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Biomedical subjects

L Olgart

Publications and source records attributed to L Olgart.

59 records · Page 4Linked to original sources
PubMedDate not supplied

Facilitated diffusion by iontophoresis of vasoactive agents to the rat incisor pulp.

The use of iontophoresis for facilitated diffusion of vasoactive agents into the dental pulp was investigated in lower incisor teeth of anaesthetized rats. Acetylcholine, carbachol and noradrenaline were iontophoresed with anodal and sodium nitroprusside with cathodal direct current through a superficial dentin exposure. Pulpal blood flow was measured with laser Doppler flowmetry. Current intensities below 100 microA of both polarities, using sodium chloride as a medium, caused no or minor afferent nerve-induced vasodilation, but excited sympathetic fibres of the pulp in a current-dependent manner. The current threshold for facilitated diffusion of acetylcholine was about 20 microA. The vascular responses to the cholinergic and noradrenergic drugs appeared within a minute after the onset of current and they were abolished by systemic administration of atropine and phenoxy benzamine, respectively. Iontophoresis of acetylcholine (40-100 microA for 20-120 s) caused a 3-fold increase of pulpal blood flow which was not dose-dependent; carbachol provoked a high-magnitude, long-lasting vasodilation and so did sodium nitroprusside. Noradrenaline caused a long-lasting vasoconstriction. In denervated rats iontophoresis of carbachol had effects similar to those seen in intact animals. None of the drugs used locally had any effect on systemic blood pressure. The results of this study indicate that iontophoresis can be used for delivery of vasoactive agents from an exposed dentin surface into the pulp in sufficient quantity to elicit drug-specific local vascular responses without causing systemic vascular effects.

Acetylcholine↗
PubMedDate not supplied

The blocking effect of iontophoretic administration of lidocaine on neurogenic vascular reactions in rat dental pulp.

The blocking effect of lidocaine on nerve-induced vascular reactions was investigated in lower incisor teeth of anaesthetized rats. Pulpal blood flow was measured with laser Doppler flowmetry. Monopolar electrical stimulation of the rat incisor evoked a biphasic vascular response: an initial vasoconstriction was followed by a long-lasting vasodilation. Iontophoresis of lidocaine on a superficially exposed dentin surface with 60 microA of anodal direct current for 20 min blocked almost completely the stimulus-induced blood flow increase for about 25 min without any systemic effects. Iontophoresis of lidocaine with 40 microA for 20 min was almost without effect. Topical application of a mixture of lidocaine and prilocaine (25 + 25 mg/ml) in deep dentinal cavities was also without effect on the neurogenic reactions. Intravenous administration of lidocaine at 5 and 10 mg/kg in rats pretreated with phenoxybenzamine reduced the stimulus-induced increase in blood flow by an average of 29% and 54%, respectively, whereas the remaining alpha-adrenoceptor resistant vasoconstriction was not influenced. The present results show that iontophoresis of lidocaine on exposed dentin blocks nerve-induced vascular responses without causing systemic effects.

Anesthetics, Local↗
PubMedDate not supplied

[The role of sensory nerves in the development of inflammation of oral tissues].

Experimental stimulation and clinical procedures applied on the tooth crown cause vascular reactions in the dental pulp of cats and rats. These reactions depend on the activation of trigeminal afferent nerves and release of neuropeptides. A brief stimulation causes vasodilation, which is mainly mediated by calcitonin gene-related peptide (CGRP). A longer stimulation results in plasma extravasation which is mediated mainly by substance P (SP) and prostaglandins in the pulp. In adjacent oral tissues the mechanisms following stimulation or local irritation are more complex and other mediators are also involved. Nitric oxide (NO) which is instantly produced in the tissues is such a novel mediator. The chemosensitive nature of the nerves involved (capsaicin sensitive) may lead to their activation also by inflammatory mediators released in the tissues. Thus, sensory nerves may modulate the progress of inflammation. Since sensory nerves in oral tissues are often the first structures to be activated during clinical procedures, tissue reactions that occur can be assumed to be initiated and perpetuated by the sensory neuropeptides. Much work is now made to modulate the sensory nerveinduced cascade of events in oral tissues to find new treatment strategies.

Animals↗