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 distribution of somatostatin (SST) throughout the nervous system suggests that this tetradecapeptide may play a physiological role in CNS in the mediation of analgesia. The present study was undertaken to evaluate the antinociceptive properties of intrathecal (IT) injection of SST in the comparison of morphine sulfate (MS) in a primate model. The study was conducted after institutional approval and adhered to the regulations of the animal research committee. Seven adult monkeys (Maccaca cyclopis Swinhoe) weighing 4-6 kg were used. In each animal a L5 laminectomy window was created to facilitate IT injection. No neurological damage from surgery was noted. With the monkey standing in a specially constructed cage, all animals randomly received the following agents at one-week interval: (1) MS 1 mg, IT; (2) SST 50 micrograms, IT; (3) SST 250 micrograms, IT; and (4) SST 250 micrograms, IT + intramuscular (IM) naloxone 400 micrograms. The measured withdrawal latency (HPWL) was converted to the maximal percentage effect (MPE %) for comparison. The HPWL was measured at predrug and 5, 15, 30, 45, 60, 90 and 120 min after injection. Venous blood sample was obtained every 15 min to determine the plasma SST level by radioimmunoassay (RIA) technique in group 3 only. The results showed that MS (1 mg, IT) produced potent antinociception (MPE 100%) for more than 2 h. Intrathecal SST 50 micrograms, however, induced mild antinociception (MPE 43%) for only a short period and a 5-fold larger dose (250 micrograms) did not significantly change the nociceptive threshold with MPE only up to 47%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The antinociceptive effect of intrathecal somatostatin in monkeys]. 168 26

The effects of the intrathecal alpha 2-agonists tizanidine and clonidine and the somatostatin analog octreotide on an experimental rat model of tactile allodynia were investigated to determine the therapeutic potential for treating chronic neuropathic pain. Allodynia was induced by ligating the rat sciatic nerve. The mechanical threshold for paw withdrawal was assessed by applying von Frey hairs to quantify analgesic actions. Mean 50% paw withdrawal thresholds were converted to the percentage of maximum possible effect (%MPE) where %MPE = (postdrug threshold-predrug threshold) divided by (15 g-predrug threshold) x 100. Dose-response curves were plotted for suppression of paw withdrawal 30 minutes after intrathecal injection of various doses of tizanidine, clonidine, and octreotide. Thresholds on the non-lesioned side were greater than 15 g. The lesioned side had baseline thresholds of less than 4.5 g. Dose-response curves were established for the antiallodynia effects of each drug. Tizanidine and clonidine at a 25-micrograms dose increased the threshold to greater than 97% of the MPE, but caused transient hindpaw weakness or sedation. No side effect was observed at a 10-micrograms dose, at which the threshold was 88-96% of MPE. Intrathecal octreotide modestly increased the threshold to only 49-67% of MPE, showing a lesser analgesic effect, although no side effect was observed at a 4-micrograms dose. The antiallodynic effects of intrathecal tizanidine and clonidine were more potent than that of octreotide.
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PMID:Effects of intrathecal nonnarcotic analgesics on chronic tactile allodynia in rats: alpha 2-agonists versus somatostatin analog. 904 98