scholarly journals Grain sorghum dust increases macromolecular efflux from the in situ nasal mucosa

1998 ◽  
Vol 84 (4) ◽  
pp. 1431-1436 ◽  
Author(s):  
Xiao-Pei Gao
Keyword(s):  
Substance P ◽  
Nasal Mucosa ◽  
Fluorescein Isothiocyanate ◽  
Grain Sorghum ◽  
Plasma Exudation ◽  
Substance P Receptor ◽  
Neurokinin 1 ◽  
Dust Extract

The purpose of this study was to determine whether an aqueous extract of grain sorghum dust increases macromolecular efflux from the nasal mucosa in vivo and, if so, whether this response is mediated, in part, by substance P. Suffusion of grain sorghum dust extract on the in situ nasal mucosa of anesthetized hamsters elicits a significant increase in clearance of fluorescein isothiocyanate-labeled dextran (FITC-dextran; mol mass, 70 kDa; P < 0.05). This response is significantly attenuated by CP-96345 and RP-67580, two selective, but structurally distinct, nonpeptide neurokinin 1 (substance P)-receptor antagonists, but not by CP-96344, the 2 R,3 Renantiomer of CP-96345 ( P < 0.05). CP-96345 has no significant effects on adenosine-induced increase in clearance of FITC-dextran from the in situ nasal mucosa. CP-96345 and RP-67580, but not CP-96344, significantly attenuate substance P-induced increases in clearance of FITC-dextran from the in situ nasal mucosa ( P < 0.05). Collectively, these data suggest that grain sorghum dust elicits neurogenic plasma exudation from the in situ nasal mucosa.

Dexamethasone attenuates grain sorghum dust extract-induced increase in macromolecular efflux in vivo

1999 ◽  
Vol 86 (5) ◽  
pp. 1603-1609 ◽  
Author(s):  
Syed R. Akhter ◽  
Hiroyuki Ikezaki ◽  
Xiao-Pei Gao ◽  
Israel Rubinstein
Keyword(s):  
Substance P ◽  
Grain Sorghum ◽  
Cheek Pouch ◽  
Site Formation ◽  
Hamster Cheek Pouch ◽  
Arteriolar Diameter ◽  
Dust Extract ◽  
Significant Concentration

The purpose of this study was to determine whether dexamethasone attenuates grain sorghum dust extract-induced increase in macromolecular efflux from the in situ hamster cheek pouch and, if so, whether this response is specific. By using intravital microscopy, we found that an aqueous extract of grain sorghum dust elicited significant, concentration-dependent leaky site formation and increase in clearance of FITC-labeled dextran (FITC-dextran; mol mass, 70 kDa) from the in situ hamster cheek pouch ( P < 0.05). This response was significantly attenuated by dexamethasone (10 mg/kg iv). Dexamethasone also attenuated substance P-induced leaky site formation and increase in clearance of FITC-dextran from the cheek pouch but had no significant effects on adenosine-induced responses. Dexamethasone had no significant effects on arteriolar diameter in the cheek pouch. On balance, these data indicate that dexamethasone attenuates grain sorghum dust extract- and substance P-induced increases in macromolecular efflux from the in situ hamster cheek pouch in a specific fashion.

Neurogenic plasma exudation mediates grain dust-induced tissue injury in vivo

1997 ◽  
Vol 272 (2) ◽  
pp. R475-R481 ◽  
Author(s):  
X. P. Gao ◽  
S. Von Essen ◽  
I. Rubinstein
Keyword(s):  
Oral Mucosa ◽  
Tissue Injury ◽  
Fluorescein Isothiocyanate ◽  
Grain Sorghum ◽  
Cheek Pouch ◽  
Site Formation ◽  
Hamster Cheek Pouch ◽  
Plasma Exudation ◽  
Neurokinin 1

The purpose of this study was to determine whether an aqueous extract of grain sorghum dust (GDE) elicits neurogenic plasma exudation in the oral mucosa in vivo. Using intravital microscopy, we found that GDE elicited significant, concentration-dependent leaky site formation and an increase in clearance of fluorescein isothiocyanate-labeled dextran (FITC-dextran; mol mass 70 kDa) from the hamster cheek pouch (P < 0.05). The selective, nonpeptide neurokinin(1) (substance P) receptor antagonists, CP-96,345 and RP-67580, but not the 2R,3R enantiomer CP-96,344, significantly attenuated GDE-induced leaky site formation and increase in clearance of FITC-dextran (P < 0.05). Indomethacin had no significant effects on GDE-induced responses. CP-96,345 had no significant effects of adenosine-induced leaky site formation and increase in clearance of FITC-dextran from the cheek pouch. We conclude that GDE elicits neurogenic plasma exudation from the oral mucosa in vivo. We suggest that this process is one mechanism whereby grain sorghum dust elicits immediate oral mucosa inflammation in vivo.

