PubMed Health⌕ Search

Biomedical subjects

A A Mathé

Publications and source records attributed to A A Mathé.

10 recordsLinked to original sources
PubMed1978

Effect of histamine on cyclic AMP levels in control and antigen-sensitized guinea pig lungs.

The effect of histamine on cyclic AMP was investigated in control and antigen-sensitized guinea pig lungs. Although histamine elevated the cyclic AMP levels in a dose-dependent manner in both groups, the response was consistently smaller in the sensitized lungs. In vivo pretreatment of control guinea pigs with histamine decreased the subsequent effect of exogenous histamine on cyclic AMP. Phosphodiesterase activity was not different in the two groups and it was not affected by histamine. These results indicate that the process of antigen sensitization results in an altered cyclic AMP response to histamine.

Animals↗
PubMed1977

Prostaglandin release by slow reacting substance from guinea pig and human lung tissue.

Slow reacting substance (SRS) injected into the pulmonary artery released prostaglandins E (PGE) and F2alpha (PGF2alpha) and the 15-keto-13, 14-dihydro PG metabolites from non-sensitized and ovalbumin sensitized, isolated, perfused guinea pig lungs. PGs were also released from lungs incubated with SRS. Sensitized lungs released more PGs in both types of preparations. Indomethacin inhibited the effect of SRS. Passively sensitized human lung fragments, in parallel to guinea pig lung, released PGE, PGF2alpha and the metabolites when incubated with SRS or antigen. In in vivo experiments, SRS and arachidonic acid given intravenously increased the airway insufflation pressure in anesthetized quinea pigs. These effects, but not the action of injected PGF2alpha and histamine, were abolished by indomethacin. The results indicate that one of the modes of SRS action is by release of PGs, and are consistent with the hypothesis that PGs are predominantly "secondary" mediators (in the temporal sense) of the antigen-antibody reaction.

Airway Resistance↗
PubMed1977

Release of histamine and formation of prostaglandins in human lung tissue and rat mast cells.

Release of histamine and prostaglandins (PGs) from human lung tissue and rat mast cells was investigated. Passively sensitized lung fragments released PGE, PGF2alpha and the 15-ketodihydro metabolites into the media with time alone. Antigen challenge liberated 20% tissue histamine and there was a twofold increase in PGs. Twice as much PGF2alpha as PGE was found. beta-Adrenergic agonists inhibited the anaphylactic release of mediators and this action was blocked by propranolol. Both PGF2alpha and PGE were consistently found in the mast cell media, demonstrating that mast cells can synthesize PGs. Anaphylaxis induced a marked liberation of histamine but not of PGs. The results indicate that the release of histamine may precede the major release of PGs and suggest that the bulk of PGs may derive from cells in the proximity of the mast cells.

Adrenergic Agonists↗
PubMed1976

Effect of epinephrine on cyclic AMP levels and adenylate cyclase and phosphodiesterase activities in control and antigen-sensitized guinea pig lungs.

Cyclic AMP levels and adenylate cyclase and phosphodiesterase activities were measured in control and ovalbumin-sensitized guinea pig lungs. Cyclic AMP levels were raised by epinephrine (0.01-10 mug/ml) in both control and sensitized lungs; the response being larger in the former group. Epinephrine (10(-9) -10(-6) M) stimulated adenylate cyclase in sensitized but had only a minimal effect in control preparations. Phosphodiesterase activities were equal in both groups. The hypersensitivity of adenylate cyclase response to epinephrine concurrent with diminished accumulation of cyclic AMP in sensitized guinea pigs indicate that antigen sensitization alters the response of the cyclic AMP system to epinephrine.

Adenylyl Cyclases↗