Biomedical subjects

L Olgart

Publications and source records attributed to L Olgart.

At least 19 recordsLinked to original sources

PubMed1998

[Breakthrough in pain research. Charting of the synaptic network may lead to new analgesics].

Increased pain fibre activity in response to tissue injury results in changes in gene expression and prolonged changes in nerves and their environment. The resulting hyperalgesia and prolonged spontaneous pain are due both to increased sensitivity of peripheral nociceptors (primary hyperalgesia) and to faciliated spinal cord transmission (secondary hyperalgesia, receptive field expansion and allodynia). Hyperexcitability of dorsal horn neurones is first triggered by increased neuronal barrage into the central nervous system ("wind-up"), and later by retrograde chemical influences from the peripheral inflammation (central sensitisation). Central transmission and hyperexcitability are mediated by excitatory amino acids (aspartate and glutamate) and by tachykinins (substance P). Normally, the net effect of the activity in a complex network of inhibitory neurones in the spinal cord ("gate control"), driven by descending projections from brain stem sites, is to dampen and counteract the spinal cord hyperexcitability produced by tissue or nerve injury. Thus, peripherally evoked pain impulses pass through a filtering process involving gamma-aminobutyric acid, glycine and enkephalins. The activity of these substances in the spinal cord usually attenuates and limits the duration of pain. In the case of persistent pain, there is evidence of pathological reduction of the supraspinal net inhibitory actions in combination with ectopic afferent input in damaged nerves. Hence, the pathology of chronic pain (neuropathic pain) differs from that of nociceptive pain and conventional pharmacological treatment of chronic central pain is usually less successful than treatment of inflammation-related pain. The many newly discovered mechanisms for the transmission and modulation of pain impulses are characterised by complex activity-dependent plasticity, which means that therapeutic strategies for persistent pain must be adapted to changing targets--either at the site of injury or at other sites in the central nervous system.

Analgesics↗

PubMed1997

[A breakthrough in the research on pain. Survey of the synaptic network may result in new analgesics].

Increased pain fibre activity in response to tissue injury results in changes in gene expression, and prolonged changes in nerves and their environment. The resulting hyperalgesia and prolonged spontaneous pain are due both to increased sensitivity of peripheral nociceptors (primary hyperalgesia) and to facilitated spinal cord transmission (secondary hyperalgesia, receptive field expansion and allodynia). Hyperexcitability of dorsal horn neurones is first triggered by increased neuronal barrage into the central nervous system ('wind-up'), and later by retrograde chemical influences from the peripheral inflammation (central sensitisation). Central transmission and hyperexcitability are mediated by excitatory amino acids (aspartate and glutamate) and by tachykinins (substance P). Normally, the net effect of the activity in a complex network of inhibitory neurones in the spinal cord ('gate control'), driven by descending projections from brain stem sites, is to dampen and counteract the spinal cord hyperexcitability produced by tissue or nerve injury. Thus, peripherally evoked pain impulses pass through a filtering process involving gamma-aminobutyric acid, glycine and enkephalins. The activity of these substances in the spinal cord usually attenuates and limits the duration of pain. In the case of persistent pain, there is evidence of pathological reduction of the supraspinal net inhibitory actions in combination with ectopic afferent input in damaged nerves. Hence, the pathology of chronic pain (neuropathic pain) differs from that of nociceptive pain, and conventional pharmacological treatment of chronic central pain is usually less successful than treatment of inflammation-related pain. The many newly discovered mechanisms for the transmission and modulation of pain impulses are characterised by complex activity-dependent plasticity, which means that therapeutic strategies for persistent pain must be adapted to changing targets--either at the site of injury or at other sites in the central nervous system.

Analgesics↗

PubMed1996

Local actions of acetylcholine on vasomotor regulation in rat incisor pulp.

