scholarly journals Bronchial hyperresponsiveness to histamine induced by intravenous administration of 13,14-dihydro-15-keto-prostaglandin F2.ALPHA. in guinea pigs.

1994 ◽  
Vol 103 (3) ◽  
pp. 91-99 ◽  
Author(s):  
Satoshi YODONAWA ◽  
Motohiro KUROSAWA
Keyword(s):  
Intravenous Administration ◽  
Guinea Pigs ◽  
Bronchial Hyperresponsiveness ◽  
Prostaglandin F2 Alpha

Bronchial responsiveness and inflammation in guinea pigs exposed to acrolein

1989 ◽  
Vol 66 (1) ◽  
pp. 171-178 ◽  
Author(s):  
G. D. Leikauf ◽  
L. M. Leming ◽  
J. R. O'Donnell ◽  
C. A. Doupnik
Keyword(s):  
Guinea Pigs ◽  
Inflammatory Mediator ◽  
Bronchial Hyperresponsiveness ◽  
Neutrophil Infiltration ◽  
Necessary Condition ◽  
Cellular Infiltration ◽  
Pulmonary Resistance ◽  
Bronchial Responsiveness ◽  
Prostaglandin F2 Alpha ◽  
Temporal Relationships

Bronchial hyperresponsiveness can be produced experimentally after inhalation of numerous nonimmunospecific stimuli; our objective was to determine whether acrolein, a component of cigarette smoke, could increase bronchial reactivity to intravenously administered acetylcholine in guinea pigs. Bronchial responsiveness was assessed twice before and 1, 2, 6, and 24 h after exposures to less than or equal to 0.01 (sham), 0.31, 0.67, 0.94, or 1.26 parts per million for 2 h (5–7 guinea pigs/group). To examine the possible relationships of responsiveness to inflammatory mediator release and cellular infiltration, bronchoalveolar lavage was performed in another 30 guinea pigs before (control) and 0, 1, 2, 6, or 24 h after exposures. Pulmonary resistance was increased immediately after exposure (5 min) and returned to control values within 30–60 min. Increased bronchial responsiveness was evident within 1 h and became maximal 2–4 h after exposure. The acetylcholine dose necessary to double resistance decreased from 104.2 +/- 7.3 to 79.6 +/- 15.9 at 1 h and was 32.5 +/- 7.9 at 2 h and 32.8 +/- 7.6 micrograms.kg-1 at 6 h. Increases in two eicosanoids, thromboxane B2 (from 167 +/- 21 to 314 +/- 77 pg/ml) and prostaglandin F2 alpha (from 98 +/- 20 to 285 +/- 62 pg/ml) occurred immediately after exposure, whereas an influx of neutrophils occurred 24 h later (from 2.2 +/- 1.2 to 11.3 +/- 3.6%). These temporal relationships suggest that neutrophil infiltration may be a sufficient but not a necessary condition for the onset of bronchial hyperresponsiveness and that injury to cells normally present in the lung are responsible for the mediators thought to influence bronchial responsiveness.

Intrathoracic Platelet Accumulation in the Guinea-Pig Induced by Intravenous Administration of Arachidonic Acid - Effect of Cyclooxygenase and Thromboxane Synthetase Inhibitors

1986 ◽  
Vol 56 (03) ◽  
pp. 311-317 ◽  
Author(s):  
P A Barrett ◽  
K D Butler ◽  
R A Shand ◽  
R B Wallis
Keyword(s):  
Arachidonic Acid ◽  
Blood Volume ◽  
Intravenous Administration ◽  
Guinea Pigs ◽  
Human Albumin ◽  
Thromboxane Synthetase ◽  
Acid Effect ◽  
Rapid Accumulation ◽  
Platelet Accumulation ◽  
High Doses

SummaryIntravenous administration of arachidonic acid to guinea-pigs caused a dose-related, rapid accumulation of 51Cr-labelled platelets in the thorax. Inhibitors of cyclooxygenase inhibited the platelet accumulation, induced by arachidonic acid (30 mg/kg), at doses which did not alter the thoracic blood volume (as measured by 131I-labelled human albumin). Thromboxane synthetase inhibitors had different effects on platelet accumulation depending on the dose. CGS 12970 (3 mg/kg) and N(1-carboxyheptyl) imidazole (100 mg/kg) reduced platelet accumulation. High doses of CGS 12970 and CGS 13080 caused an apparent enhancement of platelet accumulation which was associated with pooling of blood in the thorax, as measured by either 131I-labelled human albumin or 51Cr-labelled erythrocytes. This increase in thoracic blood volume was abolished if the guinea-pigs were also pretreated with diclofenac (1 mg/kg) in addition to the thromboxane synthetase inhibitor. Increases in thoracic blood volume were also obtained following infusions of PGI2 but not PGD2 or PGE2.

scholarly journals Role of neutral endopeptidase in endotoxin-induced bronchial hyperresponsiveness to substance P in guinea pigs

1998 ◽  
Vol 47 (1) ◽  
pp. 13-22 ◽  
Author(s):  
Shigenori Iwamae ◽  
Hideo Tsukagoshi ◽  
Takeshi Hisada ◽  
Daisuke Uno ◽  
Masatomo Mori
Keyword(s):  
Substance P ◽  
Guinea Pigs ◽  
Bronchial Hyperresponsiveness ◽  
Neutral Endopeptidase

scholarly journals The role of cysteinyl leukotrienes on lipopolysaccharide-induced bronchial hyperresponsiveness in guinea pigs

1996 ◽  
Vol 71 ◽  
pp. 305
Author(s):  
Takashi Uno ◽  
Hiroyuki Tanaka ◽  
Yoshizou Maeda ◽  
Akifumi Kogame ◽  
Hiroichi Nagai
Keyword(s):  
Guinea Pigs ◽  
Bronchial Hyperresponsiveness ◽  
Cysteinyl Leukotrienes
Sign in / Sign up

Export Citation Format

Share Document