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P Aas

Publications and source records attributed to P Aas.

At least 19 recordsLinked to original sources
PubMed1999

[Frostbite injuries].

Frostbite injuries occur mainly in toes, fingers, ears, nose and cheek. Typically an initial vasoconstriction in the skin will protect from drop in core temperature. Ice crystal development occurs when tissue temperature drops to -2 degrees C, leading to increased osmolality of the extracellular fluid and intracellular dehydration. An additional insult occurs with thawing due to reperfusion of the tissue and thereby release of inflammatory mediators. Symptoms of frostbite injury are: White-cyanotic discoloration, pain and numbness followed by hypoaesthesia. General hypothermia should be prevented and treated before managing the local frostbite injuries. Direct contact with warm skin without rubbing should be used in superficial injuries. More severe and deeper injuries should not be thawed until definite treatment could be given in a hospital. Re-freezing and mechanical influence on the injured parts must be avoided. Thawing should preferably be done in stirred water of 40-42 degrees C with mild soap. Antibiotics may be indicated when the skin barrier is broken. Surgical debridement should be postponed until a clear demarcation occurs.

Frostbite↗
PubMed1999

Phytoplanktonic and Bacterial Carbon Pools and Productivities in the Gerlache Strait, Antarctica, during Early Austral Spring.

Abstract Phytoplankton and bacterial biomass and productivities were investigated at four depths in the upper 500 m of the water column in the Gerlache Strait, Antarctica, during the prebloom period of early austral spring, from October 13 to November 4, 1995. The concentrations of all carbon pools were low, with the total particulate organic carbon (POC) concentration averaging 1.9 +/- 0.9 µM. Bacterial, protozoan, and phytoplankton carbon accounted for 21% of the total POC, indicating that detritus or unenumerated organisms comprised the bulk of the POC during this period. Larger zooplankton or protozoa, such as ciliates, may account for this difference, since microzooplankton can represent a significant fraction of the total microbial biomass. Primary and bacterial secondary production rates were also low, less than 300 and 30 ng C L(-1) h(-1), respectively. However, when production was normalized to either chlorophyll or bacterial cell number, rates were similar to those recorded during the spring bloom periods. This indicates that the cells were metabolically active during the prebloom period. Chlorophyll specific primary production averaged over the upper 80 m of the water column was 1.28 +/- 0.84 µg C µg chl(-1) h(-1), whereas the mean bacterial specific growth rate over the same depth interval was 0.34 +/- 0.24 d(-1). The overall production rates were low only because of the low abundance of cells during the prebloom period. When the site was reoccupied the following year, all measures of biomass and productivity were higher [36], emphasizing the large interannual variability in the Gerlache Strait.http://link.springer-ny.com/link/service/journals/00248/bibs/38n3p296.html</hea

Journal Article↗
PubMed1999

Early and late functional and histopathological perturbations in the rabbit ear-artery following local cold injury.

BACKGROUND: These experiments aimed to study the in vivo short and long term neurovascular regeneration after frostbite. METHODS: The rabbit central ear-artery was used as the experimental model. The effects on the noradrenergic innervation of the artery were measured in isolated vascular ring segments the first day and 2, 3-4, and 8-10 or 10-20 weeks following freezing at -9 degrees C or -18 degrees C for 15 min with slow rewarming for 7 min at room temperature. RESULTS: Two days after freezing the sympathetic nerves were completely degenerated, as observed with glyoxylic acid-induced fluorescence. The vascular isometric tension responses to exogenous noradrenaline and endogenously released noradrenaline by electrical stimulation in vitro were abolished. A varying degree of necrosis of the vascular wall was observed. Two weeks after freezing at -18 degrees C in vitro responses to exogenous noradrenaline and electrical stimulation were still abolished, then gradually approaching control levels after 10-20 weeks of in vivo regeneration. Eight and 10 weeks after injury at -9 degrees C increased vascular tension responses to exogenous noradrenaline was found. In spite of a long regeneration period the total uptake and the spontaneous and K+ (75 mM) evoked releases of [3H]noradrenaline were persistently decreased after frostbite at -18 degrees C, but they were regenerated to control levels already 10-20 weeks after -9 degrees C. Regeneration of noradrenergic nerve function, expressed as [3H]noradrenaline uptake and release and responsiveness to electrical stimulation, expressed as vascular contraction, was slower than the regeneration of the vascular smooth muscle. Myointimal hyperplasia developed in response to -9 degrees C and -18 degrees C frostbite. The uptake and the K+ evoked release of [3H]noradrenaline were particularly sensitive parameters for autonomic nerve function. CONCLUSIONS: The present findings may demonstrate important neurovascular reactions to local frostbite and may explain human sequelae following frostbite.

