Mechanical properties of the canine mitral valve: effects of autonomic stimulation
| Autor: | Donald V. Priola, M. B. Curtis |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
Inotrope
medicine.medical_specialty Sympathetic Nervous System Contraction (grammar) Physiology Heart Ventricles Autonomic Nervous System Dogs Heart Conduction System Physiology (medical) Mitral valve Internal medicine Pressure medicine Animals cardiovascular diseases Atrium (heart) Cardiac cycle business.industry Heart Electric Stimulation Electrophysiology Autonomic nervous system medicine.anatomical_structure Ventricle Circulatory system cardiovascular system Cardiology Mitral Valve Cardiology and Cardiovascular Medicine business |
| Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 262:H56-H62 |
| ISSN: | 1522-1539 0363-6135 |
| DOI: | 10.1152/ajpheart.1992.262.1.h56 |
| Popis: | Experiments were designed to determine whether the canine mitral valve actively contracts and, if so, if its mechanical activity can be modulated by the autonomic nervous system. A miniature displacement gauge was sutured to the atrial (muscular) surface of the septal leaflet in 65 dogs under pentothal sodium anesthesia during total cardiopulmonary bypass. During bypass, with blood constantly drained from the left ventricle (LV), the leaflet deflected into the LV during ventricular systole as would be expected with active contraction. With blood present in the LV, leaflet deflection was reversed, indicating a passive displacement. After application of 85% phenol to the atrial surface, ventricular displacement of the leaflet was abolished, whereas the atrial displacement was significantly augmented. There was a positive inotropic effect during sympathetic stimulation and a negative inotropic effect with parasympathetic stimulation, i.e., increased and decreased ventricular deflection, respectively. These effects of autonomic stimulation were abolished by application of phenol to the leaflet muscle. During simultaneous electrical and mechanical recordings from the valve, activation appeared to originate from the atrium, before ventricular depolarization. It was concluded that the valvular muscle actively contracts to assist in bringing the valve leaflets into early apposition. This contraction imparts a measurable level of active “stiffness” to the valve, reducing atrial displacement during ventricular systole. This “stiffness” can be modified by autonomic input and may contribute to dysfunction of morphologically normal mitral valves. |
| Databáze: | OpenAIRE |
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