EFFECT OF ALVEOLAR HYPOXIA ON PULMONARY VASCULAR RESISTANCE.
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A method is described for the partial purification of hog's antral gastrin by gel filtration and ion-exchange chromatography. Gastrin was assayed by its effect on the pH of the effluent fluid from the perfused lumen of the stomach of the anaesthetized rat. The latency of the response to gastrin given intravenously was shorter than the latency to a similar dose of histamine. The response to gastrin injected into the arterial circulation of the stomach appeared sooner than the response to gastrin injected intravenously. Iproniazid and aminoguanidine potentiated responses to gastrin. Incubation in vitro with monamine oxidase or diamine oxidase did not inactivate gastrin. Chlorpromazine and bromolysergic acid diethylamide, in doses which enhance the effects of histamine on acid gastric secretion, did not affect responses to gastrin.
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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.
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