Release of adrenaline by anaphylaxis in the guinea-pig: its effect on lung lipid content

Abstract

The study was undertaken to discover whether the catecholamines released as a result of the stress and hypoxia of anaphylaxis were responsible for the concomitant loss of lipid from the lung. A method is described whereby the respiratory rate and volume and heart-rate of conscious sensitized guinea-pig were measured and the electrocardiogram recorded during anaphylaxis induced by aerosolized antigen. After 7 days or more, some animals were anaesthetized with pentobarbitone and respiration was artificially maintained at the level recorded in the conscious state, whilst the quantity of catecholamines liberated during anaphylaxis was assayed using an extra-corporeal blood circulation to superfuse smooth muscle preparations. In other animals of the same group, it was shown that intravenous infusion of adrenaline in a similar quantity to that detected in the circulation following anaphylaxis (0.3 mug min-(-1) for 40 min) caused losses of triglyceride and partial glycerides from the lungs. Thus, the loss of choline-containing phospholipid was attributed to the direct effects of the anaphylactic reaction on the lung tissue.

Desensitization of β‐adrenergic receptors in lung injury induced by 2‐chloroethyl ethyl sulfide, a mustard analog

“…Morken et al [56] have shown that there is an immediate and sustained systemic elevation of catecholamines including epinephrine, which may set the stage for development of neutrophils-mediated acute lung injury. Furthermore, it has been reported that stress and hypoxia of anaphylaxis cause catecholamine release, loss of choline-containing phospholipids, and thereby ARDS [57]. A decrease in both β 2 -AR receptor and mRNA levels in response to chronic stimulation by β-AR agonists has been reported [33].…”