PubMed Health⌕ Search

Biomedical subjects

J Ekström

Publications and source records attributed to J Ekström.

At least 73 records · Page 4Linked to original sources
PubMed1992

Parasympathetic NANC-secretion of saliva in the mink, and effects of substance P and VIP.

In both parotid and submandibular glands a parasympathetic non-adrenergic, non-cholinergic (NANC) nerve-evoked secretion of saliva was demonstrated. Saliva evoked by exogenous substance P was poor in protein, while saliva evoked by VIP was protein-rich. In a subthreshold dose for fluid secretion VIP released protein and potentiated the responses elicited by substance P, particularly regarding the output of protein. The two neuropeptides may contribute to the parasympathetic NANC secretion of saliva in the mink. Further, agonists responsible for the secretory NANC response are also likely to contribute to the secretory response of the glands to parasympathetic stimulation in the absence of autonomic receptor blockade in this species.

Adrenergic alpha-Antagonists↗
PubMed1992

An immune stimulating complex (ISCOM) subunit rabies vaccine protects dogs and mice against street rabies challenge.

Dogs and mice were immunized with either a rabies glycoprotein subunit vaccine incorporated into an immune stimulating complex (ISCOM) or a commercial human diploid cell vaccine (HDCV) prepared from a Pitman Moore (PM) rabies vaccine strain. Pre-exposure vaccination of mice with two intraperitoneal (i.p.) doses of 360 ng ISCOM or 0.5 ml HDCV protected 95% (38/40) and 90% (36/40) of mice, respectively, against a lethal intracerebral (i.c.) dose with challenge virus strain (CVS). One 360 ng i.p. dose of ISCOM protected 87.5% (35/40) of mice against i.c. challenge with CVS. Three groups of five dogs were vaccinated intramuscularly (i.m.) with 730 ng of rabies ISCOM prepared from either the PM or the CVS rabies strains, and they resisted lethal street rabies challenge. Postexposure treatment of mice with three or four 120 ng i.m. doses of ISCOM protected 90% (27/30) and 94% (45/48), respectively, of mice inoculated in the footpad with street rabies virus, but three doses of HDCV conferred no protection. When four doses of HDCV were administered postexposure, 78% (32/41) of the mice died of anaphylactic shock; 21% (11/52) of mice had already died of rabies 4 days after the third vaccine dose was administered.

Animals↗
PubMed1991

Effects of drugs and electrical field stimulation on isolated muscle strips from rabbit pharyngoesophageal segment.

Muscle activity of isolated muscle strips from the middle pharyngeal constrictor, the inferior pharyngeal constrictor, the cricopharyngeal muscle, and the cervical esophagus of the rabbit was studied in organ baths in response to drugs and electrical field stimulation. These muscles of the pharyngoesophageal segment seem to lack an autonomic adrenergic and cholinergic innervation, as determined by responses to specific drugs. The nerve-evoked contractile responses of the two lower muscles of the segment were almost completely abolished by the curarelike drug gallamine, suggesting a somatic cholinergic nerve supply. However, in the two upper muscles, the major part of the response was resistant to gallamine, which suggests involvement of non-adrenergic, nonmuscarinic, nonnicotinic receptors in the transmission of nerve impulses in these muscles. These results suggest a differential innervation of the upper and lower pharyngeal muscles.

Animals↗
PubMed1991

On the non-adrenergic, non-cholinergic contribution to the parasympathetic nerve-evoked secretion of parotid saliva in the rat.

