Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cats were used as models of traumatic spinal cord injury. Each experimental animal received a 500 g-cm force to the exposed dura at the level of thoracic fourth vertebra. Somatosensory evoked potentials (SEPs), carotid arterial blood pressure (BP), and abdominal aorta blood flow in the treated groups were compared with those of the control group. The three treated groups received naloxone (5 mg/kg), TRH (5 mg/kg), and a combination of methyl-prednisolone sodium succinate (MP, 35 mg/kg) and epsilon-aminocaproic acid (EACA, 350 mg/kg). The SEPs which were done only in the naloxone treated group approached "normalcy" 24-26 hours after trauma as compared with the absence of SEPs in traumatized untreated group. In all three groups, the treatment increased the blood flow in abdominal aorta significantly. Morphine sulfate increased substance P (SP) immunoreactivity in the dorsal and ventral gray matter. Naloxone not only reversed this effect, it depleted SP below the saline control level. In order to establish that lipid free radicals are responsible for damage to biological membranes, their effects were also investigated in vitro: 14C-GABA uptake by mouse cortical slices which had decreased by 33% in the presence of superoxide (. O-2) generating system, horseradish peroxidase (HRP), was reduced only by 9% when superoxide dismutase was added to the medium. The latter also protected the nerve endings from damage by (. O-2) as examined by electron microscopy. It is concluded that the agents used in this study produce their ameliorating effects by virtue of their anti-inflammatory, anti-oxidant, and membrane stabilizing properties in addition to their effect on enhancing the regional microcirculation. The release of SP by naloxone may be responsible for the increase in blood flow. The consequences of traumatic injury as depicted in Fig. 1 are discussed at length.
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PMID:Prevention of damage in acute spinal cord injury by peptides and pharmacologic agents. 618 89

Tolerance to the spinal antinociceptive effects of morphine develops rapidly after its chronic administration. The mechanism involved in this phenomenon is unclear, but it is unlikely due to a direct regulation of spinal opioid peptides and their receptor binding sites. A variety of neuropeptides, especially the neurokinins and calcitonin gene-related peptide (CGRP) are concentrated in primary sensory afferents and have thus been proposed to play significant roles in spinal nociceptive mechanisms. However, their functions in the development of tolerance to the antinociceptive properties of morphine have not been explored fully. We therefore investigated the possible involvement of various sensory neuropeptides including CGRP, substance P, galanin, neurotensin and neuropeptide Y and their receptors in the dorsal horn of the spinal cord during the development of tolerance to the antinociceptive action of intrathecal morphine. Morphine sulfate (7.5 micrograms/microliters/hr) was administered continuously at lumbar level L4 using mini-osmotic pumps for 3, 5, 7 and 14 days. Tolerance to the antinociceptive effect of morphine was verified with the tail-immersion test and became evident on the 5th day of treatment. In tolerant animals, there was a marked increase in CGRP-like immunostaining and a decrease (30-45%) in [125I]human CGRP alpha binding in laminae I, II and III of the dorsal horn of the spinal cord. These changes coincided with the onset of morphine tolerance and persisted for the 14-day period during which tolerance was present. Similar changes were not observed in the immunostaining or binding of the other neuropeptides studied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerance to the antinociceptive properties of morphine in the rat spinal cord: alteration of calcitonin gene-related peptide-like immunostaining and receptor binding sites. 775 94