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Biomedical subjects

A Anggård

Publications and source records attributed to A Anggård.

At least 55 records · Page 3Linked to original sources
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

Early bone grafting in complete cleft lip and palate cases following maxillofacial orthopedics. V. A postoperative evaluation of nasal patency.

The nasal patency of children born with complete unilateral or bilateral cleft lip and palate was studied with rhinomanometry. The children had all been early bone grafted with a "four-flap" technique. The unilateral deformities were composed of two groups. One group of 39 children (mean age 17.6 years) primarily operated without preoperative orthopedics and another group of 46 children (mean age 10.8 years), where preoperative orthopedics ("T-traction") was performed before the operation. In the bilateral group, 19 children (mean age 15.1 years), preoperative retropositioning pressure and if necessary outward rotation of the lateral maxillary segments was performed before the operation. No difference of total nasal patency was found between unilateral and bilateral cleft children. The nasal cavity of the cleft side of unilateral clefts had, however, a more pronounced nasal stenosis than each cavity of bilateral clefts. In unilateral groups a significant difference in nasal patency was found between the cleft and the noncleft side. This difference was not changed by decongestion indicating a skeletal anatomical stenosis. Nasal patency did not differ between the unilateral groups. However, considering the age difference between the two groups a further improvement of nasal patency with increasing age may possibly occur in the younger "T-traction" group.

Adolescent↗
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↗
PubMed1983

Nasal meningoencephalocele. A clinical problem.

Four cases of nasal meningoencephalocele are reported. They demonstrate the importance of considering the diagnosis of nasal glioma or meningoencephalocele in adults with a nasal polyp of atypical appearance, or in infants with nasal obstruction and unilateral nasal polyp. Misdiagnosed and incorrectly handled patients with nasal meningoencephaloceles may develop serious ascending infections and/or a constant CSF leak. A thorough radiological examination including conventional and computerized tomography of the anterior cranial fossa, isotope cisternography and CT-cisternography is advocated. A multi-disciplinary approach is recommended in the diagnosis and treatment. The surgical procedure includes an anterior fossa craniotomy often in combination with a transnasal approach.

Adult↗
PubMed1982

Carbachol potentiates the cyclic AMP-stimulating effect of VIP in cat submandibular gland.

The effect of VIP and carbachol on cyclic AMP production were studied in isolated acini of the cat submandibular gland and guinea pig pancreas. VIP was almost 100 times more potent in stimulating cyclic AMP in the pancreas than in the submandibular salivary gland. Carbachol did not influence cyclic AMP in the pancreas while a 20-30% increase was seen in the submandibular gland. The addition of carbachol potentiated the cyclic AMP response to VIP in the submandibular acini while no such effect was observed in the pancreas. Atropine abolished the effect of carbachol.

Amylases↗
PubMed1982

Organizational principles in the peripheral sympathetic nervous system: subdivision by coexisting peptides (somatostatin-, avian pancreatic polypeptide-, and vasoactive intestinal polypeptide-like immunoreactive materials).

Sympathetic ganglia and some peripheral tissues of adult guinea pig and cat were analyzed by the indirect immunofluorescence technique with antisera to catecholamine-synthesizing enzymes and some peptides. In the guinea pig, noradrenergic neurons could be subdivided into three populations containing respectively (i) somatostatin-like immunoreactive material, (ii) avian pancreatic polypeptide (APP)-like immunoreactive material, and (iii) apparently only noradrenaline (NA; norepinephrine). A fourth population of sympathetic neurons was nonadrenergic and contained vasoactive intestinal polypeptide (VIP)-immunoreactive material. In the cat many noradrenergic neurons with APP and some without this peptide were seen, but no somatostatin-immunoreactive neurons were observed. Also a population of non-adrenergic, presumably cholinergic, neurons containing a VIP-like peptide was observed. These neuron populations seemed to innervate different tissues with some target specificity. For example, in the nasal mucosa of the cat, nerves containing NA/APP-like immunoreactive material (called NA/APP nerves) were found around small arteries and arterioles, whereas venules and sinusoids were surrounded by nerves containing only NA (called NA nerves). Also in the submandibular salivary gland of the cat, the NA/APP nerves surrounded arteries and arterioles, whereas NA nerves were seen in relation to acini and ducts. The sympathetic (cholinergic) VIP-containing neurons innervated blood vessels and exocrine tissue in the cat sweat glands. In the coeliac-superior mesenteric ganglion complex of the guinea pig and cat, a dense network of VIP-immunoreactive fibers was seen preferentially around noradrenergic ganglionic cell bodies lacking APP-immunoreactive material. Thus, adult peripheral sympathetic neurons can be subdivided into several categories on the basis of specific peptides. These subdivisions may innervate specific targets and may receive peptide-specific neuronal inputs.