A secretion of parotid saliva in the anaesthetized rat in response to stimulation of the parasympathetic nerve occurs in the presence of atropine and adrenoceptor antagonists, albeit reduced and transient in the face of continuous high-frequency stimulation (40 Hz). In non-atropinized rats prolonged stimulation of the parasympathetic nerve at a high frequency (40 Hz, 40 min), aiming at depletion of the neuronal stores of transmitters thought to be responsible for the non-adrenergic, non-cholinergic (NANC) secretion of parotid saliva, was performed. The magnitude of the secretory response to various stimulation frequencies (0.2-60 Hz) applied to the parasympathetic nerve was assessed before and after the period of high-frequency stimulation. The second time, the frequency-response curve was shifted to the right and, moreover, the initial maximal secretory response was not reached. Control experiments suggested that this reduction in secretory responses could be attributed neither to impaired cholinergic neurotransmission nor to decreased responsiveness of the secretory cells. The secretory responses to parasympathetic nerve stimulation after high-frequency stimulation are thought to be evoked by acetylcholine predominantly. When these responses were compared with (1) those obtained before high-frequency stimulation and thought to be evoked by acetylcholine and non-adrenergic, non-cholinergic transmitters in conjunction and (2) those depending on non-adrenergic, non-cholinergic transmitters only it appears that the non-adrenergic, non-cholinergic transmission contributes to the parasympathetic secretory response at a frequency (0.2 Hz) far below threshold frequency (5 Hz) for the non adrenergic, non-cholinergic evoked secretory response. At frequencies below 20 Hz it appears that acetylcholine and non-adrenergic, non-cholinergic transmitters interact positively thereby enhancing the secretory responses.

Animals↗
PubMed1991

Effects of stimulation of the parasympathetic and sympathetic innervations in bursts on the syntheses of polyamines, DNA and protein in salivary glands of the rat: non-adrenergic, non-cholinergic responses.

The increase in the activity of ornithine decarboxylase, the key enzyme in the formation of polyamines, in the sublingual glands of the chloralose-anaesthetized rat in response to stimulation of the parasympathetic innervation was enhanced by employing an intermittent pattern of nerve stimulation. 20 Hz in bursts delivered for 1 second every 10th second over a period of 3 hours increased the activity 1000-fold, whereas a frequency of 2 Hz delivered continuously, and thus giving rise to the same total number of impulses as the burst stimulation, increased the enzyme activity only 50-fold. Already 2 Hz in bursts caused the ornithine decarboxylase activity to increase. A parasympathetic non-adrenergic, non-cholinergic regulation of ornithine decarboxylase activity was shown in response to the two modes of stimulation. The increase to 2 and 20 Hz in bursts was 2- and 80-fold, respectively, whereas it was 29-fold to 2 Hz continuously. Increases in the concentration of the polyamine putrescine in response to burst stimulation of the parasympathetic nerve were found both in the absence and in the presence of atropine. The ornithine decarboxylase activity of the submaxillary gland was not affected by the parasympathetic stimulation. Stimulation of the sympathetic innervation was more effective in both types of glands, as to increases in the ornithine decarboxylase activity, when employing the continuous mode. In cultured tissue of the sublingual glands which, in vivo, had been subjected to parasympathetic stimulation in bursts (20 Hz), the syntheses of DNA and protein were increased as judged by the incorporation of radio-labelled thymidine and leucine; in the presence of atropine the stimulation resulted only in increased synthesis of protein.

Animals↗
PubMed1991

Atropine-resistant submandibular responses to stimulation of the parasympathetic innervation in the anaesthetized ferret.

