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L Lundblad

Publications and source records attributed to L Lundblad.

At least 37 records · Page 2Linked to original sources
PubMed1987

Neuropeptide Y and non-adrenergic sympathetic vascular control of the cat nasal mucosa.

Neuropeptide Y (NPY) coexists with noradrenaline (NA) in a population of perivascular nerves in the cat nasal mucosa. In the present study, NPY was found to exert non-adrenergic nasal vasoconstrictor actions. Postganglionic sympathetic nerve stimulation induced a release of NPY-like immunoreactivity (LI) concomitant with vasoconstriction in the nasal mucosa. About 60 and 70% of the vasoconstrictor responses upon sympathetic stimulation at 2 and 10 Hz, respectively, remained after pretreatment with phenoxybenzamine and propranolol which abolished the effects of exogenous NA. Preganglionic denervation one week prior to the experiments did not change the vasoconstrictor response to sympathetic nerve stimulation or the NA or NPY contents of the nasal mucosa. The levels of NPY-LI in the superior cervical ganglion were however reduced. After reserpine treatment, which depleted the nasal NA content by almost 90% and the NPY content by 50%, a vasoconstrictor response to nerve stimulation was still present. After reserpine treatment combined with preganglionic denervation, nerve stimulation simultaneously induced an increased output of NPY-LI and a marked long-lasting vasoconstriction which was not influenced by phenoxybenzamine and propranolol. The reserpine-induced depletion of NA was not influenced by preganglionic denervation while the reduction in the nasal content of NPY-LI was prevented. In conclusion, NPY could be a non-adrenergic mediator of sympathetic vascular effects in cat nasal mucosa.

Animals↗
PubMed1987

Capsaicin-sensitive nerves and the cutaneous allergy reaction in man. Possible involvement of sensory neuropeptides in the flare reaction.

The effects of local capsaicin pretreatment on the cutaneous triple response reaction induced by allergen exposure or anti-IgE were studied in man. Acute exposure of the human skin to capsaicin caused a burning sensation and a clearcut flare reaction but no wheal response. Upon repeated administration these local reactions to capsaicin disappeared. The flare component and the subjective itching sensation of the cutaneous allergy reaction to rat antigen in sensitized persons or anti-IgE in non-allergic persons were then markedly reduced. Two weeks after capsaicin pretreatment the flare response to allergen was not significantly changed compared to the control reaction, suggesting a reversible effect of capsaicin treatment. The wheal component of the allergy or anti-IgE reaction was, however, not influenced by capsaicin pretreatment, indicating that the wheal and flare components are caused by different mechanisms. It is concluded that capsaicin sensitive sensory nerves are of importance for the human cutaneous triple response reaction induced by allergen exposure. Thus, secondary release of mediators, such as CGRP or tachykinins from sensory nerve branches, may contribute to the flare component of this reaction. Furthermore the itching sensation seems to be dependent to a large extent on capsaicin-sensitive nerves. However, sensory nerves seem to have less importance for the wheal reaction, i.e. the protein extravasation response.

Adult↗
PubMed1984

Local and systemic capsaicin pretreatment inhibits sneezing and the increase in nasal vascular permeability induced by certain chemical irritants.

The effects of local exposure to chemical irritants and mechanical stimulation on sneezing reflexes have been studied in normal and capsaicin-pretreated, conscious guinea-pigs. The influence of local and systemic capsaicin pretreatment on vascular permeability to plasma proteins and the cardiovascular effects of local application of capsaicin to the nasal mucosa have also been studied in anaesthetized animals. Local application of capsaicin (threshold dose 3 microM), nicotine (threshold dose 300 microM) or formalin to the nasal mucosa induced reflex sneezing discharges. Systemic or local capsaicin pretreatment abolished or reduced the sneezing responses to capsaicin and formalin. The response to nicotine was also reduced following local pretreatment with capsaicin, while the response to systemic pretreatment with capsaicin was only slightly affected. The sneezing response to mechanical stimulation was not affected by capsaicin pretreatment. Pretreatment with a local anaesthetic induced a similar dose-dependent inhibition of the sneezing responses to both capsaicin and nicotine. Local application of disodium cromoglycate to the nasal mucosa reduced the sneezing response to capsaicin, but not that to nicotine. Local pretreatment with the 3 mM and 30 mM capsaicin solution inhibited the increase in vascular permeability to plasma proteins in the nasal mucosa induced by i.v. capsaicin. Local pretreatment with capsaicin did not result in any reduction in the capsaicin-induced permeability in the ureter, suggesting that such treatment did not have any major systemic toxic effects. However, a small, acute increase in respiratory insufflation pressure, indicating broncho constriction, was seen when the 30 mM capsaicin solution was applied to the nasal mucosa.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Inhibition of cigarette smoke-induced oedema in the nasal mucosa by capsaicin pretreatment and a substance P antagonist.

