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Biomedical subjects

L Olgart

Publications and source records attributed to L Olgart.

At least 55 records · Page 3Linked to original sources
PubMed1983

Responses of feline intradental sensory nerves to hyperosmotic stimulation of dentin.

The responses of intradental sensory nerves to hyperosmotic solutions of sucrose (4M) and calcium chloride (6M) applied in dentinal cavities were studied in anesthetized cats. Nerve impulse activity was recorded from canine teeth after application of the test solutions in shallow and deep cavities. In shallow cavities (thickness of remaining dentin, about 500 micron) sucrose and calcium chloride caused an immediate and transient excitation of the nerves in 3 out of 15 teeth and in 8 of 12 teeth, respectively. Treatment of such cavities with lactic acid (1M) increased the frequency of nerve responses to 100%. When applied in deep cavities (thickness of remaining dentin, 0-50 micron), sucrose induced a burst of impulses followed by continuous nerve activity, whereas calcium chloride decreased the nerve excitability. Our results support the hypothesis that solutions exerting an effective osmotic pressure excite the intradental nerves by an indirect mechanism when applied on the dentin and that they exert a direct effect on nerves when in contact with the pulp. In addition, it is suggested that acids produced in carious dentin may facilitate the induction of pain by hyperosmotic stimuli.

Action Potentials↗
PubMed1983

Alterations in intradental nerve responsiveness induced by electrical stimulation of the inferior alveolar nerve in the cat.

The effects of antidromic nerve stimulation on intradental nerve activity were studied by recording sensory nerve impulses from canine teeth in anaesthetized cats. Nerve responses to application of a solution of hypertonic sodium chloride (0.76 M) in dentinal cavities at various intervals before and after antidromic stimulation of the inferior alveolar nerve were compared. Low-intensity stimulation (2 V, 60 Hz, 0.02 ms) did not affect the nerve responses to subsequent applications of the hypertonic solution. In contrast, high-intensity stimulation (10 V, 10 Hz, 5 ms) induced biphasic changes in the intradental nerve activity, consisting of a transient, increased nerve response to sodium chloride during the first few minutes after stimulation, followed by a period (40 min) of decreased responses. Systemic pretreatment with phentolamine did not influence these effects, whereas after administration of mepyramine and cimetidine the nerve stimulation induced increased responses during a period of 50 min. Local application of substance P in dentinal cavities reduced the nerve responses to subsequent applications of hypertonic sodium chloride, thus mimicking the depressant effect of antidromic stimulation. This inhibitory effect of substance P was abolished by pretreatment with antihistamines. The present results show that electrical stimulation of the inferior alveolar nerve at intensities high enough to excite sensory C fibres alters the responsiveness of intradental nerves. Such changes probably reflect a neurogenic inflammatory-like reaction in the pulp, in which substance P and histamine take part.

Alveolar Process↗
PubMed1981

Tissue concentration and release of substance P-like immunoreactivity in the dental pulp.

The concentration of substance P-like immunoreactivity (SPLI) was determined in dental pulps from cat, dog and man by radioimmunoassay. Pulps from mature cats showed the highest SPLI-levels (mean 32 pmol/g); these are comparable to or higher than those found in any other organ outside the central nervous system. The SPLI concentrations were lower in pulp from immature teeth. The immunological and chromatographic behaviour of the pulpal SPLI from cat and man resembled that of synthetic substance P (SP), indicating that the assayed substance is closely related to or identical with SP. Release of pulpal SPLI in canine teeth was evoked by stimulation of the inferior alveolar nerve in anaesthetized cats. In 9 of 16 experiments the amounts of SPLI found in pulp suprafusates following stimulation (4-31 fmol) were larger than those in unstimulated controls (0-7 fmol). Stimulation also reduced the pulpal tissue concentration of SPLI to 60% of that in homologous control pulps. The high concentration of SPLI found in the dental pulp and the demonstration of nerve-induced release strengthen the hypothesis that SP serves some function in the dental pulp.

Adolescent↗
PubMed1981

Depletion of substance P-like immunoreactivity in the cat dental pulp by antidromic nerve stimulation.