Adrenergic Fibers↗
PubMed1999

Effect of alpha-trinositol on interstitial fluid pressure, oedema generation and albumin extravasation in experimental frostbite in the rat.

1. The anti-inflammatory effect of alpha-trinositol (D-myo-inositol-1,2,6-trisphosphate) on oedema formation, microvascular protein leakage and interstitial fluid pressure (Pif) in rat skin after frostbite injury, was investigated. Alpha-trinositol (40 mg kg body weight(-1)) was administered intravenously as a bolus both before and/or in the interval between freezing and thawing of the tissue. 2. Pif was measured in rat paw skin with micropipettes connected to a servo-controlled counterpressure system. Oedema formation was estimated by measuring the increase in total tissue water content (wet weight minus dry weight divided by dry weight). Albumin extravasation (i.e., the difference between the plasma equivalent space for 125I- and 131I-human serum albumin (HSA) circulating for different time intervals) was used to estimate the microvascular leakage. 3. Compared to untreated animals, alpha-trinositol given pre- and/or post-freeze reduced total tissue water and albumin extravasation as well as the fall in Pif in injured tissue significantly (P<0.05). Alpha-trinositol given only post-freeze reduced total tissue water and albumin extravasation from 4.46+/-0.93 and 2.37+/-1.12 to 2.51+/-0.29 and 0.36+/-0.18 ml g dry weight(-1), respectively (P<0.05). 4. Pif fell from -0.8+/-0.2 mmHg pre-freeze to -3.4+/-1.0 mmHg (P<0.05) at 20 min after tissue injury (circulatory arrest) and was attenuated by treatment with alpha-trinositol. 5. We conclude that alpha-trinositol exerts its anti-oedematous effect by acting on the extracellular matrix, attenuating the lowering of Pif as well as on the microvascular wall, thereby decreasing the protein extravasation.

Animals↗
PubMed1996

In vitro effects of toxogonin, HI-6 and HLö-7 on the release of [3H]acetylcholine from peripheral cholinergic nerves in rat airway smooth muscle.

The purpose of this work was to evaluate the possible non-reactivating effects of toxogonin (1,1'[oxybis(methylene)]bis[4-[hydroxyimino) methyl]pyridinium]-dichloride), HI-6 (1-[[[(4-aminocarbonyl)pyridinio] methoxy]methyl]-2-[(hydroxyimino)methyl]pyridinium-dichloride) and HLö-7 (pyridinium, 1-[[[4-(aminocarbonyl)pyridino]methoxy] methyl]-2,4-bis-[(hydroxyimino)methyl]diiodide) on the release of acetylcholine from cholinergic nerves. The oximes have been tested in our rat bronchial smooth muscle model, with respect to the effects of oximes on the K+ (51 mM)-evoked release of [3H]acetylcholine in the presence and absence of soman (1.0 microM). Toxogonin (100 microM) had no effect on the K(+)-evoked release of [3H]acetylcholine in the presence or absence of soman (1.0 microM). Similar results were found for HI-6 (100 microM). In contrast, HLö-7 (100 microM) enhanced the K(+)-evoked release of [3H]acetylcholine in the absence of soman. In the presence of soman HLö-7 did not alter the release of [3H]acetylcholine induced by K+ stimulation. The potentiating effect of HLö-7 on the release of [3H]acetylcholine could be blocked by the L-, N- and P-Ca2+ channel blockers verapamil (0.1 and 1.0 microM), omega-conotoxin GVIA (1.0 microM) and omega-agatoxin IV-A (0.2 microM), respectively. Muscarinic receptor antagonists (atropine (10 microM), pirenzepine (M1) (1.0 microM) and methoctramine (M2) (1.0 microM) had no effects on the HLö-7 (100 microM)-enhanced release of [3H]acetylcholine. Protein kinase inhibitors (H-7 (20 microM), calphostin C (1.0 microM) and KN-62 (10 microM) inhibited the HLö-7 (100 microM)-enhanced K(+)-evoked release of [3H]acetylcholine. The results showed that only HLö-7 had a direct enhancing effect on the release of acetylcholine through activation or opening of Ca2+ channels and a subsequent protein phosphorylation in the nerve terminal.