The effect of cigarette smoke on vascular permeability in the rat nasal mucosa was studied using the Evans blue extravasation method. Exposure to smoke from cigarettes induced a significant extravasation of Evans blue in the nasal mucosa of normal rats, suggesting an increased vascular permeability to plasma proteins. The oedema response was correlated to tar, nicotine and vapour phase components in the smoke. The smoke-induced permeability effect was abolished in rats pretreated neonatally with capsaicin. Also, systemic or local pretreatment with [D-Arg, D-Pro, D-Trp, Leu]Substance P, a substance P antagonist, inhibited the permeability response to cigarette smoke. Insertion of a glass-fibre filter, which removes the particulate phase of the smoke (including nicotine), did not significantly reduce the permeability response. The present findings suggest that the smoke-induced oedema in the rat nasal mucosa is not caused by nicotine but by vapour-phase irritants, which activate capsaicin-sensitive C-fibre afferents. These neurons then release agents such as substance P or a related tachykinin which increase permeability to plasma proteins.

Animals↗
PubMed1984

Capsaicin sensitive sensory neurons mediate the response to nasal irritation induced by the vapour phase of cigarette smoke.

Cigarette-smoke exposure in awake guinea-pigs induced reproducible nose wipings with the fore-paws. This behaviour was used as a model to study the mechanisms underlying the irritant effect of cigarette smoke. The nose wipings upon smoke exposure were abolished after local anaesthesia of the nasal mucosa, which indicates that this response was due to activation of nasal protective reflexes. Removal of the particulate phase of the smoke including nicotine using a Cambridge filter only slightly reduced the wiping response, and nicotine-free cigarettes also induced marked irritation. This suggests that irritant chemicals in the vapour phase of the smoke caused this effect. Systemic capsaicin pretreatment, which is known to cause a functional impairment of chemosensitive C-fibre afferents, abolished the nose wiping behaviour seen upon smoke exposure. Local pretreatment of the nasal mucosa with capsaicin also significantly reduced the number of smoke-induced nose wipings. It is concluded that smoke-induced irritation, as indicated by nose wipings, is primarily due to activation of capsaicin-sensitive sensory nerves in the nasal mucosa by vapour-phase components.

Animals↗
PubMed1984

Mechanisms for reflexive hypertension induced by local application of capsaicin and nicotine to the nasal mucosa.

The cardiovascular effects of locally applied nicotine and capsaicin to the nasal mucosa were studied in anaesthetized guinea-pigs. Local application of capsaicin (0.3-30 microM) or nicotine (0.3-30 mM) induced dose-dependent increases in arterial blood pressure, mainly due to an increase in peripheral vascular resistance. The capsaicin and nicotine responses were abolished after local anaesthesia and markedly reduced (to about 20% of control) by combined pretreatment with phentolamine and propranolol, suggesting reflexogenic sympathetic activation. Systemic capsaicin pretreatment abolished the hypertensive effect of capsaicin (30 microM) and reduced the response to nicotine application to about 25% of control (p less than 0.001). Local capsaicin pretreatment of the nasal mucosa one week earlier also significantly reduced the capsaicin response (p less than 0.05), while the nicotine-induced increase in blood pressure was not significantly changed. The present findings suggest the presence of two afferent mechanisms in the nasal mucosa which induce hypertension upon chemical irritation. The capsaicin response is dependent upon capsaicin-sensitive afferents. The nicotine response involves mainly capsaicin-sensitive neurons and, in addition, a minor component which is resistant to capsaicin pretreatment. Thus, the hypertensive effect of nicotine applied locally to the nasal mucosa seems to be mainly mediated via sensory mechanisms other than the sneezing response which is not dependent on capsaicin sensitive nerves.

Administration, Intranasal↗
PubMed1983

Effects of antidromic trigeminal nerve stimulation in relation to parasympathetic vasodilation in cat nasal mucosa.