Tissue levels of substance P-like immunoreactivity (SPLI) were determined by radioimmunoassay in incubated cat dental pulps with and without previous electrical stimulation of the inferior alveolar nerve (I.A.N.). The ability of the dental pulp to degrade substance P (SP) was also studied. The pulpal SPLI levels in teeth incubated at 37 degrees C for up to 240 min immediately after removal from the jaws did not differ from those in contralateral unincubated teeth. Following I.A.N. stimulation (3-45 min at 10 V, 15 Hz and 5 ms) and subsequent incubation (30 min at 37 degrees C) of the teeth the SPLI levels in ipsilateral pulps were significantly lower (45% reduction) than those in contralateral unstimulated controls. Incubation of homogenized pulp tissue at 37 degrees C with synthetic bovine SP or 125I-Tyr8-SP led to rapid inactivation of SP, whereas similar incubation of whole blood with 125I-Tyr8-SP had little effect. Endogenous SPLI levels were also rapidly reduced (50% reduction within 3 min) in incubated pulp homogenates. Incubation at a lower temperature (22 degrees C) resulted in a somewhat reduced rate of degradation and incubation with boiled homogenates failed to inactivate SP. The results indicate that the pulp contains enzymes capable of destroying SP and that within the nerve terminals SP is stored in such a way that it is protected against degradation. The data obtained also provide further evidence for a nerve evoked release of SP.

Animals↗
PubMed1981

Evidence that substance P is a mediator of antidromic vasodilatation using somatostatin as a release inhibitor.

The effect of somatostatin on nerve-induced vasodilatation and the release of substance P (SP) was studied in the dental pulp of anesthetized cats. Changes in pulpal blood flow were determined by measuring the rate of disappearance of a local depot of radioactive tracer. The release of SP was studied indirectly by determining the residual amounts of substance P-like immunoreactivity (SPLI) in the pulps by radioimmunoassay. Electrical stimulation (3 min at 10 V, 15 Hz and 5 ms) of the distal end of the cut inferior alveolar nerve (IAN) increased pulpal blood flow. After pretreatment (10 min) with somatostatin (30 pmol/min) similar nerve stimulation was without effect on pulpal blood flow. Intra-arterial infusion of somatostatin (30 pmol/min) had no effect on pulpal blood flow and did not influence the vasodilator response to SP. Following IAN stimulation (3--45 min) and subsequent incubation (30 min, 37 degrees C) of the lower canine teeth, the SPLI levels in ipsilateral pulps were significantly lower (47.5% reduction) than those in contralateral, unstimulated controls. In cats pretreated with somatostatin (30 pmol/min for 10 min, i.a.) similar nerve stimulation (3 min) did not reduce the pulpal SPLI levels as compared to controls. The results show that nerve-induced vasodilatation and release of SPLI are inhibited by somatostatin. They are consistent with the hypothesis that vasodilatation in the cat dental pulp produced by stimulation of the IAN is mediated by substance P.

Alveolar Process↗
PubMed1980

Vasodilatation in the dental pulp produced by electrical stimulation of the inferior alveolar nerve in the cat.

The effects of nerve stimulation on blood flow were studied in the dental pulp of anesthetized cats. Changes in iodide disappearance rate (k-value) from dentinal cavities were used to determine changes in pulpal blood flow. Electrical stimulation of the distal end of the cut inferior alveolar nerve after alpha-adrenoceptor blockade (phentolamine, 3 mg/kg) consistently resulted in a rapid increase in disappearance rate. The first stimulation produced the greatest response (an average increase in k-values of 60%) and repeated stimulations showed a successive attenuation in response, the fourth stimulation usually having no effect. A progressive decrease in resting k-values was observed after the first stimulation, indicating an impaired exchange function of the capillary vessels. Systemic pretreatment with propranolol (0.5--1 mg/kg), atropine (3 mg/kg), mepyramine (3 mg/kg) and cimetidine (3 mg/kg) did not influence the rapid increase in k-values produced by the nerve stimulation. The experiments show that vasodilatation in the cat dental pulp produced by stimulation of the inferior alveolar nerve is not mediated by common efferent vasodilatory mechanisms and strengthen the hypothesis that the sensory nerve axon reflex mechanism is involved.

Animals↗
PubMed1978

Inhibition of compound 48/80-induced intradental sensory nerve activity by disodium cromoglycate and serotonin antagonists.