Acetylcholine↗
PubMed1996

Extract of the marine alga Prymnesium patelliferum induces release of acetylcholine from cholinergic nerves in the rat bronchial smooth muscle.

An extract of the marine algal flagellate Prymnesium patelliferum enhanced the spontaneous as well as the K+ evoked (51 mM K+) release of [3H]acetylcholine and endogenous acetylcholine from autonomic cholinergic nerves of rat bronchial smooth muscle. The effects were concentration-dependent and reversible. The enhancement of the K+ evoked release by the algal extract was partly dependent on extracellular Ca2+ and was significantly suppressed by the organic Ca2+ blockers omega-conotoxin GVIA (1 microM), diltiazem (100 microM), nifedipine (100 microM) and flunarizine (100 microM). The enhancement of the spontaneous release seemed Ca2+ independent and not sensitive to the Na+ channel blocker tetrodotoxin. Sphingosine (20 microM), a protein kinase C inhibitor, strongly potentiated the enhancement of spontaneous release of [3H]acetylcholine induced by the algal extract whereas another protein kinase C inhibitor. 1-(5-quinolinesulphonyl)-2-methylpiperazine (H-7) (20 microM), was without effect. A similar potentiation as seen with sphingosine was observed with procaine (100 microM) and flunarizine (100 microM). The results indicate that the enhancement of the K+ evoked release of [3H]acetylcholine by the toxic extract of P. patelliferum was partly caused by activation of voltage-dependent Ca2+ channels. The increase in the spontaneous release of [3H]acetylcholine and endogenous acetylcholine induced by the algal extract alone may be caused by an ionophore-like property of the algal extract. This effect of the algal extract may be enhanced by compounds that facilitate the interaction of the algal toxin with the plasma membrane such as the lipophilic compounds flunarizine, procaine and sphingosine.

Acetylcholine↗
PubMed1994

Responses of noradrenergic nerves in rabbit ear-artery before and after experimental frost-bite.

Experiments were designed to determine the effects of sub-zero temperatures on the function of the noradrenergic innervation of a peripheral blood-vessel. The central ear-artery of the rabbit was used for this purpose. The ear was exposed to temperatures of -6, -9 or -18 degrees C in vivo for 15 min. After 1 day (24 h) or 6 days in vivo, the central ear-artery was dissected free, incubated in [3H]-noradrenaline (NA) and stimulated in vitro with high potassium (75 mM) for 5 min to evoke release of [3H]-NA. The release of [3H]-NA was Ca(2+)-dependent. One day after exposure to -6, -9 or -18 degrees C, increases of 45-57 and 44-72% and a reduction of 12-35% were observed, respectively, in three successive potassium-evoked NA-releases. After 6 days in vivo an increase of 30-34% was observed following exposure to -6 degrees C, while no alteration was observed after exposure to -9 degrees C. A reduction of 84-89% was recorded after exposure to -18 degrees C. Following this exposure to -18 degrees C, there was also a great reduction in the evoked release of [3H]-NA compared with the spontaneous release, whereas this correlation did not change after exposure to -6 and -9 degrees C. The total uptake of [3H]-NA was unchanged after freezing the tissue at -6 degrees C, but was substantially reduced after exposure to -9 and -18 degrees C. A short period of in vivo restoration (6 days, enhanced the uptake of [3H]-NA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effect of pyridostigmine pretreatment, HI-6 and Toxogonin treatment on rat tracheal smooth muscle response to cholinergic stimulation after organophosphorus inhalation exposure.