1. Submandibular salivary and vascular responses to stimulation of the peripheral end of the chorda-lingual nerve at 20 Hz continuously for 60 min were investigated in anaesthetized ferrets, in which the sympathetic innervation to the gland was cut, in the presence and absence of atropine (2.0 mg kg-1). 2. Both the increase in submandibular salivary flow and protein output, which occurred in response to nerve stimulation, were substantially reduced following the administration of atropine, the latency was greatly increased thereby, and both responses were more transient but neither was abolished by atropine. The fall in submandibular vascular resistance was not significantly affected by atropine, either in respect of extent or duration. 3. Chorda-lingual stimulation produced an increase in the output of vasoactive intestinal peptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP) in the submandibular venous effluent blood. Each of these responses was maximal within the first 10 min after the onset of stimulation and declined thereafter. The time-scales of both the CGRP and SP responses were similar to those of the atropine-resistant secretory responses, both being quite short-lived, whereas the output of VIP (like the atropine-resistant vascular response) was significantly greater than the basal value throughout the whole of the 60 min period of stimulation. 4. The CGRP response was completely abolished by pre-treatment with atropine, whereas the outputs of both VIP and SP were significantly enhanced thereby. Both the submandibular vascular and secretory responses to chorda-lingual stimulation were almost completely suppressed following the administration of hexamethonium, and there was then no detectable release of peptidergic agonists from the gland. 5. The atropine-resistant submandibular salivary secretory responses were completely abolished by pre-treatment with a tachykinin inhibitor [( D-Arg1, D-Cl2 Phe5, Asn6, D-Trp7,9, Nle11]-SP; 0.75 mg kg-1) without affecting the fall in submandibular vascular resistance. 6. Following pre-treatment with hexamethonium, I.V. bolus injections of methacholine, SP and CGRP elicited increases in submandibular blood flow and secretion of saliva. VIP caused an increase in blood flow without overt secretion, although it is known to increase secretion of protein and to potentiate the secretory response to SP. Taken together, all these results are consistent with the contention that VIP contributes to the vasodilator response to stimulation of the para-sympathetic innervation in this gland and that both SP and CGRP are likely to contribute to the secretory response.

Animals↗
PubMed1990

VIP-containing nerve fibres in the submandibular gland of the dog and protein secretion in vitro in response to VIP.

Previously, administration of VIP has been shown to elicit no flow of saliva from the submandibular gland of the dog. However, in the present study we found VIP to cause release of protein in vitro from canine submandibular gland tissue. Furthermore, VIP-containing nerve fibres were demonstrated in large numbers in association with acini. Thus, VIP may be involved in the nervous regulation of salivary protein secretion in the dog.

Animals↗
PubMed1990

Increased immunogenicity of a non-amphipathic protein (BSA) after inclusion into iscoms.

Bovine serum albumin (BSA) was used as a non-amphipathic model protein to be included into iscoms. Pretreatment at an acidic pH (2.5) was used to reveal hydrophobic regions, after which BSA could be integrated. In immunization experiments in mice the BSA iscoms induced long lasting and considerably higher serum antibody responses than non-treated monomeric BSA or BSA aggregated by acidic treatment.

Animals↗
PubMed1990

Neuropeptide-containing nerve fibers in the pharynx of the rabbit.

The distribution of peptide-containing nerve fibers in the pharyngeal region of rabbits was studied by immunocytochemistry. Neuropeptide Y (NPY)-containing fibers were numerous around blood vessels and moderate in number among bundles of striated muscle fibers. A few NPY-containing fibers were seen around seromucous glands and beneath the epithelium. Nerve fibers containing vasoactive intestinal peptide (VIP) were numerous around seromucous glands and moderate in number around blood vessels, bundles of muscle, and in the subepithelial layer. A few nerve fibers containing substance P (SP) were seen around blood vessels, seromucous glands, among bundles of muscle, and in the subepithelial layer. Nerve fibers containing calcitonin gene-related peptide (CGRP) were numerous. They were distributed close to blood vessels, among bundles of muscle, in the subepithelial layer, and within the epithelium. A conspicuous finding was the occurrence of CGRP within motor end plates of striated muscle.

Animals↗
PubMed1990

Effects of repeated infusions of substance P and vasoactive intestinal peptide on the weights of salivary glands subjected to atrophying influences in rats.