Tannic acid elicits neurogenic plasma exudation from the in situ hamster cheek pouch

1998 ◽  
Vol 274 (1) ◽  
pp. R237-R242
Author(s):  
Xiao-Pei Gao
Keyword(s):  
Tannic Acid ◽  
Biosynthetic Pathway ◽  
Fluorescein Isothiocyanate ◽  
Cheek Pouch ◽  
Site Formation ◽  
Hamster Cheek Pouch ◽  
Plasma Exudation ◽  
Synthase Inhibitor

The purpose of this study was to determine whether tannic acid elicits neurogenic plasma exudation from the oral mucosa in vivo and, if so, whether this response is transduced in part by thel-arginine-nitric oxide (NO) biosynthetic pathway. Using intravital microscopy, we found that suffusion of tannic acid elicits significant concentration-dependent leaky site formation and increase in clearance of fluorescein isothiocyanate-dextran (molecular mass 70 kDa) from the in situ hamster cheek pouch ( P < 0.05). These effects are significantly attenuated by two selective, but structurally distinct, nonpeptide neurokinin-1 (NK1) receptor antagonists, CP-96,345 and RP-67580, but not by CP-96,344, the 2R,3R enantiomer of CP-96,345. N G-nitrol-arginine methyl ester (l-NAME), an NO synthase inhibitor, but notd-NAME, significantly attenuates tannic acid-induced responses.l-Arginine, but notd-arginine, reverses the attenuating effects of l-NAME. We conclude that tannic acid elicitsl-arginine-NO biosynthetic pathway-dependent neurogenic plasma exudation from the in situ hamster cheek pouch.

Ovalbumin increases macromolecular efflux from the in situ nasal mucosa of allergic hamsters

1998 ◽  
Vol 84 (1) ◽  
pp. 169-176 ◽  
Author(s):  
Xiao-Pei Gao ◽  
Syed R. Akhter ◽  
Israel Rubinstein
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Nasal Mucosa ◽  
Biosynthetic Pathway ◽  
Fluorescein Isothiocyanate ◽  
Significant Time ◽  
Hoe 140 ◽  
Subsequent Activation

Gao, Xiao-Pei, Syed R. Akhter, and Israel Rubinstein.Ovalbumin increases macromolecular efflux from the in situ nasal mucosa of allergic hamsters. J. Appl. Physiol. 84(1): 169–176, 1998.—The purpose of this study was to determine whether bradykinin mediates ovalbumin-induced increase in macromolecular efflux from the nasal mucosa of ovalbumin-sensitized hamsters in vivo and, if so, whether thel-arginine/nitric oxide biosynthetic pathway transduces, in part, this response. We found that suffusion of ovalbumin onto the in situ nasal mucosa of ovalbumin-sensitized hamsters, but not of controls, elicited a significant time- and concentration-dependent increase in clearance of fluorescein isothiocyanate-labeled dextran (mol mass, 70 kDa; P < 0.05). HOE-140, but not des-Arg9,[Leu8]-bradykinin, and N G-l-arginine methyl ester (l-NAME), but not N G-d-arginine methyl ester, significantly attenuated ovalbumin-induced responses.l-Arginine, but notd-arginine, abolished the effects ofl-NAME.l-NAME also significantly attenuated bradykinin-, but not adenosine- induced increase in macromolecular efflux from the in situ nasal mucosa. Overall, these data suggest that ovalbumin increases macromolecular efflux from the in situ nasal mucosa of ovalbumin-sensitized hamsters, in part, by producing bradykinin with subsequent activation of thel-arginine/nitric oxide biosynthetic pathway.

Differential expression of two isoforms of the neurokinin-1 (substance P) receptor in vivo

1996 ◽  
Vol 719 (1-2) ◽  
pp. 8-13 ◽  
Author(s):  
Patrick W. Mantyh ◽  
Scott D. Rogers ◽  
Joseph R. Ghilardi ◽  
John E. Maggio ◽  
Christopher R. Mantyh ◽  
...  
Keyword(s):  
Substance P ◽  
Differential Expression ◽  
Substance P Receptor ◽  
Neurokinin 1

Paradoxical effect of salbutamol in a model of acute organophosphates intoxication in guinea pigs: role of substance P release

2007 ◽  
Vol 292 (4) ◽  
pp. L915-L923 ◽  
Author(s):  
Jaime Chávez ◽  
Patricia Segura ◽  
Mario H. Vargas ◽  
José Luis Arreola ◽  
Edgar Flores-Soto ◽  
...  
Keyword(s):  
Substance P ◽  
Guinea Pigs ◽  
Smooth Muscle Contraction ◽  
In Vivo Experiments ◽  
Intracellular Ca ◽  
Neurokinin 1 ◽  
Substance P Release