Animals↗
PubMed1982

Complementary role of vasoactive intestinal polypeptide (VIP) and acetylcholine for cat submandibular gland blood flow and secretion.

The effects of local intraarterial infusions of VIP, acetylcholine (ACh), substance P, isoprenaline and bradykinin on submandibular gland blood flow and salivary secretion were studied in cats. It was found that VIP (10(-14) to 10(-10) mol/min) caused an atropine resistant vasodilation but no salivary secretion. Several hundred fold higher doses of exogenous VIP had to be infused than the amounts of VIP seen in the venous outflow during maximal nerve stimulation at a similar vasodilatory response. ACh infusions (5 X 10(-12) to 5 X 10(-8) mol/min) caused both a muscarinic vasodilation and salivary secretion. ACh was about 100 times less potent than VIP as a vasodilating agent. Both ACh and VIP induced in high doses a vasodilatory response similar to that seen during parasympathetic nerve stimulation at 15 Hz. ACh by itself did in the present doses, however, only induce about 50-60% of the maximal secretory response. Combined infusions of ACh and VIP, had mostly an additive effect on vasodilation. The salivatory volume response to ACh was potentiated by VIP and to a smaller extent also by isoprenaline. This potentiating effect may be due to a direct effect on secretory elements as well as partly to the additional increase in blood flow. Bradykinin was about 1 000 times less potent than VIP as a vasodilating agent. Substance P (10(-9) mol/min) only caused a weak vasodilation. Since there is evidence that ACh and VIP coexist within the same neurons and are both released upon parasympathetic nervous activation, the present findings suggest that the secretory and vasodilatory responses may be caused by an interaction between these two agents.

Acetylcholine↗
PubMed1981

Vasoactive intestinal polypeptide and cholinergic mechanisms in cat nasal mucosa: studies on choline acetyltransferase and release of vasoactive intestinal polypeptide.

Quantitative immunohistochemical analysis of the sphenopalatine ganglion in normal cats revealed that virtually all ganglion cells (98.5%) were immunoreactive to vasoactive intestinal polypeptide (VIP). After surgical removal of this ganglion, the content of both VIP and choline acetyltransferase (acetyl-CoA:choline O-acetyltransferase, EC 2.3.1.6), a specific marker for cholinergic neurons, was decreased to about 70-80% in the nasal mucosa. In contrast, in animals subjected to sympathectomy combined with sensory (trigeminal) denervation, no significant change in VIP or choline acetyltransferase was found in the nasal mucosa. The present findings strongly suggest that a large proportion of the VIP neurons in the sphenopalatine ganglion contain choline acetyltransferase. This further supports the view that VIP is present in a population of autonomic cholinergic neurons innervating exocrine glands in the cat. In contrast, the ciliary ganglion contained high levels of choline acetyltransferase but no VIP. Parasympathetic nerve stimulation (15 Hz) caused a maximal vasodilation and a 500-fold increase in VIP output from the nasal mucosa. The plasma VIP immunoreactivity eluted at the same position as porcine VIP on gel permeation chromatography. Atropine pretreatment, which is known to abolish nasal secretion, caused a further 3-fold increase in VIP output during the nerve stimulation (15 Hz). Simultaneously, a markedly prolonged duration of the vasodilatory response was observed. The increased output of VIP during parasympathetic nerve stimulation by atropine pretreatment suggests that the transmitter acetylcholine may inhibit the release of the coexisting peptide--i.e., VIP--via muscarinic autoreceptors.

