[Systemic management of a patient with Marfan's syndrome during dental treatment].
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Biomedical subjects
Publications and source records attributed to T Shibutani.
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To investigate a physiological function of substance P (SP) present in the peripheral ending of sensory neurons, we determined immunoreactive SP (iSP) levels in the s.c. perfusate and the amount of edema evoked in rat paw by noxious heat stimulation. We found that immersion of rat paw into hot water (47 degrees C) for 30 min led to a significant increase of iSP in the perfusate and about 50% increase in paw volume. Neonatal pretreatment with capsaicin inhibited significantly the increase in both iSP and paw volume evoked by noxious heat stimulation. Acute and chronic denervation of the sciatic and saphenous nerves also inhibited the heat-evoked iSP release and edema remarkably. Intraplantar injection of SP evoked an increase in paw volume in dose-dependent manner. This increasing effect of SP on paw volume was more substantial than that produced by histamine. Simultaneous treatment with stem bromelain and emorfazone decreased significantly the heat-evoked iSP release and edema. These results suggest that 1) SP produced by noxious heat stimulation in the periphery may be released from the afferent fibers with small-diameter, 2) bradykinin may intervene in this SP release and 3) SP released in the periphery may be closely related to the edema formation of the thermal injury reaction.
The superficial layer in subnucleus caudalis of the brain-stem trigeminal sensory nuclear complex (SpVc) in the rabbit was perfused with artificial cerebrospinal fluid using a push-pull perfusion cannula system. Immunoreactive substance P (iSP) and [Met5]enkephalin (iME) released into the perfusates following electrical stimulation of the lower incisor pulp were measured. An increase in the release of iSP and iME lasting for 1 h or more was observed following electrical stimulation with 40 V. The increase in iSP release depended on the intensity of stimulation. Systemic morphine (10 mg/kg i.v.) completely inhibited the stimulus-evoked iSP release and this inhibition was antagonized by pretreatment with naloxone (5 mg/kg i.v.). The stimulus-evoked iSP release was also inhibited by local application of morphine (10(-6) M) or the opioid peptide [D-Ala2,Met5]enkephalinamide (10(-4) M). However, the local application of naloxone (5 X 10(-7) M) only partially antagonized the inhibitory effects of locally applied morphine and the opioid peptide. These results suggest that there is a functional interaction between SP and enkephalin systems in the superficial layer of SpVc for the regulation of dental pain transmission.
Effects of noxious electrical tooth stimulations and intraarterial administration of bradykinin or inhalation of volatile anesthetics on substance P content in the diencephalon-mesencephalon, pons-medulla and the spinal cord were examined in the rat. Noxious stimulation by electrical long duration stimulation (type 2) of tooth pulp caused an increase of substance P content in the ponsmedulla. Inhalation of volatile anesthetics such as methoxyflurane and diethylether produced an increase of substance P content in the spinal cord; and in addition, methoxyflurane produced a decrease of substance P content in ponsmedulla. However, halothane did not produce any changes in substance P content in any parts of the central nervous system (CNS). These results suggest that volatile anesthetics such as diethyl-ether and methoxyflurane act on the substance P neuron and may modulate pain transmission through the action of substance P in the pons-medulla or the spinal cord.
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Immunohistochemical identification of glycosaminoglycans (GG) in salivary pleomorphic adenomas (63 cases) was made to evaluate chondrogenesis in modified myoepithelial cell regions. Monoclonal antibodies (MoAbs) to GGs were used in conjunction with specific enzyme digestion, and chondroitin 4S proteoglycan (C4SPG), chondroitin 6S PG(C6SPG), dermatan sulfate PG(DSPG), heparan sulfate PG(HSPG) and keratan sulfate PG(KSPC) were identified. Modified myoepithelial cells showing fibrillar and plasmatoid shapes contained KSPG (68%), DSPG (32%) and CSPG(C6SPG:22%, C4SPG:33%). Foci of chondroidally changed cells stained intensely for KSPG (53%), and less so for CSPG(C6SPG:22%, C4SPG:33%), and DSPG (19%). Perinuclear matrix in chondroidal tissue reacted most strongly. Almost all types of modified myoepithelial cells, or outer layer tumor cells of tubulo-ductal structures, produced or synthesized CSPG, DSPG, and HSPG. Certain cells located in hyalinous and myxomatous tissues may undergo chondroidal metaplasia, and clusters of such cells may produce GGs and PGs in the perinuclear zone similar to those GGs in matrix synthesized in chondroidal tissue. GG-synthesizing cells might continuously produce KSPG until the cartilage matrix is completed.
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