Organophosphates induce bronchoobstruction in guinea pigs, and salbutamol only transiently reverses this effect, suggesting that it triggers additional obstructive mechanisms. To further explore this phenomenon, in vivo (barometric plethysmography) and in vitro (organ baths, including ACh and substance P concentration measurement by HPLC and immunoassay, respectively; intracellular Ca2+ measurement in single myocytes) experiments were performed. In in vivo experiments, parathion caused a progressive bronchoobstruction until a plateau was reached. Administration of salbutamol during this plateau decreased bronchoobstruction up to 22% in the first 5 min, but thereafter airway obstruction rose again as to reach the same intensity as before salbutamol. Aminophylline caused a sustained decrement (71%) of the parathion-induced bronchoobstruction. In in vitro studies, paraoxon produced a sustained contraction of tracheal rings, which was fully blocked by atropine but not by TTX, ω-conotoxin (CTX), or epithelium removal. During the paraoxon-induced contraction, salbutamol caused a temporary relaxation of ∼50%, followed by a partial recontraction. This paradoxical recontraction was avoided by the M2- or neurokinin-1 (NK1)-receptor antagonists (methoctramine or AF-DX 116, and L-732138, respectively), accompanied by a long-lasting relaxation. Forskolin caused full relaxation of the paraoxon response. Substance P and, to a lesser extent, ACh released from tracheal rings during 60-min incubation with paraoxon or physostigmine, respectively, were significantly increased when salbutamol was administered in the second half of this period. In myocytes, paraoxon did not produce any change in the intracellular Ca2+ basal levels. Our results suggested that: 1) organophosphates caused smooth muscle contraction by accumulation of ACh released through a TTX- and CTX-resistant mechanism; 2) during such contraction, salbutamol relaxation is functionally antagonized by the stimulation of M2 receptors; and 3) after this transient salbutamol-induced relaxation, a paradoxical contraction ensues due to the subsequent release of substance P.

Neural regulation of lysozyme secretion from tracheal submucosal glands of ferrets in vivo

1991 ◽  
Vol 71 (3) ◽  
pp. 939-944 ◽  
Author(s):  
B. Davis ◽  
H. C. Tseng
Keyword(s):  
Substance P ◽  
Peripheral Nerves ◽  
Specific Marker ◽  
Cell Secretion ◽  
P Content ◽  
Submucosal Glands ◽  
Serous Cell ◽  
The Central Nervous System

To investigate how central and peripheral nerves affect lysozyme secretion from tracheal submucosal glands in ferrets we injected substance P (20 nmol/kg in 200 microliters) intracisternally or intravenously into anesthetized artificially ventilated ferrets. We collected 3-ml samples from a perfused (3 ml/5 min) segment of trachea in situ during 15 min before and 45 min after injection of substance P. Content of lysozyme, a specific marker of tracheal submucosal gland serous cell secretion in ferrets, was measured spectrophotometrically in each sample. Intracisternal substance P increased peak lysozyme output threefold compared with baseline. This increase was abolished completely by cutting both superior laryngeal nerves (SLN) and was partially inhibited by atropine, phentolamine, or propranolol. Intravenous substance P increased peak lysozyme output 10-fold compared with baseline. This increase was partly abolished by cutting both SLN. We concluded that intracisternal substance P stimulated the central nervous system (CNS) and activated cholinergic, adrenergic, and nonadrenergic noncholinergic secretomotor nerves to tracheal glands and that intravenous substance P increased lysozyme secretion both by acting directly on tracheal glands and indirectly on the CNS to activate secretomotor nerves.

scholarly journals Dexamethasone attenuates acute macromolecular efflux increase evoked by smokeless tobacco extract

1999 ◽  
Vol 87 (2) ◽  
pp. 619-625 ◽  
Author(s):  
Xiao-Pei Gao ◽  
Syed R. Akhter ◽  
Hiroyuki Ikezaki ◽  
Dennis Hong ◽  
Israel Rubinstein
Keyword(s):  
Oral Mucosa ◽  
Smokeless Tobacco ◽  
Fluorescein Isothiocyanate ◽  
Cheek Pouch ◽  
Site Formation ◽  
Hamster Cheek Pouch ◽  
Acute Increase ◽  
Tobacco Extract

The purpose of this study was to determine whether dexamethasone attenuates the acute increase in macromolecular efflux from the oral mucosa elicited by an aqueous extract of smokeless tobacco (STE) in vivo, and, if so, whether this response is specific. Using intravital microscopy, we found that 20-min suffusion of STE elicited significant, concentration-related leaky site formation and an increase in clearance of fluorescein isothiocyanate-labeled dextran (FITC-dextran; mol mass 70 kDa) from the in situ hamster cheek pouch ( P < 0.05). This response was significantly attenuated by dexamethasone (10 mg/kg iv). Dexamethasone also attenuated the bradykinin-induced leaky site formation and the increase in clearance of FITC-dextran from the cheek pouch. However, it had no significant effects on adenosine-induced responses. Dexamethasone had no significant effects on baseline arteriolar diameter and on bradykinin-induced vasodilation in the cheek pouch. Collectively, these data indicate that dexamethasone attenuates, in a specific fashion, the acute increase in macromolecular efflux from the in situ oral mucosa evoked by short-term suffusion of STE. We suggest that corticosteroids mitigate acute oral mucosa inflammation elicited by smokeless tobacco.

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