Animals↗
PubMed1981

Vascular effects of slow reacting substance (SRS) in the cat nasal mucosa and the appearance of a SRS-like principle in cat nasal secretion on nerve stimulation.

Stimulation of parasympathetic secreto-vasomotor nerve fibres in cat nasal mucosa produced nasal secretions with biological activity similar to cat paw SRS. The biologically active principle was purified by ethanol extraction, Amberlite XAD-2 and anion exchange chromatography. It had elution characteristics common with cat paw SRS but different to those of prostaglandin F2 alpha. The biological activity on the guinea pig ileum was antagonized by FPL 55712. In the cat intraarterial administration of cat paw SRS resulted in a dose-dependent but modest increase in nasal blood flow whereas local blood content was not affected. Provided SRS has similar effects on human nasal blood flow the importance for SRS as a mediator for nasal congestion in allergic rhinitis or parasympathetically induced vasomotor rhinitis seems less likely.

Angiotensin II↗
PubMed1981

Complementary role of vasoactive intestinal polypeptide (VIP) and acetylcholine for cat submandibular gland blood flow and secretion. I. VIP release.

The effects of parasympathetic and sympathetic nerve stimulation on VIP release in relation to blood flow and secretion were studied in the cat submandibular salivary gland. Parasympathetic nerve stimulation caused a marked VIP overflow (over thousand fold increase in VIP output) into the venous effluent from the gland which was simultaneous with profuse salivation and an about 10-15 fold increase in blood flow. The VIP output was dependent on the stimulation frequency, the duration of the stimulation period as well as the glandular blood flow. At 15 Hz maximal VIP output (about 4 fmol per impulse) was obtained after about 5 min of stimulation simultaneously with the maximum of the maintained phase of vasodilation. About 50 pmol VIP was recovered in the venous effluent from the gland during 1 h of maximal nerve stimulation. The VIP output after 1 h, was only about 20% of maximal, however, suggesting that the storage reserves and/or resupply of VIP might be running out. Under physiological conditions (frequencies less than or equal to 6 Hz) it was estimated that the axonal transport mechanism should be sufficient for replacement of VIP. At lower frequencies (2 and 6 Hz) the VIP output was parallel to vasodilation and secretion, while at a high frequency (15 Hz) a much more pronounced VIP output was seen. The increased overflow at 15 Hz may either be due to an actual increase in release or to a saturation of local VIP inactivating mechanisms. When stimulated simultaneously, the parasympathetic vasodilator mechanism seemed much more potent than sympathetic vasoconstriction. Since VIP may be present in cholinergic neurons, data from the literature concerning acetylcholine release are discussed in relation to the observed VIP output.

Acetylcholine↗
PubMed1981

Complementary role of vasoactive intestinal polypeptide (VIP) and acetylcholine for cat submandibular gland blood flow and secretion. II. Effects of cholinergic antagonists and VIP antiserum.

The effects of atropine and hexamethonium on submandibular vasodilation, secretion and VIP release in response to parasympathetic nerve stimulation were studied in cats. It was found that salivary secretion was completely atropine sensitive at all frequencies. The vasodilatory response was characterized by an initial phase (most marked at lower frequencies) followed by a maintained phase (most pronounced at high frequencies). Atropine reduced the initial phase at all frequencies while the maintained phase was reduced only at low stimulation frequencies. At 15 Hz the maintained blood flow response was paradoxically increased after atropine, particularly with regard to the duration. The increase in blood flow after atropine was accompanied by an about eight fold increase in VIP output as compared to control stimulations at 15 Hz. This may suggest that the acetylcholine levels regulate the VIP release in a feed-back system via muscarinic autoreceptors. No increase in VIP output by atropine was, however, observed at 2 Hz while a small but significant increase was found at 6 Hz. Treatment with VIP antiserum reduced both phases of the vasodilation as well as the secretion in response to stimulation at 2 Hz. Thus, VIP and acetylcholine seem to be important for both phases of vasodilation as well as for salivary secretion. The relative contributions of VIP and acetylcholine are, however, hard to evaluate since atropine appears to increase VIP release. This fact complicates the characterization of cholinergic and noncholinergic vasodilator mechanisms by the use of atropine. Hexamethonium treatment abolished both the vasodilation, the secretion and the VIP release seen during parasympathetic nerve stimulation implying that it was preganglionic and that the preganglionic transmitter is acetylcholine which activates postganglionic transmitter is acetylcholine which activates postganglionic neurons via nicotinic receptors. Somatostatin had no blocking effect on parasympathetic mechanisms in the cat submandibular gland.