Local actions of acetylcholine on vasomotor regulation in rat incisor pulp were investigated in anaesthetized animals. Pulpal blood flow was measured with laser Doppler flowmetry. lontophoresis (40 or 60 muA for 20 s) with acetylcholine or carbachol on an exposed dentin surface caused a biphasic response: an initial vasoconstriction was followed by an atropinesensitive vasodilation. The vasoconstrictor response was enhanced by 171% in the presence of atropine, whereas in control experiments, using isotonic saline as a medium for the direct current, similar vasoconstriction was unaffected by atropine. Carbachol-induced vasodilation was significantly reduced by 30% after intravenous injection of the nitric oxide synthesis blocker N omega-nitro-L-arginine methyl ester (10 mg kg-1), and the remaining vasodilation was abolished by atropine. The present results support the concept of a cholinergic modulation of sympathetic vasoconstrictor function and of a partial contribution of nitric oxide in carbachol-induced vasodilation in rat incisor pulp.

Acetylcholine↗

PubMed1996

Neural control of pulpal blood flow.

Blood flow of mammalian dental pulp is under both remote and local control. There is evidence for the existence of parasympathetic nerves in the pulp, but functionally the cholinergic influence is weak, and the physiological significance of this autonomic system seems to be low. The evidence for sympathetic vasoconstrictor nerves in the pulp is robust, and there is convincing support for the contention that these nerves play a physiological role, operating via release of noradrenaline and neuropeptide Y. However, there is no significant functional evidence in support of sympathetic beta-adrenoceptor-mediated vasodilation in the pulp. The local control of blood flow involves a subset of intradental sensory nerves. By virtue of their neuropeptide content, these afferent fibers cause vasodilation and inhibit sympathetic vasoconstriction in response to painful stimulation of the tooth. Such locally governed control may serve to meet immediate demands of the pulp tissue. A locally triggered reflex activation of sympathetic nerves in the pulp may modulate this control and limit its magnitude. Thus, there are competitive interactions between local and remote vascular controls which may be put out of balance in the injured and inflamed dental pulp.

Animals↗

PubMed1995

Haemodynamic and immunohistochemical studies of rat incisor pulp after denervation and subsequent re-innervation.

The effects of injury to the inferior alveolar nerve on the distribution of neuropeptides and neurogenic blood-flow reactions were studied in rat mandibular dental pulp. In normal incisor pulps, calcitonin gene-related peptide (CGRP)-like immunoreactivity was common, while substance P- and neurokinin (NKA)-positive nerve fibres were much less abundant. There were no signs of vasoactive intestinal peptide-like, neuropeptide Y-like or 5-hydroxytryptamine-like immunoreactivity. In normal pulps, electrical stimulation (100 microA, 5 ms, 15 Hz for 30 s) of the tooth crown resulted in transient vasoconstriction followed by vasodilation, which was enhanced after alpha-adrenoceptor blockade. At 3 days-4 weeks after unilateral nerve section there were no signs of CGRP-, substance P- and NKA-immunoreactivity, and there was no vasodilation in response to tooth stimulation. The vasoconstrictor response was also absent during this period but at 4 weeks postoperatively a weak response was obtained and after 7 weeks the vasoconstrictor response had regained normal amplitude. At 7 weeks postoperatively, a large number of CGRP-positive fibres had reappeared and at 11 weeks the pattern of CGRP-immunoreactivity was normal. However, substance P- and NKA-immunoreactivity were not found at 7 or 11 weeks after surgery. Vasodilator responses appeared at 7 weeks, and showed normal amplitude at 11 weeks after the creation of the nerve lesion. The results show that during nerve regeneration, sympathetic vasoconstriction was regained earlier than neurogenic vasodilation in rat incisor teeth. The reappearance of neurogenic vasodilation after nerve injury was temporarily associated with the presence of CGRP-immunoreactivity in regenerating trigeminal afferent nerves.

Adrenergic alpha-Antagonists↗

PubMed1995

Enhanced formation of secondary dentin in the absence of nerve supply to feline teeth.

