{'fraction_non_alphanumeric': 0.024703557312252964, 'fraction_numerical': 0.015810276679841896, 'mean_word_length': 5.938356164383562, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Relationships between Responsiveness of the Bronchi to Acetylcholine and Cyclic AMP Response of Lymphocytes to Beta1‐ and Beta2‐Adrenergic Receptor Stimulation in Patients with Asthma

Decreased response of beta‐adrenergic receptor has been considered to he one of the causes of increased responsiveness of the bronchi in asthma. Since beta‐adrenergic receptor has two subtypes, beta1 and beta2, and the bronchodilating effect of beta stimulants is mediated by beta2‐receptor, responsiveness of the bronchi is expected to correlate to the cyclic AMP response of lymphocytes to a beta2‐stimulant. Responsiveness of the bronchi was expressed as respiratory threshold to acetylcholine (RT‐Ach), which was the minimal concentration of acetylcholine solution to cause an initial decrease of FEV1 of more than 20% of the baseline value. Beta1 and heta2‐responses were expressed as the increments of cyclic AMP content of 106 lymphocytes incubated with norepinephrine (beta1‐stimulant) and salbutamol (beta2‐stimulant).