic patients for significant periods, suggesting that this agent can be a useful clinical tool for the treatment of acromegaly.
 ...
PMID:Effect of a single administration of somatostatin analogue (SMS 201-995) on GH, TSH and insulin secretion in patients with acromegaly. 288 93

In the present investigation, the antinociceptive effect of somatostatin (SST) was assessed after intrathecal injection in rats. It was found that the peptide caused antinociception, hind limb paralysis and neuronal damage of the spinal cord in a dose-dependent manner. The threshold dose for antinociception was lower (approximately 10 micrograms) than that (approximately 30 micrograms) giving rise to chronic motor impairment associated with necrotic changes and loss of an immunohistochemical marker for motoneurons in the spinal cord. It is concluded that the 'neurotoxic' potential of SST should be considered in further clinical trials.
Pain 1988 Jan
PMID:Antinociceptive and 'neurotoxic' actions of somatostatin in rat spinal cord after intrathecal administration. 289 26

We determined the effects on nociceptive threshold and motor function of dynorphin-gene products, dynorphin A-(1-32) (DYN A-(1-32), DYN A-(1-8), DYN B and DYN B-29 and the non-opioid peptides somatostatin, neurotensin and salmon calcitonin (s-CT) after intrathecal administration in the rat. DYN A-(1-32) (25 nmol) produced maximal elevation of tail-flick latency accompanied by severe hind limb paralysis and tail flaccidity lasting 6 h and still present at 24 h in several animals. Antinociception evaluated by the vocalization test wore off within 2 h. A lower dose of the peptide (6.25 nmol) did not alter the tail-flick reflex and motor function but significantly elevated the vocalization threshold. The other dynorphins showed weaker, short-lasting activity on the nociceptive threshold, the order of potency being as follows: DYN B-29 greater than DYN B greater than DYN A-(1-8). On the other hand, at the high doses DYN B (100 nmol) and DYN B-29 (50 and 100 nmol) caused moderately severe hind limb paralysis whereas DYN A-(1-8) did not cause any motor impairment up to the dose of 100 nmol. MR 1452, a relatively preferential antagonist of the kappa opioid receptor, prevented both the antinociceptive and motor effects of dynorphins. Intrathecal somatostatin (25 nmol) had a profile of activity superimposable on that of DYN A-(1-32): long-lasting (up to 24 h) elevation of tail-flick latency with hind limb paralysis, and a shorter (4 h) elevation of the vocalization threshold. MR 1452 did not modify these effects. Intrathecal neurotensin (25 nmol) and s-CT (0.5 nmol) did not alter tail-flick latency or vocalization threshold. However, adopting the hot plate as the analgesimetric test, both peptides elevated the time of hind paw licking, taken as an index of nociception. No signs of motor dysfunction were observed at the doses employed.
Pain 1988 Oct
PMID:Distinguishable effects of intrathecal dynorphins, somatostatin, neurotensin and s-calcitonin on nociception and motor function in the rat. 290 71

Concentrations of somatostatin-like immunoreactivity in cerebrospinal fluid were significantly reduced in chronic pain patients compared to control patients without chronic pain. This difference was not influenced by demographic or clinical characteristics. Somatostatin has been shown to be a neurotransmitter in animal nociception; pharmacologic doses of this substance have moderated human pain. Our findings provide evidence that somatostatin may be involved in the pathogenesis of the chronic pain state.
Pain 1988 May
PMID:Alterations in cerebrospinal fluid concentrations of somatostatin-like immunoreactivity in chronic pain patients. 296 47

The onset of therapeutic effectiveness of carbamazepine is generally very rapid in the treatment of seizure and paroxysmal pain disorders, shows some lag in the treatment of mania, and exhibits the longest lag in depression. These time course variations may indicate that different mechanisms underlie the efficacy of carbamazepine in the differential neuropsychiatric syndromes. Biochemical and pharmacological data suggest that the anticonvulsant effects of carbamazepine are related to "peripheral-type" benzodiazepine and alpha 2-noradrenergic receptor systems and to its ability to stabilize sodium channels. GABAB (baclofen-like) actions appear to be involved in antinociceptive, but not anticonvulsant, effects. The relatively acute time course of antimanic efficacy may be related to the above-mentioned mechanisms or to other effects related to systems postulated to be altered in the manic syndrome. These effects might include carbamazepine's ability to increase acetylcholine in the striatum, decrease probenecid-induced levels of CSF homovanillic acid (HVA) in man and dopamine turnover in animals, decrease CSF norepinephrine in manic patients, inhibit adenylate cyclase activity (in response to norepinephrine, dopamine, adenosine, or ouabain), decrease GABA turnover, or act as a vasopressin agonist. Efficacy in depression may be related to actions in man that take time or chronic drug administration to develop, such as increases in plasma tryptophan, decreases in CSF somatostatin, decreases in thyroid indices, and increases in urinary free cortisol excretion and, in animals, increases in substance P sensitivity and increases in brain adenosine receptors. The ability of carbamazepine to block the development of lidocaine- and cocaine-induced seizures also requires chronic administration, suggesting that these seizure models may provide a unique perspective for understanding mechanisms of time-dependent effects.
 ...
PMID:Time course of clinical effects of carbamazepine: implications for mechanisms of action. 328 May 60