This investigation was designed to study the formation of secondary dentin in permanent teeth of young cats after denervation. In eight animals, cervical dentin was exposed bilaterally in the mandibular canines, 7-10 d after unilateral resection of the inferior alveolar nerve. The observation intervals were 30 d, 90 d and 180 d, after which histological examination of dentin was performed. In order to verify the loss and regeneration of pulpal innervation and an intact blood supply, blood flow responses to electrical stimulation of the tooth and to i.v. injections of substance P (SP) were recorded by laser Doppler flowmetry before and at 7-10 d after denervation, at the end of the experiments, and at predetermined intermediate intervals. SP-induced vasodilation was significantly enhanced at 1 wk and 30 d postoperatively and was normalized to control values at 90 and 180 d. Vasodilation in response to electrical tooth stimulation, which was absent after denervation, reappeared after 90 d in two of four cats. There was no irregular dentin formation under the exposed dentin at any time in denervated or control teeth. Formation of regular secondary dentin appeared to be enhanced on the denervated side at 30 d and 90 d postoperatively, whereas at 180 d there was no difference between sides. The results indicate that intradental nerves influence secondary dentin formation in feline permanent teeth.

Animals↗

PubMed1994

Involvement of substance P but not nitric oxide or calcitonin gene-related peptide in neurogenic plasma extravasation in rat incisor pulp and lip.

The possible involvement of the neuropeptides substance P and calcitonin gene-related peptide (CGRP) in the development of neurogenic plasma extravasation in the lower lip, gingiva and incisor pulp was examined in anaesthetized rats by means of the Evans blue method and by using newly developed blockers of substance P (CP-96,345) and CGRP (CGRP8-37). Electrical stimulation of the inferior alveolar nerve (15 V, 2 ms, 10 Hz) for 5 min significantly increased the Evans blue content of the ipsilateral lip, gingiva and pulp by 60 (p < 0.01), 62 (p < 0.01) and 92% (p < 0.05), respectively (n = 8). Pretreatment with CP-96,345 (total dose: 1.5 mg/kg, intravenously) counteracted the dye leakage in the lip and pulp but not in the gingiva (n = 6). The inactive enantiomer (CP-96,344, 1.5 mg/kg, n = 8) or the nitric oxide synthesis inhibitor (N omega-nitro-L-arginine methyl ester hydrochloride, 10 mg/kg, n = 7) did not reduce the stimulation-induced dye extravasation in any of the tissues. Pretreatment with CGRP8-37 (0.3 mg/kg, n = 7) did not significantly influence the development of neurogenic extravasation in the lip and incisor pulp, but it slightly attenuated extravasation in the gingiva. The results indicate that the afferent nerve-induced dye extravasation in the lip and pulp, but not in the gingiva, is to a large extent mediated by substance P acting via neurokinin-1 receptors. There was no evidence for an involvement of nitric oxide or CGRP in neurogenic extravasation in rat incisor and lip.

Animals↗

PubMed1994

Nerve-pulp interactions.

Pulpal haemodynamics are naturally intermeshed with inflammatory responses. Cellular and humoral factors may be the vehicles that aid in physiological regulation, but when these systems are overly activated, they may lead to pathological changes. Sensory nerves may initiate inflammatory reactions when activated, and interestingly, recent findings show that vasoconstrictor nerves in the pulp can inhibit the release of neurally stored vasoactive and inflammatory mediators. Thus, there are options for endogenous control of inflammation. Perhaps a variation in the effectiveness of such control can explain why symptoms of hypersensitivity and pain are so unpredictable and individual. What naturally occurring agents are involved in early tissue changes and how do they act? Some agents exert their effects both on vessels and nerves. Thus, there is an intriguing mutual interplay between nerves and tissue reactions. A prolonged, painful stimulation may generate increased blood flow and inflammation, and vice versa, inflammation may lead to pain. This complexity of mechanisms generates many questions that need answers.

Animals↗

PubMed1994

CGRP (8-37) reduces the duration but not the maximal increase of antidromic vasodilation in dental pulp and lip of the rat.

