Role of Hyperreactivity of Bronchial and Pulmonary Vascular Muscle to Acetylcholine and Histamine in Anaphylactic Shock in Rabbits and Guinea-Pigs

1965 ◽  
Vol 27 (1) ◽  
pp. 35-45
Author(s):  
J. Ng ◽  
Y.M. Seys ◽  
G.J. Hildebrand
Keyword(s):  
Guinea Pigs ◽  
Anaphylactic Shock ◽  
Vascular Muscle

scholarly journals STUDIES ON THE LOCALIZATION OF CIRCULATING ANTIGEN-ANTIBODY COMPLEXES AND OTHER MACROMOLECULES IN VESSELS

1963 ◽  
Vol 118 (4) ◽  
pp. 503-513 ◽  
Author(s):  
Charles G. Cochrane
Keyword(s):  
Mast Cell ◽  
Guinea Pigs ◽  
Anaphylactic Shock ◽  
Disease States ◽  
Forssman Antigen ◽  
Circulating Antigen ◽  
Antigen Antibody ◽  
Direct Attack ◽  
Experimental Disease

Localization of circulating antigen-antibody complexes in vessels of guinea pigs by means of anaphylactic shock was found to be mediated by histamine that was released at the time of anaphylaxis. The source of the histamine may have been the mast cell as noted in studies employing a direct attack on the mast cells by octylamine. Platelets played apparently little to no role in guinea pigs in the anaphylactic deposition of circulating complexes. Rat anaphylatoxin was found to cause vascular localization and symptoms of anaphylaxis identical with that brought about by antigen-antibody anaphylaxis. This also was found to be dependent upon the release of histamine. Antibody against Forssman antigen in the vessel walls of the guinea pigs also led to deposition of circulating complexes. This was found not to be histamine dependent. The possible role of local increase in vascular permeability in certain experimental disease states in the localization of circulating complexes is discussed.

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.

Putative antihyperpyretic factor induced by LPS in spleen of guinea pigs

2005 ◽  
Vol 289 (3) ◽  
pp. R680-R687 ◽  
Author(s):  
Carlos Feleder ◽  
Vit Perlik ◽  
Ying Tang ◽  
Clark M. Blatteis
Keyword(s):  
Kupffer Cells ◽  
Guinea Pigs ◽  
Collateral Circulation ◽  
Splenic Vein ◽  
Inhibitory Factor ◽  
Febrile Response ◽  
Temperature Changes ◽  
The Core ◽  
Temporally Correlated

We reported previously that the onset of LPS-induced fever, irrespective of its route of administration, is temporally correlated with the appearance of LPS in the liver and that splenectomy significantly increases both the febrile response to LPS and the uptake of LPS by Kupffer cells (KC). To further evaluate the role of the spleen in LPS fever production, we ligated the splenic vein and, 7 and 30 days later, monitored the core temperature changes over 6 h after intraperitoneal (ip) injection of LPS (2 μg/kg). Both the febrile response and the uptake of LPS by KC were significantly augmented. Like splenectomy, splenic vein ligation (SVL) increased the febrile response and LPS uptake by KC until the collateral circulation developed, suggesting that the spleen may normally contribute an inhibitory factor that limits KC uptake of LPS and thus affects the febrile response. Subsequently, to verify the presence of this factor, we prepared splenic extracts from guinea pigs pretreated with LPS (8 μg/kg ip) or pyrogen-free saline, homogenized and ultrafiltered them, and injected them intravenously into splenectomized (Splex) guinea pigs pretreated with LPS (8 μg/kg ip). The results confirmed our presumption that the splenic extract from LPS-treated guinea pigs inhibits the exaggerated febrile response and the LPS uptake by the liver of Splex guinea pigs, indicating the presence of a putative splenic inhibitory factor, confirming the participation of the spleen in LPS-induced fever, and suggesting the existence of a novel antihyperpyretic mechanism. Preliminary data indicate that this factor is a lipid.

scholarly journals Role of PGE2 in Neurotransmission from Pre- to Post-Ganglionic Hypogastric Nerves of Guinea Pigs.

1992 ◽  
Vol 58 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Akikazu Fujita ◽  
Tadayoshi Takeuchi ◽  
Fumiaki Hata ◽  
Osamu Yagasaki
Keyword(s):  
Guinea Pigs

scholarly journals Role of thromboxane-A2 and cholinergic mechanisms in bronchoconstriction induced by cigarette smoke in guinea-pigs

1996 ◽  
Vol 9 (12) ◽  
pp. 2468-2473 ◽  
Author(s):  
K. Matsumoto ◽  
H. A Izawa ◽  
H. Inoue ◽  
S. Takata ◽  
M. Shigyo ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Cholinergic Mechanisms

Nitric Oxide: A Mediator in Anaphylactic Shock in Guinea-Pigs

1996 ◽  
Vol 7 (1) ◽  
Author(s):  
Yitzchak Abend ◽  
Yaakov Ashkenazy ◽  
Valentin Witzling ◽  
Dan Feigl ◽  
David Geltner ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Guinea Pigs ◽  
Anaphylactic Shock
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