Adult respiratory distress syndrome (ARDS): the pathophysiologic role of catecholamine-kinin interactions.
The pathophysiology of the adult respiratory distress syndrome (ARDS) seems to be based on a cybernetic imbalance of the central nervous system (CNS), with activation of secondary peripheral effectors (PE). Lung vascular hyperpermeability is a crucial feature of PE actions in ARDS. Kinins (Bk), as PE, are important vascular hyperpermeability-inducing factors, with potential participation in ARDS induction. To test this hypothesis, we produced experimental ARDS in male Wistar rats using the anterior hypothalamic nuclei lesion model. Adrenalectomy, adrenal demedullation and denervation, alpha-adrenergic blockade, and catecholamine (CA) depletion reduced ARDS severity whereas beta-adrenergic blocking and CA uptake I inhibition resulted in a potentiated aspect. The Bk depletion or inhibition of the generation of these peptides resulted in attenuation of the pathologic features of ARDS. Bk half-life prolongation produced intense potentiation of the respiratory syndrome. This work suggests that Bk and CA systems are interactive and interdependent in their pathogenic actions on lungs in ARDS, involving, probably, a reciprocally-activating mechanism.
D000313:Adrenal Medulla / Q000294:innervation; D000315:Adrenalectomy; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D007025:Anterior Hypothalamic Nucleus / Q000293:injuries; D001920:Bradykinin / Q000378:metabolism; D002199:Capillary Permeability; D002395:Catecholamines / Q000378:metabolism; D003714:Denervation; D008168:Lung / Q000098:blood supply; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012128:Respiratory Distress Syndrome / Q000503:physiopathology*
D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D001920:Bradykinin