The ex vivo contraction response of the rat tracheal smooth muscle was examined after 10 min in vivo inhalation of soman and/or pretreatment with pyridostigmine and/or post-exposure treatment with HI-6 ([[[(4-aminocarbonyl)pyridinio]methoxy]methyl]-2[(hydroxy imino) methyl]pyridinium dichloride) or Toxogonin (1,1'-[oxybis-(methylene)]bis[4-[(hydroxyimino)methyl]-py rid inium] dichloride). In vivo pretreatment with pyridostigmine was achieved by subcutaneous (s.c.) implantation of an osmotic pump that delivered pyridostigmine continuously (0.01 mg/h) in the neck region of the rat 18 h before soman exposure. The ex vivo cholinergic tracheal smooth muscle response increased during the first 60 min after soman exposure in animals pretreated with pyridostigmine. The amplitude of the contraction response in pyridostigmine pretreated animals was about 60% of control, compared to 15% of control without pyridostigmine pretreatment. Pyridostigmine pretreatment also produced significant recovery of the total cholinesterase (ChE) activity in plasma, but not in trachea and lung. Intraperitoneal (i.p.) injection of HI-6 or Toxogonin (50 mg/kg), immediately after 10 min inhalation exposure to soman, also significantly improved the ex vivo cholinergic contraction response of the trachea (decapitation 15 min after oxime administration). The recovery of the physiological response with Toxogonin was, however, not stable. HI-6 was superior to Toxogonin with respect to the initial airway contraction response, and the response increased up to a stable level not significantly different from control. There was no significant reactivation of the ChE activity after treatment with the oximes. Combination of pyridostigmine pretreatment and oxime treatment enhanced the recovery of the tracheal contraction response and the ChE activity in the trachea compared to treatment with oximes alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1993

The effect of experimental frost-bite on the responses of the rabbit ear-artery to adrenergic and electrical stimulation.

The aim of the present investigation was to study the effect of sub-zero temperatures on the adrenergic activated, smooth muscle-contraction of a peripheral blood-vessel. The central ear-artery of the rabbit was used for this purpose. The artery was stimulated to contract in vitro by activation of phentolamine sensitive, post-junctional, alpha-adrenoceptors by use of noradrenaline, or by noradrenaline released from noradrenergic nerves in the blood-vessel following electrical field stimulation. The effect of freezing the tissue in vivo for 15 min at sub-zero temperatures (-4, -6 and -9 degrees C) was studied in vitro. Exposure to -4 and -6 degrees C did not alter the apparent affinity (ED50) of noradrenaline significantly, when measured immediately, or 2 or 6 days after exposure. The maximal response to noradrenaline was reduced by approximately 54, 74 and 100% following exposure to -4, -6 and -9 degrees C, respectively. The response was completely restored after 2 and 6 days of regeneration in vivo following exposure to -6 degrees C, whereas the response after exposure to -9 degrees C was restored by only about 8 and 30% after 2 and 6 days regeneration, respectively. The maximal response to electrical field stimulation, which was completely inhibited by tetrodotoxin and phentolamine, was reduced by approximately 92% after exposure for 15 min to -4 and -6 degrees C, while it was completely inhibited after exposure to -9 degrees C. The response was restored by only 15-20% following 2 and 6 days in vivo after exposure to -6 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effect of calcium antagonists (omega-conotoxin GVIA, verapamil, gallopamil, diltiazem) on bronchial smooth muscle contractions induced by soman.

The effect of the calcium antagonists omega-conotoxin GVIA, verapamil, gallopamil and diltiazem was investigated on in vitro bronchial smooth muscle contraction in the rat induced by the nerve agent soman. Soman inhibits the acetylcholinesterase activity irreversibly. The effect of the calcium channel antagonists on contractions induced by electrical field stimulation and carbachol was also investigated, in order to elucidate the mechanism by which calcium antagonists inhibit the soman induced contraction. omega-Conotoxin GVIA reduced the bronchial smooth muscle contraction induced by electrical field stimulation with an almost complete inhibition at approximately 1.0 x 10(-6) M. The soman induced contraction was only inhibited by 15% at a concentration of 3.0 x 10(-6) M omega-conotoxin GVIA. The organic calcium antagonists verapamil, gallopamil and diltiazem reduced both electrically and soman induced smooth muscle contraction. Complete inhibition of the contractions induced by soman was achieved at 1.4 x 10(-4) M for verapamil and gallopamil, while diltiazem inhibited the contraction to 7% of control at 1.4 x 10(-4) M. Verapamil, gallopamil and diltiazem increased the EC50 for carbachol significantly, while omega-conotoxin GVIA had no effect. None of the calcium antagonists had any effect on the maximal contraction induced by carbachol. Verapamil, gallopamil and diltiazem blocked, however, sub-maximal contractions induced by carbachol (10(-7)-10(-5) M) resulting in a right-shift of the dose response curve. The results show that omega-conotoxin GVIA inhibits the calcium-dependent release of acetylcholine which causes contraction of airway smooth muscle, while it has no effect on smooth muscle contraction induced by soman.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholinesterase↗
PubMed1991

Effect of AH5183 (vesamicol) on cholinergic transmission in intact airway smooth muscle.

