Amerikanische Gesellschaft für Hirudotherapie

Elastase in hyperpnea-induced guinea pig airway constriction

Research article published in European journal of pharmacology (1998)

Zuletzt aktualisiert: June 18, 2026Geprüft von: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Preclinical (animal)ArzneimittelentwicklungLai YL · European journal of pharmacology, 1998

Abstract

Aerosolized elastase has been shown to produce airway constriction in guinea pigs. In this study, we examined whether endogenous elastase plays a role in isocapnic hyperpnea-induced airway constriction using an elastase inhibitor, eglin-c. The study was divided into three experiments. In the first experiment, we used an elastase inhibitor, eglin-c, to suppress hyperpnea-induced bronchoconstriction. Twenty-two young male Hartley guinea pigs were divided into three groups: control (n=8), eglin-c(1) (a lower dose of eglin-c, n=7), and eglin-c(2) (a higher dose of eglin-c, n=7). In the second experiment, we tested whether eglin-c affects pulmonary function following 15 min of normal air ventilation in two groups of animals: control (n=8) and eglin-c (n=8). In the third experiment, animals were divided into two groups: control (n=7) and compound 48/80 (a mast cell degranulating agent, n=7). Airway function was examined in the anesthetized-paralyzed animal. In the first and third experiments, 15 min of isocapnic hyperpnea caused marked decreases in dynamic respiratory compliance, forced expiratory flow at 0.1 s and maximal expiratory flow at 50% total lung capacity, demonstrating hyperpnea-induced airway constriction. This bronchoconstriction was significantly attenuated by eglin-c and by pretreatment with compound 48/80. In the second experiment, eglin-c did not significantly affect bronchial function following normal air ventilation. These data suggest that elastase released from mast cells directly or indirectly induces hyperpnea-induced bronchoconstriction.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal ArticleResearch Support, Non-U.S. Gov't
Indexed MeSH termsAnimalsBody WeightBronchoconstrictionGuinea PigsHyperventilationLungMalePancreatic ElastasePeak Expiratory Flow RateProteinsRespiratory Function TestsSerpins

Zusammenfassung

Research article relevant to leech therapy and its derived compounds.

Warum dies für die Hirudotherapie relevant ist

This study examined whether endogenous elastase plays a role in isocapnic hyperpnea-induced airway constriction in anesthetized guinea pigs, using the elastase inhibitor eglin-c across three experimental conditions. Eglin-c significantly attenuated hyperpnea-induced decreases in dynamic respiratory compliance, forced expiratory flow, and maximal expiratory flow, while not significantly affecting pulmonary function during normal air ventilation. Pretreatment with compound 48/80, a mast cell degranulating agent, similarly attenuated bronchoconstriction, suggesting that elastase released from mast cells contributes to hyperpnea-induced airway constriction. The abstract identifies eglin-c only as an elastase inhibitor and contains no reference to leeches, leech saliva, leech origin, or hirudotherapy; the study is an animal model investigation with no leech involvement.

Zitation

Elastase in hyperpnea-induced guinea pig airway constriction

Lai YL · European journal of pharmacology, 1998

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