In this study the newly developed blockers of substance P (CP-96,345) and calcitonin gene-related peptide (CGRP8-37) were used to examine whether substance P and CGRP are involved in the afferent nerve induced vasodilation in the rat lower incisor pulp and lip. Electrical stimulation of the inferior alveolar nerve (10 V, 2 ms, 10 Hz, 30 s) in the presence of phenoxybenzamine (3 mg kg-1) induced an immediate vasodilation in the pulp and lip (52 and 186% increase in blood flow respectively, n = 12) with a long duration. Infusion of 2 mg kg-1 CP-96,345, a dose that inhibited the vasodilator effects of substance P (5-25 ng kg-1) in oral tissues, did not have any effect on antidromic vasodilation in either tissue. After infusion of CGRP8-37 (0.3 mg kg-1) the duration of the antidromic vasodilation in the pulp and lip was significantly reduced by 72 and 67% respectively (P < 0.05, n = 4), whereas the maximal increase of the response was unaffected. The blocking effect of the drug was short-lasting. When combined infusions of CP-96,345 and CGRP8-37 were given, a similar reduction in the duration of antidromic vasodilation in the pulp and lip occurred but in this case the amplitude of vasodilation in the pulp was reduced (from 35 +/- 9 to 12 +/- 3%, P < 0.05, n = 4). However, in the lip, the amplitude of vasodilation was not significantly reduced. The present findings indicate an involvement of CGRP in the mediation of the late phase of antidromic vasodilation in rat oral tissues and a role of substance P in the initiation of antidromic vasodilation in the incisor pulp.

Afferent Pathways↗

PubMed1993

Cat dental pulp after denervation and subsequent re-innervation: changes in blood-flow regulation and distribution of neuropeptide-, GAP-43- and low-affinity neurotrophin receptor-like immunoreactivity.

The effects of unilateral extramandibular inferior alveolar nerve injury on pulpal blood-flow responses to electrical stimulation and i.v. injections of substance P (SP) in cat mandibular canine teeth with a dentinal lesion were investigated with laser Doppler flowmetry. After blood-flow recordings, the teeth were fixed and the pulps were examined with light and electron microscopy. The distribution of pulpal SP, neurokinin A (NKA), calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), growth-associated protein (GAP-43) and low-affinity neurotrophin receptor (LANR)-like immunoreactivity was examined with immunohistochemical fluorescence microscopy. Blood-flow recordings, performed at 10 days and 1 month postoperatively, showed that vasodilation, occurring in control teeth after bipolar electrical stimulation of the tooth crown, was absent in the denervated pulps, whereas at 3 months, five of six teeth had regained responsiveness, although at a low level. There was enhanced vasodilation (by 370%) to SP injections (400 fmol i.v.) at 10 days in denervated pulps. Such supersensitivity was reduced at 1 month despite the apparent lack of nerve fibers, and the response fell further towards the level in control teeth at 3 months when pulpal axons reappeared. At 10 days and 1 month postoperatively, light and electron microscopy demonstrated that surgery had resulted in total pulpal denervation. At 3 and 6 months, a large number of regenerated pulpal axons reappeared, in accordance with previous findings. At 10 days and 1 month after nerve transection immunohistochemistry showed a complete loss of pulpal immunoreactivity to all the neuropeptides that were studied. At 3 and 6 months, neuropeptide immunoreactivity reappeared but far fewer number of pulpal nerve fibers were SP-, NKA- and CGRP-immunoreactive than under normal conditions, as demonstrated by double-labeling experiments with GAP-43- or LANR-antiserum. The results indicate that pulpal hemoregulatory functions, which are lost after denervation, do not return to normal levels after nerve regeneration. This malfunction may be caused by inadequate target re-innervation and/or a deficiency of neuropeptides in the re-innervated pulp.

Animals↗

PubMed1993

Differential effects of nitric oxide synthesis inhibition on basal blood flow and antidromic vasodilation in rat oral tissues.