Acetylcholine↗
PubMed1980

Cellular localization of peptides in neural structures.

By means of the immunohistochemical technique of Coons and collaborators, numerous peptide-containing neurons have been observed in the brain, spinal cord and periphery. These neurons may contain peptides such as substance P, vasoactive intestinal polypeptide (VIP), enkephalin or somatostatin. Some systems are very extensive. For example, immunoreactive substance P has been observed in more than 30 cell groups in the central nervous system, in primary sensory neurons, in sensory neurons in the vagus nerve and in taste buds, and in intestinal neurons. Thus, one and the same peptide can be utilized at many different levels in the nervous system. Several examples are now known where a regulatory peptide occurs together with a classical transmitter, such as a catecholamine, in the same neuron, which suggests the possibility that a neuron can release more than one transmitter substance. Of particular interest is the occurrence of VIP in presumed cholinergic neurons innervating exocrine glands in the cat, and the coexistence of a cholecystokinin (CCK)-like peptide in dopamine neurons projecting mainly to limbic areas. In the former system VIP seems to be responsible mainly for vasodilation, whereas acetylcholine mainly causes secretion. Furthermore, combined infusion of both substances in very low doses results in a marked potentiation of the secretory and vasodilatory responses. Thus, we have an example where two putative transmitters, released from the same nerve endings, seem to cooperate to activate a physiological response (secretion). With regard to the central CCK/dopamine neurons the type of interaction between the two coexisting transmitter candidates is at present unclear. It is suggested that elucidation of different types of coexistence phenomena may advance our understanding of chemical transmission at synapses under normal and pathological conditions, and may lead to new approaches to the treatment of some nervous disorders.

Adrenocorticotropic Hormone↗
PubMed1980

Vasoactive intestinal polypeptide in cholinergic neurons of exocrine glands: functional significance of coexisting transmitters for vasodilation and secretion.

By a combination of the indirect immunofluorescence technique with acetylcholinesterase (acetylcholine acetylhydrolase, EC 3.1.1.7) staining, it was shown that vasoactive intestinal polypeptide (VIP) is present in cholinergic (acetylcholinesterase-rich) neurons involved in control of secretion and vasodilation in exocrine glands of cat. The submandibular salivary gland was used as a functional model. Preganglionic nerve stimulation induced an atropine-resistant, hexamethonium-sensitive vasodilation and release of VIP into the venous outflow from the gland and an atropine- and hexamethonium-sensitive secretion. Infusion of VIP antiserum reduced both the vasodilation and secretion. Infusion of VIP caused vasodilation only, whereas acetylcholine caused both vasodilation and secretion. Simultaneous infusion of VIP and acetylcholine in low doses resulted in a marked potentiation of both vasodilation and secretion. The present morphological and functional data support the following hypothesis for regulation of vasodilation and secretion in exocrine glands. Preganglionic cholinergic nerves activate, via nicotinic receptors, postganglionic neurons, causing concomitant release from the same nerve endings of two coexisting putative transmitters, acetylcholine and VIP. Acetylcholine produces mainly secretion by a muscarinic action and VIP causes mainly vasodilation, but the two substances seem to cooperate directly or indirectly in both types of response. Thus, the coexistence of two putative neurotransmitters, VIP and acetylcholine, in one neuron may explain the dual effector response (i.e., the cholinergic secretion and the atropine-resistant vasodilation) caused by nerve stimulation in exocrine glands.

Acetylcholinesterase↗