Modifications in the regression of the acute inflammation caused by a beta-adrenergic effect unbalanced by the alpha-component ("biased beta-effect").
A biased beta-adrenergic effect was produced either by blocking the alpha-adrenergic component of endogenous catecholamines using phentolamine or by application of isoproterenol. Both experimental conditions led to a prolongation of the lymphocyte phase of the inflammatory process. A beta-bias also curbed the activity of a substance (or substances) inhibiting the ingress of lymphocytes into the site of inflammation (subcutaneously injected Sephadex) around the fourth and fifth day after the onset of inflammation. This lack in activity is evidently connected with the prolonged lymphocyte phase.
D000818:Animals; D002395:Catecholamines / Q000378:metabolism; D002465:Cell Movement; D003911:Dextrans; D007249:Inflammation / Q000378:metabolism* / Q000473:pathology; D007545:Isoproterenol / Q000494:pharmacology; D008214:Lymphocytes / Q000503:physiopathology; D008297:Male; D010646:Phentolamine / Q000494:pharmacology; D051381:Rats; D011941:Receptors, Adrenergic / Q000378:metabolism*; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000378:metabolism*; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000378:metabolism*
D002395:Catecholamines; D003911:Dextrans; D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; C025614:sephadex; D007545:Isoproterenol; D010646:Phentolamine