The role of nitric oxide in the mediation of (a) antidromic and (b) substance P-induced vasodilation in the pulp, lip, oral mucosa and submandibular gland was investigated in anaesthetized rats by means of laser Doppler flowmetry. Bolus or continuous infusion of N omega-nitro-L-arginine methyl ester (L-NAME) increased mean arterial blood pressure and reduced basal blood flow in the pulp but not in the lip. Electrical stimulation of the inferior alveolar nerve, in the presence of phenoxybenzamine, resulted in a long lasting vasodilation in lower lip and incisor pulp. Infusion of L-NAME enhanced the antidromic vasodilation in both lip and pulp. Pretreatment with L-arginine prevented these effects. Administration of the enantiomer (D-NAME) did not exert any effect on basal blood flow and on antidromic vasodilation. Infusion of substance P resulted in a transient vasodilation in all of the oral tissues studied. L-NAME reduced this vasodilation in the submandibular gland (only the lower doses) but it potentiated the responses in the pulp and oral mucosa. Pretreatment with L-arginine prevented the potentiated responses in the pulp and those induced by the lower doses of substance P in the oral mucosa. Thus, nitric oxide appears to differentially regulate the basal blood flow and the antidromic or substance P-induced vasodilation in the microvasculature of the lip and dental pulp.

Amino Acid Oxidoreductases↗

PubMed1993

Localization of NADPH-diaphorase activity in the dental pulp, periodontium and alveolar bone of the rat.

In this study we examined the presence and localization of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) activity in the dental pulp, periodontal tissues and alveolar bone of the rat. The presence of NADPH-d activity was also examined in cat pulp. The rat histochemical analysis revealed the presence of prominent NADPH-d activity both in cells of the sub-odontoblastic cell layer and in the odontoblasts, in the root as well as in the coronal pulp regions. In the pulpal horns, odontoblasts often had long processes with a high level of labelling indicating NADPH-d activity extending through the predentin and dentin. Moreover, endothelial cells of pulpal blood vessels were positive for NADPH-d in both species. However, no clearcut examples were found of pulpal nerve fibres positive for NADPH-d in the rat or cat and denervation performed in rats did not alter the enzyme staining patterns. In the periodontal tissue, NADPH-d activity was localized to cells on the alveolar bone surface of the periodontal ligament and, in addition, alveolar bone marrow crypts were filled with intensely labelled cells. In the gingival papillae, NADPH-d activity was observed in the basal cell layer of the epithelium. Endothelial cells of periodontal and gingival blood vessels showing positive staining for NADPH-d were occasionally noted.

Alveolar Process↗

PubMed1993

Evans blue extravasation in rat dental pulp and oral tissues induced by electrical stimulation of the inferior alveolar nerve.

Whether increased extravasation of plasma protein may occur in the rat incisor pulp as a result of antidromic stimulation of afferent nerves was investigated, and this preinflammatory reaction compared with that in adjacent soft tissues. In anaesthetized rats, the inferior alveolar nerve was exposed and stimulated electrically (10-15 V, 2 ms, 10 Hz for 30 s or 5 min). Blood flow changes in the lower lip and incisor pulp were recorded by laser Doppler flowmetry. Increased vascular permeability in the lip, gingiva and pulp was indirectly determined by means of the Evans blue dye method and spectrophotometric analysis. Stimulation of the inferior alveolar nerve for 30 s, in the presence of the alpha-adrenergic blocker phenoxybenzamine (3 mg/kg), increased blood flow in the lip by 172 +/- 16% and in the pulp by 38 +/- 5% as compared to basal blood flow. Intravenous (i.v.) administration of atropine (1 mg/kg), chlorisondamine (3 mg/kg), timolol (150 micrograms/kg), cimetidine plus mepyramine (3 mg/kg of each), methysergide (1 mg/kg) and diclofenac sodium (3 mg/kg) was without effect on this response. Acute pretreatment with capsaicin (1-3 mg/kg, i.v.), however, abolished the vasodilation in the pulp and reduced that in the lip by 58% (p < 0.05). In untreated animals, stimulation of the inferior alveolar nerve for 5 min increased the Evans blue content in the ipsilateral lip by 164% (p < 0.001), gingiva by 55% (p < 0.01) and pulp by 67% (p < 0.01). Pretreatment (i.v.) with a combination of cimetidine and mepyramine counteracted the dye extravasation only in the gingiva.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Inhibitory influence of sympathetic nerves on afferent nerve-induced extravasation in the rat incisor pulp upon direct electrical stimulation of the tooth.