1. The long-term influence of substance P (SP) and vasoactive intestinal peptide (VIP) on rat salivary gland weight was investigated after parasympathetic denervation or on feeding soft food. 2. The parotid gland lost about one-third of its weight within 4-5 days following parasympathetic post-ganglionic denervation or change in dietary regimen, from pellets to liquid diet, thought to reduce nerve reflex activity. 3. Daily i.v. infusions with SP or VIP diminished or largely prevented the fall in parotid gland weight, whereas infusions with pentagastrin, bethanechol and saline had no effect. The infusions were preceded by administration of alpha- and beta-adrenoceptor antagonists; these antagonists were also given to the control animals. 4. The effect of SP and VIP on the parotid gland weight appeared to be related to cell size rather than to cell number, as judged by measurements of RNA and DNA. 5. Observations on the two other major salivary glands underlined the fact that different gland types in the same animal behave differently. Parasympathetic preganglionic denervation (decentralization) lowered the weights of the sublingual and submandibular glands, whereas liquid diet only reduced the weight of the sublingual gland. SP and VIP did not affect the weights of the submandibular glands, but VIP prevented the slight fall in sublingual gland weight induced by liquid diet. 6. The present results suggest a trophic role in rats for SP and VIP on parotid glands and for VIP on sublingual glands. Such an influence may be exerted naturally as a result of their release from nerves containing these peptides around acini.

Animals↗
PubMed1990

Protein secretion in salivary glands of cats in vivo and in vitro in response to vasoactive intestinal peptide.

In anaesthetized cats exogenous vasoactive intestinal peptide failed to elicit any secretion of saliva from the submandibular and parotid glands. However, protein release from both glands occurred in response to VIP in the presence of alpha- and beta-adrenoceptor blocking agents and was dose-dependent. This response was revealed by means of a subsequent washout flow of saliva evoked by intravenous injections of methacholine or stimulations of the parasympathetic innervation. The submandibular glands responded to vasoactive intestinal peptide at a lower dose than the parotid glands. In the presence of atropine (but in the absence of adrenoceptor blockers), stimulation of the parasympathetic chorda-lingual nerve, which of itself elicited no secretion of saliva, contributed to the release of protein within the submandibular gland, since the output of protein in response to a subsequent stimulation of the sympathetic innervation was increased. Vasoactive intestinal peptide administered in combination with methacholine or during ongoing parasympathetic nerve-induced salivary secretion revealed positive interactions, particularly with respect to protein release. In-vitro protein release in response to vasoactive intestinal peptide was also demonstrated by perfusing small pieces of the two glands in the presence of muscarinic and adrenoceptor blockers. As in vivo, submandibular tissue responded at a lower concentration of vasoactive intestinal peptide than the parotid tissue. One to two weeks after combined parasympathetic and sympathetic denervation of the parotid glands, the glands were sensitized to vasoactive intestinal peptide when tested in vitro. It is concluded that vasoactive intestinal peptide or a structurally related peptide is a potential transmitter in the parasympathetic control of protein secretion in salivary glands of cats.

Animals↗
PubMed1990

Polyamines and long-term disuse of rat parotid glands.

A decrease in nerve reflex activation for 7-14 days, induced by a liquid diet, caused the rat parotid gland to lose weight, involving reduction in both cell size and number. In the atrophied glands, the activity of ornithine decarboxylase, the key enzyme in polyamine formation, and the levels of the polyamines putrescine, spermidine and spermine were found to be lowered. The present results are compatible with a role for polyamines in cellular growth.

Animals↗
PubMed1990

Neuropeptides and disuse of the rat parotid gland.

Rats were fed a liquid diet with the aim of decreasing nervous reflex activity in the parotid glands. In rats killed after 21 days on this diet the glands were atrophied and the total amounts of the neuropeptides, substance P, vasoactive intestinal peptide and calcitonin gene-related peptide, were lower than in control glands.

Animals↗
PubMed1990

Submandibular responses to stimulation of the parasympathetic innervation in bursts in the anaesthetized ferret.

