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)

Two acromegalic patients with severe headache, persisting after pituitary adenomectomy followed by radiotherapy in one, were treated with the somatostatin analogue SMS 201-995. Both had been resistant to conventional headache therapy and experienced dramatic and rapid relief after the first injection of the analogue. This result persisted with long-term treatment of the drug. Although the mechanism of action of SMS 201-995 in pain remains unclear, the rapid and efficacious analgesic effect of this compound may be one more indication for its use in pituitary tumors associated with cephalalgias.
Clin J Pain 1990 Sep
PMID:Headache in acromegaly: dramatic improvement with the somatostatin analogue SMS 201-995. 213 20

1. Cysteamine is formed by degradation of coenzyme A (CoA) and causes somatostatin (SS), prolactin and noradrenaline depletion in the brain and peripheral tissues. 2. Cysteamine influences several behavioral processes, like active and passive avoidance behavior, open-field activity, kindled seizures, pain perception and SS-induced barrel rotation. 3. Cysteamine has several established (cystinosis, radioprotection, acetaminophen poisoning) and theoretical (Huntington's disease, prolactin-secreting adenomas) indications in clinical practice. 4. Pantethine is a naturally occurring compound which is metabolized to cysteamine. 5. Pantethine depletes SS, prolactin and noradrenaline with lower efficacy compared to that of cysteamine. 6. Pantethine is well tolerated by patients and has been suggested to treatment of atherosclerosis. The other possible clinical indications (alcoholism, Parkinson's disease, instead of cysteamine) are discussed.
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PMID:Preclinical and clinical studies with cysteamine and pantethine related to the central nervous system. 227 50

In cats, intracellular dye injection of single sensory neurones of known fibre type and sensory modality has been combined with peptide immunohistochemistry. There was no clear relationship between the sensory function of a neurone and the presence of the neuropeptides substance P, somatostatin, cholecystokinin and vasoactive intestinal polypeptide, in its cytoplasm. In particular, substance P was not detected in many nociceptive sensory neurons even though it could be demonstrated with the same technique in many sensory neurones which did not have cutaneous receptive fields. These results mean that the role, if any, of these neuropeptides in the transmission of pain, must be regarded as complex.
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PMID:Neuropeptides in physiologically identified mammalian sensory neurones. 241 Aug 16

Improved knowledge about biochemical mechanisms underlying pain suppression by CNS electric stimulation is one condition for the further advancement of this form of treatment. In 6 patients treated with PVG stimulation and in 14 with spinal cord stimulation the concentration of substance P-like immunoreactivity in lumbar CSF increased significantly following stimulation. However, these changes may be unspecific and not directly related to the suppression of pain. Measurements of somatostatin, cholecystokinin, vasoactive intestinal polypeptide, neurotensin and monoamine metabolites in CSF showed no changes related to stimulation and the ensuing pain relief. Possible reasons for these negative findings are discussed.
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PMID:Possible neurohumoral mechanisms in CNS stimulation for pain suppression. 242 25

Substance P, present in primary sensory neurones, seems to take part in nociceptive transmission within the trigeminal system. Substance P, released by peripheral axons of these neurones, induces vasodilatation, plasma extravasation, miosis, conjunctival and nasal congestion. All these effects bear some similarity to symptoms of cluster headache and migraine attack. Opiates and somatostatin inhibit the release of substance P from primary sensory neurones and relieve both pain and autonomic symptoms of cluster headache attack. Plasma substance P-like immunoreactivity was decreased during spontaneous attack of cluster headache and migraine and during histamine precipitated attack of cluster headache. Taken together these data suggest that substance P and endogenous opioids could be implicated in the pathophysiology of cluster headache and migraine.
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PMID:Substance P and enkephalins: a creditable tandem in the pathophysiology of cluster headache and migraine. 243 12

An isolated spinal cord-tail preparation of the newborn rat was developed and used for studying the effects of various drugs. The cord and the tail were separately perfused with oxygenated artificial cerebrospinal fluid. Application of capsaicin in a small amount to the tail induced a depolarizing response of the lumbar ventral root (L3-L5) lasting for about 30 sec. The stimulating action of capsaicin was potentiated by previous perfusion of the tail with a medium containing prostaglandin E1 or E2. The capsaicin-induced nociceptive reflex was depressed by application to the spinal cord of morphine, Met-enkephalin, dynorphin (1-13), somatostatin, adenosine, GABA and a substance P (SP) antagonist [D-Arg1, D-Pro2, D-Trp7,9, Leu11]SP, and potentiated by bicuculline. The present preparation will be useful for the future studies on pain and analgesic drugs.
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PMID:Effect of a substance P antagonist on capsaicin-induced nociceptive reflex in the isolated spinal cord-tail preparation of the rat. 244 68