Previous studies have shown that sympathetic nerve stimulation reduces afferent nerve-induced vasodilation by mechanisms unrelated to vasoconstriction in the rat incisor pulp. The present investigation concerned whether similar modulatory mechanisms might also influence neurogenic plasma extravasation in dental pulp. Rat mandibular incisors were electrically stimulated and blood flow reactions in the pulp were recorded by laser Doppler flowmetry. Plasma extravasation in the incisor pulp, gingiva and lip were indirectly assessed by the Evans-blue method. Stimulation of teeth with 50 microA (5 min) did not cause increased dye accumulation in the stimulated pulps whereas stimulation with 100 microA significantly increased the dye content in ipsilateral pulps by 32% as compared to controls; 100 microA stimulation was without effect in unilaterally denervated animals. Tooth stimulation with 50 microA (5 min), in the presence of either the alpha-adrenergic blocker phenoxybenzamine (3 mg/kg), or the alpha 1-adrenergic antagonist prazosin (50 micrograms/kg), as well as in chronically sympathectomized animals, significantly increased the Evans-blue content in the stimulated pulps by 47, 83 and 86%, respectively. Application of short trains of impulses (same number of impulses as for the continuous stimulation but producing minimal vasoconstriction) resulted in some dye accumulation, which was enhanced in the ipsilateral pulps in the presence of prazosin (100 micrograms/kg) or after acute resection of the superior cervical sympathetic ganglion by 70 and 64%, respectively. The Evans-blue content in the lip and gingiva was uninfluenced by the tooth stimulation. The results indicate that activation of sympathetic nerves inhibits the afferent nerve-induced plasma extravasation in rat incisor pulp and this effect is mediated by alpha-adrenoceptors not associated with vasoconstriction.

Animals↗

PubMed1993

Activation of sympathetic nerves exerts an inhibitory influence on afferent nerve-induced vasodilation unrelated to vasoconstriction in rat dental pulp.

In order to elucidate a possible influence of the sympathetic nervous system on afferent nerve function, rat mandibular incisors were electrically stimulated and blood flow changes monitored in the incisor pulp of untreated and sympathectomized animals by a laser Doppler flowmeter. Monopolar electrical stimulation of the tooth (200 microA, 5 ms, 40 Hz, 1 s) in normal animals resulted in a transient reduction in pulpal blood flow (PBF) (16% reduction, n = 10) followed by a small but long-lasting increase (11% increase). After administration of phenoxybenzamine or phentolamine (3 mg kg-1, i.v.) the initial dip in PBF was reduced by 59% (P < 0.001) while the subsequent increase was enhanced by 185% (P < 0.001). Similarly, infusion of prazosin (50 micrograms kg-1, i.v.) and idazoxan (0.5 mg kg-1, i.v.) significantly enhanced the increase in PBF by 118 and by 79%, respectively. In chronically sympathectomized animals the increase in PBF was 250% larger than that seen in untreated animals (P < 0.001). This increase in PBF was not further enhanced after alpha-adrenergic blockade. Acute resection of the superior cervical sympathetic ganglion, also resulted in some enhancement (by 56%) of the stimulation-induced increase in PBF (P < 0.01, n = 6). The increase in PBF was unaffected by infusion of timolol (150 micrograms kg-1) and atropine (1 mg kg-1) but was totally abolished by intravenous pre-treatment with capsaicin (1-3 mg kg-1). The present results suggest that activation of sympathetic nerves exerts inhibitory effects on the afferent nerve-induced vasodilation in the rat incisor pulp unrelated to sympathetic vasoconstriction.

Adrenergic alpha-Antagonists↗

PubMed1992

Immuno-electron-microscopic localization of laminin and collagen type IV in normal and denervated tooth pulp of the cat.