Local application of compound 48/80 induced long lasting nerve activity in intradental sensory nerves in the teeth of cats and dogs. This effect was inhibited by pretreatment with disodium cromoglycate (DSCG) given locally (2 X 10(-2) M) or i.a. (20 mg/min). DSCG did not have any effect on the nerve excitability per se, as judged from the responses to hypertonic NaCl and air blasta applied to exposed dentin before and after administration of DSCG. Local treatment with lysergic acid diethylamide (0.1--1 mg/ml) and methysergide (0.05--0.5 mg/ml) selectively reduced or inhibited the compound 48/80 induced nerve activity. Systemic administration of methysergide (12.5 microgram/kg) prevented the excitatory effects of compound 48/80 but was without effect when administrated during a state of established activity. The present findings support the hypothesis that compound 48/80 has an indirect effect on intradental sensory nerves and indicate that vascular reactions take part in intradental sensory nerve excitation.

Action Potentials↗
PubMed1977

Comparative effects of adrenaline and felypressin (octapressin) on consecutive sections of the vascular bed in canine adipose tissue.

Blood flow and tissue volume were recorded in the isolated canine subcutaneous adipose tissue, enclosed in a plethysmography. Adrenaline and felypressin (octapressin) were infused intra-arterially at doses producing a blood flow reduction of approximately 60%. Adrenaline (4.6-23 ng/min) caused an initial reduction in tissue volume, indicating a constriction of capacitance vessels. Octapressin (0.46-9.2 ng/min) had no effect on tissue volume. Neither adrenaline or octapressin caused appreciable filtration or absorption, suggesting that the pre- to postcapillary resistance ration remained unchanged. In contrast to sympathetic stimulation and noradrenaline, adrenaline significantly reduced the capillary filtration coefficient (CFC) by 34%, the change in CFC being related to the flow reductions, while octapressin did not reduce CFC sffect of adrenaline on precapillary sphincter sections and on capacitance vessels is greater than that of octapressin in doses producing similar flow reductions.

Adipose Tissue↗
PubMed1977

Effects of adrenaline and felypressin (octapressin) on blood flow and sensory nerve activity in the tooth.

The present investigations in cats were designed to study the effects of local anaesthetics containing adrenaline and felypressin (octapressin) on dental pulp function. Intradental sensory nerve excitability was measured using electrodes placed in dentinal cavities in canine teeth. Changes in pulp blood flow were measured using the disappearance rate of a radioactive tracer placed in the same cavities. Injections (0.5 ml) of lidocaine (20 mg/ml) - adrenaline (12.5 microng/ml) or prilocaine (30 mg/ml) - octapressin (0.54 microng/ml) were given supraperiosteally in the apical area of the tooth. Adrenaline either alone or with lidocaine caused almost complete inhibition of pulp blood flow within a few minutes. This effect was followed by a total inhibition of the sensory nerve activity. In most cases there was a recovery of both functions after 3 hours. Octapressin, on the other hand, had no inhibitory effects on pulp blood flow or sensory nerve activity. Lidocaine and prilocaine were also without effect. These findings indicate a different mode of action of the two vasoconstrictors and suggest that octapressin may be preferred in infiltration anaesthesia during treatment of the vital tooth.

Action Potentials↗
PubMed1975

The excitatory action of acetylcholine on intradental sensory units.

In order to test the hypothesisthat ACh mediates the transmission of pain stimuli from dentin to sensory intradental nerve endings the following experiments were performed. Intradental nerve impulses were recorded by means of low impedance electrodes inserted in dentinal cavities in the tooth of the cat. An air blast proved to be an efficient physical stimulus to excite the intradental nerves. Local application of acetylcholine caused a similar response. This respinse to acetylcholine was followed by a transient blockage to repeated application. The response to acetylcholine could be blocked by d-tubocurarine, atropine, succinylcholine and hexamethonium administered locally. In contrast, the response to physical stimuli (air blasts) could not be blocked by these drugs. Moreover, during the period of depression following acetylcholine the preparation responded to physical stimuli. These findings suggest that acetllcholine is not a mediator in the intradental pain transmission provoked by physical stimuli.

Acetylcholine↗