1. Submandibular salivary and vascular responses to different patterns of stimulation of the parasympathetic innervation have been investigated in anaesthetized ferrets in the presence and absence of atropine. 2. At low stimulus frequencies likely to fall within the physiological range (0.5-2.0 Hz continuously; 5.0-20.0 Hz in 1 s bursts at 10 s intervals) secretion of fluid and protein were both potentiated by the bursting pattern of stimulation and the latency of the secretory response was reduced. Over a somewhat lower range (0.5-1.0 Hz continuously; 5.0-10.0 Hz in bursts) the submandibular vascular response was also significantly potentiated by employing this intermittent pattern of stimulation. Above these frequency ranges no such potentiation occurred. 3. Pre-treatment with atropine (2.0 mg kg-1) blocked the submandibular secretory responses to stimulation of the chorda-lingual nerve at these low frequencies and the residual responses at higher frequencies were not significantly affected by changing the pattern of stimulation. The vascular response was somewhat reduced after atropine but that which persisted was enhanced by stimulating in bursts. 4. It is concluded that the release of some transmitter from postganglionic terminals in the submandibular gland of the ferret must be potentiated by the arrival of action potentials at short intervals and possible mechanisms are considered.

Anesthesia, Intravenous↗
PubMed1989

Depletion of large dense-cored vesicles from parasympathetic nerve terminals in rat parotid glands after prolonged stimulation of the auriculotemporal nerve.

Large dense-cored vesicles (60-100 nm in diameter) have been assessed electron-microscopically in terminal parasympathetic axons at acinar neuro-effector sites in rat parotid glands. Their numbers in control unstimulated glands have been compared with those in the contralateral glands of the same animals after prolonged nerve stimulation. Bilateral postganglionic sympathectomy had been undertaken 4-6 weeks previously to remove adrenergic axons from the glands. Stimulation of the postganglionic parasympathetic nerve to the gland--the auriculotemporal nerve--for 80 min at 40 Hz caused a significant depletion of large dense-cored vesicles from the terminal axons. This depletion corresponded in time and magnitude to the depletion of vasoactive intestinal peptide and substance P from the glands that had been found previously to occur under identical conditions. This adds support to the belief that the neuropeptides are stored in such vesicles and that these vesicles release their contents at neuro-effector sites as a result of propagated impulse formation in the axons.

Animals↗
PubMed1989

Effects of capsaicin pretreatment on neuropeptides and salivary secretion of rat parotid glands.

1. 'Atropine-resistant' secretion of saliva in response to parasympathetic stimulation may reflect antidromic activation of sensory nerve fibres. In this investigation, the effect of pretreatment in the rat with capsaicin (total dose of 125 mg kg-1, s.c.), was determined. 2. In the parotid glands substance P (SP)/calcitonin gene-related peptide (CGRP)-containing nerve fibres around ducts and blood vessels disappeared after capsaicin, while periacinar SP-containing fibres (devoid of CGRP) and CGRP-containing fibres (devoid of SP) remained. Vasoactive intestinal peptide (VIP)-containing nerve fibres seemed to be unaffected. The parotid content of SP and CGRP was reduced by 11 and 36% respectively, while that of VIP remained unchanged. 3. The weights of the parotid glands and their sensitivity to the secretagogues methacholine and SP, injected intravenously, were unchanged as was the response to stimulation of the auriculo-temporal nerve in the presence and absence of atropine. 4. In contrast to capsaicin pretreatment, parasympathetic denervation of the parotid gland reduced the weight of the gland and produced an increase in the response to methacholine and SP. 5. For comparison, the effectiveness of the capsaicin treatment on neuropeptide content was determined in the urinary bladder. The bladder of capsaicin-pretreated rats increased in weight (21%) and in VIP content (31%), while the content of SP and CGRP was reduced by 86 and 94%, respectively. SP- and CGRP-containing nerve fibres were virtually eliminated, while VIP-containing nerve fibres seemed unaffected. 6. In conclusion, antidromic activation of primary afferent (capsaicin-sensitive) C-fibres does not contribute significantly to the 'atropine-resistant' secretory response of the parotid gland to stimulation of the parasympathetic nerve.

Animals↗