A study has been made of the involvement of spinal peptidergic neurons in ascending tracts at lumbar-sacral levels in rats, by combining the retrograde transport of a protein-gold complex with immunocytochemistry. Ten neuropeptides have been considered for their presence in the cells of origin of the following six ascending tracts, including some involved in pain transmission: the spinosolitary tract, the medial and lateral spinoreticular tracts, the spinomesencephalic tract, the spinothalamic tract and the postsynaptic dorsal column tract. Although there was overlap in the distribution of several of the types of peptidergic cells and some ascending tract cells only a very small percentage of long ascending tract cells were found to contain neuropeptides. Most (90%) of those peptidergic ascending tract cells, however, were clearly congregated in two distinct spinal regions: the lateral spinal nucleus and the region surrounding the central canal (including lamina X). Ascending tract cells in both of these regions contained a wide variety of neuropeptides. Immunoreactivities for a total of seven different peptides were seen. The lateral spinal nucleus had the highest percentage of neuropeptide containing ascending tract cells; cells of all the four populations of peptidergic neurons lying in this region were involved in supraspinal projections; they stained for vasoactive intestinal polypeptide, bombesin, substance P or dynorphin and their axons projected in the spinomesencephalic, spinoreticular and spinosolitary tracts. The region surrounding the central canal contained bombesin-, enkephalin-, cholecystokinin- and somatostatin-immunoreactive ascending tract cells; these cells were found at the origin of the spinothalamic, spinomesencephalic, spinoreticular and spinosolitary tracts. In this region only the cells staining for substance P were not involved in supraspinal projections. The peptidergic ascending tract cells in other spinal regions were few; they were found in either lamina I or lateral part of lamina V. Ascending tract lamina I cells reacted for dynorphin or vasoactive intestinal polypeptide and their axons projected in the spinosolitary and spinomesencephalic tracts. Ascending tract lamina V cells reacted for somatostatin and were found at the origin of the medial component of the spinoreticular tract. It is proposed that peptidergic ascending tract cells form minor but distinct subgroups within each ascending tract. Each of the ascending tracts are divisible into peptide- and nonpeptide-containing groups of cells which convey information in a parallel fashion.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:neuropeptides in long ascending spinal tract cells in the rat: evidence for parallel processing of ascending information. 336 49

Pain is a complex phenomenon involving both neurophysiological and psychological components. Pathophysiological mechanisms involve neural pathways, and a variety of pain-producing substances and modulating mechanisms. These include acetylcholine, serotonin, histamine, bradykinin, prostaglandins, substance P, somatostatin, cholecystokinin, vasoactive intestinal polypeptide, noradrenaline and endogenous opioid peptides. In assessing patients with pain, it is essential to evaluate the cause of the pain, its severity, type, location, duration, quality, and response to therapies, among other factors. The measurement of pain is dependent on subjective responses, which are evaluated by methods which have been well developed over the last three decades. Alleviation of pain by non-drug treatments must be considered as well as use of pharmacological treatments. These include psychological support, placebos, relaxation training, biofeedback, hypnosis, heat, cold, physical supports and surgery. Oral drugs are generally preferable to parenteral drugs, as are drugs with few side effects and low addictive liability. Both overtreatment and undertreatment are to be avoided. Patients can be expected to differ in their needs and responses, and economic considerations ought not be ignored. Newer approaches to pain management include self-administration of parenteral drugs, the search for new types of analgesics and appreciation of the relationship between age, sex, race, etc. and the response to analgesics. Tricyclic antidepressants, phenothiazines and the new non-steroidal anti-inflammatory drugs have pointed the way to possible improvements in our ability to tailor specific drugs to the needs of individual patients.
 ...
PMID:The management of pain. 355 78


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>