The effect of the vesicular acetylcholine (ACh) transport blocker trans-2-(4- phenyl-piperidino)-cyclohexanol (AH5183) was studied in bronchial smooth muscle during activation of the vagus nerve. AH5183 inhibited in a dose-dependent manner the Ca(2+)-sensitive electrically induced smooth muscle contractions in vitro with a half-inhibitory concentration (IC50) of 1.6 +/- 0.4 microM. The inhibition was complete within 68 +/- 1 min (n = 8) at approximately 20 microM AH5183 and was partly reversible after washing of the preparations. AH5183 (20 microM) reduced the level of endogenous ACh by 47.4 +/- 7.6% (n = 4) during this time period. The effect of AH5183 is most likely prejunctional, since the contractions induced post-junctionally by carbachol were not altered by AH5183. The irreversible anticholinesterase, soman, increased the tonus of airway smooth muscle as a result of accumulation of spontaneously released ACh from prejunctional leakage. AH5183 had no effect on this increase of muscle contraction. The present results show that the nerve-evoked release of ACh comes from an AH5183-sensitive pool, probably a vesicular pool, whereas leakage of ACh presumably comes from the cytoplasmic pool in airway smooth muscle.

Acetylcholine↗
PubMed1991

Prejunctional stimulation of cholinergic nerves in rat airway smooth muscle by an adenosine analogue.

The effect of 5'-N-ethylcarboxamidoadenosine (NECA) on rat bronchial smooth muscle was examined in vitro. Both the nerve mediated muscle contraction induced by electrical stimulation and the potassium evoked release of [3H]ACh were enhanced by NECA. The apparent affinity (EC50) of NECA in the contraction experiments was 0.30 +/- 0.06 microM. The adenosine (ADO) receptor antagonist, 8-phenyltheophylline (8-PT), inhibited the NECA induced potentiation of both the electrical induced contraction and the potassium evoked release of [3H]ACh. The EC50 and intrinsic activity of exogenous ACh were not altered in the presence of NECA (1 microM) in experiments where smooth muscle contraction were measured, indicating that NECA has a prejunctional effect and not a postjunctional effect on muscarinic receptors. The new A2 specific ADO receptor agonist 2-p-(2-carboxyethyl)-phenethylamino-5'-N-ethylcarboxamidoadenosine (CGS 21680) and ADO also enhanced the nerve-mediated contraction (EC50 = 35 +/- 8 microM and 69 +/- 20 microM, respectively). 8-PT (10 microM) and enprofylline (ENPF) (10 microM) inhibited the electrically induced contraction by 55 +/- 16% and 45 +/- 5% respectively. The potassium evoked release, however, was stimulated 56 +/- 6% and 39 +/- 7% by 50 microM 8-PT and ENPF respectively. The results provide evidence for a NECA specific ADO receptor in rat bronchi that is most likely prejunctional. Stimulation of this receptor, which may be of an A2 receptor subtype, enhances the nerve mediated release of ACh and thereby induce contraction of the bronchial smooth muscle.

Adenosine↗
PubMed1990

Amino acids as modulators of cholinergic nerves in airways.

The bronchial smooth muscle of rat was examined for contractile responses to excitatory amino acids. The electrical field stimulation (EFS) which induces release of ACh, induced contraction which was enhanced by exogenous L-glutamate (L-glu). The ED50 of L-glu was 3.5 +/- 0.1 mM. Inhibition of the release by TTX or by HC-3 completely abolished the potentiation of the EFS-induced contraction by L-glu. The effect of L-glu is therefore probably a prejunctional effect. Concentrations of L-glu higher than 22 mM inhibited the EFS evoked contractions, and enhanced the tonus of the muscle by a postjunctional stimulation. The ED50 of ACh was not altered by L-glu. In contrast, an increase of the intrinsic activity (alpha) of ACh was seen, providing evidence for a postjunctional potentiation of ACh induced contraction. L-glu did not inhibit AChE-activity at concentrations up to 50 mM, indicating that the effect is not due to an accumulation of ACh. A relaxation of the EFS-induced bronchial smooth muscle contraction was seen with high concentrations of D-glu, L-asp, L-alpha-amino adipate and ibotenate. Neither L-GDEE nor DL-APV had any inhibitory effect on L-glu and L-asp induced alteration of EFS-evoked contraction or on the L-glu enhanced tonus of the bronchial smooth muscle. Kainate, NMDA and quisqualate had only minor transient potentiating effects on the EFS-induced contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1990

Evidence for prejunctional M2 muscarinic receptors in pulmonary cholinergic nerves in the rat.

