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At least 1,063 records · Page 59Linked to original sources
PubMed1984

Histamine and slow reacting substance in acid-induced pneumonitis.

Acid pneumonitis was produced in 18 dogs by the tracheal instillation of 3 ml/kg 0.1 N hydrochloric acid. Arterial and mixed venous oxygen tension, static compliance and pulmonary capillary wedge pressure were measured during a 2-hour observation period. Plasma histamine (measured by the enzymatic isotopic assay) increased from 1.7 +/- 0.2 ng/ml (mean +/- SE) before acid injury to 13.5 +/- 1.9 ng/ml after injury (p less than 0.05). In one group of 7 control dogs, 3 ml/kg of normal saline produced no increase in plasma histamine. Pulmonary edema secretions from acid injured animals had a histamine level of 30.3 +/- 3.8 ng/ml and slow reacting substance was detected in 7 of 11 animals. The slow reacting substance was an antihistamine-resistant, ethanol extractable substance that contracted guinea pig ileum. Lung weight-body weight ratio PaO2, and static compliance were different with acid pneumonitis compared to controls. Total protein was not different in the tracheal secretions compared to plasma. We conclude that histamine and slow reacting substance are released in this animal model of acid pneumonitis and may be important in the pathogenesis of the lung injury.

Animals↗
PubMed1980

Identification of leukotriene C-1 as a major component of slow-reacting substance from rat mononuclear cells.

Slow-reacting substance (SRS) was produced by rat peritoneal mononuclear cells after stimulation with the ionophore A23187. The SRS consisted of two main components as judged by high-pressure liquid chromatography (HPLC) on Florisil. The larger and more polar component consisted mainly of leukotriene (LT) C-1 as judged by ultraviolet spectroscopy, mass spectrometry (after desulfurization), amino acid analysis, and conversion by soybean lipoxygenase. Comparisons with authentic LTC-1 showed identity on reverse phase HPLC and guinea pig ileum bioassay. The latter methods are known to distinguish between LTC-1 and stereoisomers of LTC-1.

Amino Acids↗
PubMed1980

Effect of the 5-hydroperoxide of eicosatetraenoic acid and inhibitors of the lipoxygenase pathway on the formation of slow reacting substance by rat basophilic leukemia cells; direct evidence that slow reacting substance is a product of the lipoxygenase pathway.

Previous studies in a line of rat basophilic leukemia (RBL 1) cells have indicated that the slow reacting substance (SRS) made during stimulation with the divalent cation ionophore, A23187, is derived from arachidonic acid (AA). In the present report, various inhibitors of AA metabolism were compared with regard to their effects on SRS formation and incorporation of radioactivity from [1-14C]-AA into known metabolites of the lipoxygenase and cyclooxygenase pathways. An apparently close parallel between lipoxygenase product formation and SRS synthesis is demonstrated. In addition, exogenous 5-hydroperoxy-eicosatetraenoic acid (5-HPETE) has been shown to markedly enhance SRS synthesis, even when A23187 is absent. The data provide very strong evidence that SRS is produced through the lipoxygenase pathway.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1981

Mechanisms of contraction induced by partially purified slow reacting substance from human polymorphonuclear leukocytes and leukotriene D in guinea pig ileal smooth muscle.

On the basis of the experiments described here, we suggest that the mechanism of action of SRS in guinea pig ileal longitudinal muscle is very similar to that used by other agonists in this preparation, namely interactions at a specific receptor to activate Ca++ channels leading to Ca++ influx and mechanical response. SRS responses differ in 1 important respect from those produced by other agonists. SRS and leukotriene D cause the generation of a slower contraction, which has a greater resistance to reversal by washing. The basis for this unique and prolonged duration of action is unknown but may represent an exceptionally tight, or even irreversible, association with a membrane component. Current studies on the structure of SRS may be helpful in this regard. Although not definitive, this report clearly indicates that a SRS "receptor" is, in fact, present on smooth muscle and that it utilizes a pool of calcium channels common to all smooth muscle agonists.

Animals↗