High threshold stimulation of the trigeminal nerve in sympathectomized cats caused an atropine and hexamethonium resistant vasodilation in the nasal mucosa. Stimulation of efferent parasympathetic neurons to the nose caused a partially atropine sensitive vasodilation which was abolished by hexamethonium. Combined trigeminal and parasympathetic nerve stimulation did not reveal any obvious functional interactions between these two systems. Local intra-arterial infusions of substance P, VIP and acetylcholine caused a dose dependent vasodilation in the nasal mucosa. The relative vasodilatory potencies were substance P greater than to VIP greater than acetylcholine. Local infusions of capsaicin, known to release substance P from nerve endings, caused a marked longlasting biphasic vasodilation which was atropine and hexamethonium resistant. In conclusion, the present findings illustrate the presence of two vasodilator mechanisms of different nervous origin in the nasal mucosa. The trigeminal response is probably mediated via release of substance P, while the parasympathetic effect seems to be caused by acetylcholine and VIP.

Acetylcholine↗
PubMed1983

Nasal autonomic innervation with special reference to peptidergic nerves.

Studies of the nasal autonomic innervation in cat, rat and man have demonstrated the presence of Substance P (SP), Vasoactive Intestinal Polypeptide (VIP) and Pancreatic Polypeptide (PP) immunoreactivity in the classical pathways. SP was principally confined to the sensory neurones with nerve endings in the spinal trigeminal nucleus, around sphenopalatine ganglion cells and around blood vessels as well as under or within the nasal epithelium. VIP was located to parasympathetic postganglionic cholinergic neurones innervating blood vessels and glands. PP was found in a population of nor-adrenergic ganglion cells in the superior sympathetic ganglia and innervating arteries in the mucosa selectively. The recent findings suggest a hypothesis of a local reflex arch involving antidromic vasodilation by afferent, capsaicin sensitive SP neurones and parasympathetic VIP-cholinergic neurones in the efferent response.

Animals↗
PubMedDate not supplied

The mechanism of action of the anti-herpes virus compound 2,3-dimethyl-6(2-dimethylaminoethyl)-6H-indolo-(2,3-b)quinoxaline.

The compound 2,3-dimethyl-6(2-dimethylaminoethyl)6H-indolo-(2,3-b)quinoxaline (B-220) has been shown to exhibit potent antiviral activity against herpes simplex virus type 1 (HSV-1), varicella-zoster virus (VZV) and cytomegalovirus (CMV). The mechanism of antiviral action of B-220 against HSV-1 has been studied; from the results it appears that B-220 binds by intercalation into the DNA helix and then disturbs steps that are vital for viral uncoating.

Adsorption↗
PubMedDate not supplied

Interobserver variations in assessment of antral disease from direct sinoscopic observations compared to video recordings.

We tested the reliability of visual clinical sinoscopic observations by using video recordings. An edited video tape was made from the video-recorded bilateral antral sinoscopies of nine patients included in a prospective case series of inflammatory maxillary sinus disease in critically ill patients. An expert panel of four consultant ENT surgeons made individual appraisals of the video using a structured form. They had only been informed in general about the study, but had no further case knowledge in order to avoid all biases. Concordance and interobserver variabilities in the expert panel were compared in pairs. The assessments of the expert panel were compared with the observations of the performer, who was biased through individual case knowledge. Nine patients, either nasotracheally intubated or tracheotomized, had ventilator treatment for more than 7 days. One ENT surgeon performed all sinoscopies and made the direct observations. Satisfactory agreement was found on mucosal alterations. The concordance of recognizing bacterial infection was almost perfect. However, the assessment of redness from a video recording displayed only chance agreement. The differences between kappa statistic values within the expert panel group compared to the comparisons of performer versus expert panel were not significant. The case knowledge of the sinoscopist did not alter the assessments markedly and thus seemed only to have minor influence. Video recording as a method for second opinion was shown to be a useful technique, but will have to be further developed.

Adult↗
PubMedDate not supplied

Increased vascular permeability in rat nasal mucosa induced by substance P and stimulation of capsaicin-sensitive trigeminal neurons.

Electrical stimulation of the maxillary branches of the trigeminal nerve induced an increase in vascular permeability to macromolecules and an interstitial edema in the nasal mucosa of the rat, as indicated by extravasation of Evans blue. In animals that had been treated neonatally with capsaicin, the effect of trigeminal nerve stimulation was abolished. Local application of capsaicin or substance P (SP) also induced a significant Evans blue extravasation in the nasal mucosa. In capsaicin-pretreated animals the effect of SP was still present, while the permeability increase induced by capsaicin was abolished. In conclusion, chemogenic irritation of the nasal mucosa by capsaicin induces edema probably via a local axon reflex inducing release of SP. Capsaicin-sensitive SP-containing afferents in the nasal mucosa may also be involved in the pathogenesis of nasal congestion seen in various types of rhinitis.

Animals↗