1. The effects of muscarinic antagonists considered to be selective for M1 receptors (pirenzepine) and for M2 receptors (gallamine and methoctramine) were used to investigate the existence of prejunctional muscarinic receptors on cholinergic nerves in the rat lung. The tracheal tube preparation was used in vitro, and contraction of the trachealis muscle was induced by electrical field stimulation (EFS) and by application of an exogenous muscarinic agonist (pilocarpine), and measured as an increase in intraluminal pressure in the tube. 2. The muscarinic antagonists, gallamine and methoctramine, enhanced the contractions induced by nerve stimulation, while contractions elicited by exogenous application of pilocarpine were inhibited by the antagonists. 3. In contrast, pirenzepine blocked contractions induced by both EFS and pilocarpine in a dose-dependent manner (EC50 0.1 microM) due to blockade of the postjunctional muscarinic receptors on airway smooth muscle. Potentiation of the response to EFS was never seen with this antagonist. 4. The muscarinic agonist, pilocarpine, caused a slow maintained increase in tone of the tracheal tube and at the same time reduced the contractions induced by EFS. This inhibitory effect was blocked by gallamine and methoctramine. 5. The results suggest that prejunctional inhibitory muscarinic receptors may be localised on the parasympathetic cholinergic nerve terminals innervating tracheal smooth muscle in the rat. This confirms previous findings obtained by measuring transmitter release in this species. The present results suggest that these receptors are of the M2 subtype. Blockade of these autoreceptors with gallamine or methoctramine would increase the output of acetylcholine (ACh) and thereby enhance the nerve-induced contraction of tracheal smooth muscle.

Animals↗
PubMed1989

Stimulation of peripheral cholinergic nerves by glutamate indicates a new peripheral glutamate receptor.

The bronchial smooth muscle of the rat was examined for contractile responses to excitatory amino acids. The nerve-mediated contraction induced by electrical field stimulation was enhanced by exogenous L-glutamate (L-Glu). The apparent affinity (ED50) of L-Glu was 3.5 +/- 0.1 mM. Both tetrodotoxin and hemicholinium-3 completely abolished the electrical field-induced contraction and therefore the potentiation by L-Glu, which indicates that L-Glu has a prejunctional effect. Concentrations of L-Glu higher than 22 mM inhibited the electrical field-induced contractions and enhanced the tonus of the smooth muscle by postjunctional stimulation. The ED50 of exogenous ACh was not altered by L-Glu. High concentrations (62 mM) of L-Glu increased the intrinsic activity (alpha) of ACh, indicating a postjunctional potentiation of ACh-induced contractions. L-Glu did not inhibit the activity of acetylcholinesterase, therefore the postjunctional potentiation was not due to ACh accumulation. Inhibition of the electrical field-induced contraction was seen with high concentrations of D-Glu, L-aspartate (L-Asp), L-alpha-amino adipate and ibotenate. Neither glutamate diethyl ester nor 2-amino-5-phosphonovalerate had any inhibitory effects on the L-Glu- and L-Asp-induced alterations of the electrical field-stimulated contraction or on the L-Glu-enhanced tonus of the bronchial smooth muscle. Kainate, N-methyl-D-aspartate, quisqualate and N-acetyl-aspartyl-glutamate had only minor transient potentiating effects on the electrical field-induced contraction. The results provide evidence for a L-Glu receptor in rat bronchi that has a different specificity for glutamate agonists and antagonists than the L-Glu receptor described in the CNS. The receptor seems to be located prejunctionally and enhances nerve-mediated responses and thereby stimulates the bronchial smooth muscle to contract. The possible involvement of this type of receptor in the 'Chinese restaurant syndrome' is discussed.

Amino Acids↗