title: Catecholamines in hyperpnoea-induced airway constriction of guinea pigs.
abstract: 1. We found previously that propranolol augments hyperpnoea-induced bronchoconstriction (HIB). This study was performed to investigate the underlying mechanism of this aug- menting action of propranolol. 2. In the first series, 45 young Hartley guinea-pigs were divided into five groups: control; propranolol; adrenalectomy; metoprolol and reserpine. Each animal underwent three periods: baseline, hyperpnoea, and recovery. For each animal 1 ml of arterial blood was sampled during the baseline and recovery periods. 3. Treatments of propranolol, metoprolol, and reserpine caused significant decreases in both dynamic respiratory compliance (Crs) and forced expiratory volume in 0.1 s (FEV0.1) during the baseline period. Hyperpnoea caused slight but not significant decreases in Crs, FEV0.1, and maximal expiratory flow at 50% total lung capacity (TLC) (V(max50)) during the recovery period in the control group. Propranolol, but not other treatments, significantly augmented these decreases (indicating HIB). Plasma noradrenaline and adrenaline levels in the reserpine group were not detectable. The above treatments or hyperpnoea did not induce any significant effect on the plasma noradrenaline level. Plasma adrenaline level of the control group was higher than that of either adrenalectomy or reserpine group during the baseline and the recovery periods. 4. In the second series, we avoided repeated blood samplings. Forty-eight animals were evenly divided into two groups: control and propranolol. Each group was again evenly divided into three subgroups: baseline; hyperpnoea, and recovery. Five minutes into the recovery period, we demonstrated HIB in the control group. In terms of V(max50), this HIB was significantly augmented by propranolol. Plasma noradrenaline and adrenaline levels, however, were not significantly altered by either hyperpnoea or propranolol. 5. Taken together, these data suggest that propranolol-augmented HIB has no direct relationship with decreased catecholamine activity.
authors.affiliation: Department of Physiology, College of Medicine, National Taiwan University, Taipei, Taiwan.
authors.forename: Y L
authors.initials: YL
authors.lastname: Lai
authors.forename: S C
authors.initials: SC
authors.lastname: Lee
authors.forename: L C
authors.initials: LC
authors.lastname: Lai
authors.forename: F C
authors.initials: FC
authors.lastname: Hu
authors.forename: T L
authors.initials: TL
authors.lastname: Tsai
authors.forename: Y F
authors.initials: YF
authors.lastname: Tsai
mesh_terms: D000315:Adrenalectomy; D018759:Adrenergic Uptake Inhibitors / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000403:Airway Resistance / Q000187:drug effects / Q000502:physiology; D000818:Animals; D016084:Bronchoconstriction / Q000187:drug effects / Q000502:physiology*; D002395:Catecholamines / Q000097:blood*; D006168:Guinea Pigs; D006985:Hyperventilation / Q000503:physiopathology*
chemical_list: D018759:Adrenergic Uptake Inhibitors; D000319:Adrenergic beta-Antagonists; D002395:Catecholamines