Evaluation of the Autonomic Nervous System in a Canine Model of Chronic Embolic Pulmonary Hypertension
Background Sildenafil improves autonomic dysfunction caused by pulmonary hypertension (PH) in humans, but its effect is unknown in dogs with PH. This prospective study aimed to evaluate the autonomic nervous system function of a canine model of chronic embolic PH (CEPH) and the autonomic nervous sys...
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Published in | Veterinary research communications Vol. 44; no. 2; pp. 73 - 81 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Dordrecht
Springer Netherlands
01.05.2020
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | Background
Sildenafil improves autonomic dysfunction caused by pulmonary hypertension (PH) in humans, but its effect is unknown in dogs with PH. This prospective study aimed to evaluate the autonomic nervous system function of a canine model of chronic embolic PH (CEPH) and the autonomic nervous system function of a canine model of CEPH in which sildenafil was administered.
Methods
This study used five clinically healthy female beagle dogs. Evaluation parameters included hemodynamic parameters, heart rate (HR) and heart rate variability (HRV). Each evaluation parameter was compared before and after creating the CEPH model (before, BL; after, CEPH
BL
) and between the CEPH
BL
model and after the administration of sildenafil (1 mg/kg, BID) in the CEPH model dogs (CEPH
Sil
).
Results
In the CEPH
BL
model, the hemodynamic parameters indicated cardiac hypofunction, and HR was significantly increased and HRV was significantly decreased compared with BL. Further, in the CEPH
Sil
model, the hemodynamic parameters suggested improvement in cardiac function, and HRV was significantly increased.
Conclusions
From the results of the CEPH model dogs, autonomic dysfunction was shown to occur in PH dogs. In addition, the administration of 1 mg/kg of sildenafil to CEPH model dogs may improve autonomic dysfunction. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0165-7380 1573-7446 |
DOI: | 10.1007/s11259-020-09774-z |