The present study examines the effects of intrathecal administration of selected peptides on nociceptive responses in the rat. Each peptide was delivered via a chronically implanted catheter to the L5 vertebral level. In the tail flick test, VIP (0.65-6.5 nmoles) produced a dose-dependent decrease in reaction time (RT) from 1 to 6-16 min after injection; 6.5 nmoles decreased RT to 37% of control value at 1 min after injection. Galanin (0.65-6.5 nmoles) produced a dose-dependent increase in reaction time at 1 and 6 min; at high doses, many of the rats failed to flick the tail. CGRP (6.5 nmoles) produced a small, transient decrease in RT to 73% of control values at 1 min; 3.25 nmoles were without effect. CSF and 6.5 nmoles of somatostatin, TRH and angiotensin II were without effect. At high doses of galanin and CGRP, rats vocalized to innocuous touch of the tail, as reported for substance P. Von Frey hairs were thus applied to the tail after 6.5 nmoles of VIP, galanin, CGRP or substance P. Vocalization in response to a previously innocuous pressure stimulus was observed at 30 s after injection in all rats given galanin and some rats given CGRP or substance P; the effect lasted 4-8 min. VIP and CSF had no effect. These results suggest that VIP, galanin, CGRP and substance P may act as excitatory agents in nociceptive pathways and that specific peptides may function in the different types of pain modalities; VIP in thermal, galanin in mechanical and substance P and CGRP in both.
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PMID:Effects of intrathecal administration of neuropeptides on a spinal nociceptive reflex in the rat: VIP, galanin, CGRP, TRH, somatostatin and angiotensin II. 245 92

Pharmacological, percutaneous celiac plexus blockade is often inefficient in the treatment of pain in chronic pancreatitis. Lack of efficiency could be due to incomplete denervation of the plexus; however, a method for measuring the completeness of celiac plexus blockade is not yet available. We have, therefore, monitored the physiological completeness of pharmacological percutaneous celiac blockade with 40 ml 25% ethanol by measuring the effect of posture on heart rate, blood pressure, hepato-splanchnic vascular resistance, and pancreatic hormone concentrations before and after celiac plexus block in 6 patients with chronic pancreatitis. Blood pressure decreased and heart rate increased after the block (P less than 0.025), whereas no significant change was found in hepato-splanchnic vascular resistance nor in the change of these parameters during transition from the supine to standing position. Pancreatic hormones (C-peptide, free insulin, glucagon, pancreatic polypeptide and somatostatin) did not change in response to standing, either before or after the block. The cardiovascular variables were normalized the day after the block, and all the patients were in their habitual state regarding pain after 1 week. In conclusion, pancreatic hormone concentrations in response to standing are not useful for monitoring celiac plexus block, whereas heart rate, blood pressure and hepato-splanchnic blood flow may yield useful information. From such measurements it was concluded that permanent denervation of the celiac plexus was not achieved in our patients after injection of 40 ml 25% ethanol.
Pain 1989 Sep
PMID:Monitoring of celiac plexus block in chronic pancreatitis. 213 12

Twenty-seven patients with postoperative enterocutaneous fistulas were treated with parenteral nutrition and SMS 201-995 (100 micrograms/8 hours, subcutaneously), a long half-life somatostatin analogue. At the time SMS 201-995 was started, 11 patients had low output fistulas (less than 1000 ml/48 hours), 11 patients had high output fistulas (above 1000 ml/48 hours), and 5 patients had fistulas sitting in large abdominal wall defects. Within 24 hours of treatment, a mean reduction of 55% of the fistula output was observed. Fistula site or output before treatment had no influence on the magnitude of output reduction. Spontaneous closure was achieved in 77% of the patients after a mean of 5.8 +/- 2.7 days of treatment with this drug. Two patients died (7.4%). Pain at the injection site was referred by 15% of the patients but no other side effects were observed. Glucose intolerance was not observed. SMS 201-995 has been shown to be very useful in the conservative treatment of enterocutaneous fistulas because of its ability to rapidly reduce fistula output and accelerate spontaneous closure.
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PMID:Treatment of 27 postoperative enterocutaneous fistulas with the long half-life somatostatin analogue SMS 201-995. 250 Sep

This paper reports the phenomenon of dependence to a somatostatin octapeptide analog used for the treatment of acromegaly and severe headache. The mechanism of this dependence is still unknown, but could be based on the interaction of the somatostatin analog with opioid receptors. Analgesia may be at least partially supported by the opioid modulation of pain transmission, but also by general "appetitive" behavioral activation due to the effect of somatostatin on its receptors.
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PMID:The development of dependence to an octapeptide somatostatin analog: contribution to the study of somatostatin analgesia. 254 10


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