The distribution of laminin-like immunoreactivity in adult normal and denervated cat mandibular tooth pulps was studied by the use of fluorescence microscopy and pre-embedding immunogold electron microscopy. Immunoreactivity to collagen IV was also assessed in order to distinguish basement membranes. In normal pulps, light-microscope laminin-like immunoreactivity was strong along blood vessels and Schwann cell sheaths, and a faint immunoreactivity was seen also in the odontoblast layer. Electron microscopy confirmed the laminin-like immunoreactivity of endothelial and Schwann cell basement membranes at all pulpal levels. In the odontoblast layer and the predentine, nerve-like structures lacking basement membranes but possessing strong membrane laminin-like immunoreactivity were encountered. In addition, a clear-cut laminin-like immunoreactivity of plasma membranes of the somata and processes of odontoblasts was seen. Observations on denervated pulps as well as pulps in which nerve regeneration had taken place did not reveal any changes in the pattern of laminin-immunoreactivity in basement membranes or odontoblasts. Distribution of collagen IV-like immunoreactivity was very similar to laminin-like immunoreactivity in basement membranes of blood vessels and Schwann cells, and appeared unaffected by denervation. The odontoblasts and nerve-like profiles in the odontoblast layer were devoid of collagen IV-like immunoreactivity. We propose that odontoblast-associated laminin could be of significance as guidance for regenerating terminal pulpal nerve fibers to appropriate targets.

Animals↗

PubMed1992

Activation of sympathetic fibres in the pulp by electrical stimulation of rat incisor teeth.

Previous studies of the sympathetic nerve supply of the rat mandibular incisor pulp have shown conflicting results. Here, the neurovascular control of the rat lower incisor pulp was investigated by stimulating the tooth crown and the cervical sympathetic trunk electrically and monitoring blood-flow changes in the pulp by laser Doppler flowmetry. In addition the presence of noradrenaline (NA) in the pulp and gingiva was examined biochemically in untreated and sympathectomized animals by high-performance liquid chromatography. The tissue concentrations of NA in the pulp were 11-fold greater than those of gingiva. Surgical sympathectomy significantly reduced the NA content in the pulp by 76%. Monopolar electrical stimulation of teeth (25-50 microA) for 1 min resulted in a frequency-dependent reduction followed by an increase in pulpal blood flow. At 16 Hz the reduction in blood flow was 65% and the subsequent increase was 9%. After intravenous administration of the alpha-adrenoceptor antagonist phentolamine, the stimulation-induced reduction in pulpal blood flow was diminished by 94% while the increase was significantly enhanced (from 9 to 40%). Infusion of the beta-adrenoceptor antagonists propranolol and timolol significantly reduced this increase in blood flow by 53 and 55%, respectively. Preganglionic sympathetic nerve stimulation also induced a frequency-dependent reduction followed by a slight increase in pulpal blood flow. This reduction in blood flow was almost abolished after alpha-adrenergic blockade and there was no subsequent increase. These findings suggest that there are sympathetic nerve fibres in rat incisor pulp and that they are activated upon monopolar electrical stimulation of teeth resulting in alpha- and beta-adrenoceptor mediated blood-flow responses.

Adrenergic Fibers↗

PubMed1992

Effects of autonomic reflexes on tooth pulp blood flow in man.

In 15 subjects, laser-Doppler flowmetry (LDF) was used to investigate whether the nervous control of pulpal blood flow (PBF) is affected by three tests known to excite the sympathetic nervous system. For comparison, skin blood flow was similarly recorded. Dynamic exercise (bicycle ergometer, 5 min, 90-100 W) in eight subjects was accompanied by a rise in PBF. PBF was increased by the cold pressor test (2 min) in eight subjects, while in five the flow decreased or remained unaffected. The isometric hand grip (2 min, 30% MVC) and the subsequent muscle ischaemia (2 min) led to a rise in PBF in two subjects and a fall in four. Following unilateral anesthesia of the mandibular nerve, PBF in five subjects became unresponsive to dynamic exercise or the cold pressor test, indicating pressure autoregulation. All three tests triggered increases in mean arterial pressure (MAP) and heart rate (HR). Skin blood flow usually increased in response to the tests, but could also decrease, and often changed in a direction opposite to that of PBF. It is concluded that the circulation of blood in the human tooth is affected by evoked changes in autonomic nerve activity, involving activation of both vasodilator and vasoconstrictor nerves to vessels serving the tooth.

Adult↗