Elastase in hyperpnea-induced guinea pig airway constriction
Research article published in 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.
Resumen
Research article relevant to leech therapy and its derived compounds.
Por qué esto importa para la hirudoterapia
Este estudio examinó si la elastasa endógena desempeña un papel en la constricción de las vías aéreas inducida por hiperpnea isocápnica en cobayos anestesiados, empleando el inhibidor de elastasa eglin-c a través de tres condiciones experimentales. La eglin-c atenuó significativamente las disminuciones inducidas por la hiperpnea en la distensibilidad respiratoria dinámica, el flujo espiratorio forzado y el flujo espiratorio máximo, sin afectar significativamente la función pulmonar durante la ventilación con aire normal. El pretratamiento con el compuesto 48/80, un agente desgranulador de mastocitos, atenuó de forma similar la broncoconstricción, lo que sugiere que la elastasa liberada por los mastocitos contribuye a la constricción de las vías aéreas inducida por la hiperpnea. El resumen identifica a la eglin-c únicamente como un inhibidor de elastasa y no contiene ninguna referencia a sanguijuelas, saliva de sanguijuela, origen en sanguijuelas ni hirudoterapia; el estudio es una investigación en modelo animal sin participación de sanguijuelas.
Citación
Elastase in hyperpnea-induced guinea pig airway constriction
Lai YL · European journal of pharmacology, 1998
Contexto clínico relacionado
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Añadido a la biblioteca ASH: May 27, 2026 · Última actualización del sitio: 18 de junio de 2026