Progressive development of cardiomyopathy following altered autonomic activity in status epilepticus
| Autor: | Ivan A. Sammut, Joanne C. Harrison, Morgayn I. Read, Dominic Michael McCann, D. Steven Kerr, Rebecca N. Millen |
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| Rok vydání: | 2015 |
| Předmět: |
Cardiomyopathy
Dilated Male Sympathetic nervous system Sympathetic Nervous System Physiology Aconitine Cardiomyopathy Blood Pressure Status epilepticus Autonomic Nervous System Rats Sprague-Dawley Norepinephrine Status Epilepticus Heart Rate Fibrosis Physiology (medical) Heart rate Excitatory Amino Acid Agonists medicine Animals Myocytes Cardiac Kainic Acid business.industry Myocardium Arrhythmias Cardiac Stroke Volume Stroke volume Voltage-Gated Sodium Channel Agonists medicine.disease Rats Autonomic nervous system Blood pressure medicine.anatomical_structure Anesthesia Vacuoles medicine.symptom Cardiomyopathies Cardiology and Cardiovascular Medicine business |
| Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 309:H1554-H1564 |
| ISSN: | 1522-1539 0363-6135 |
| DOI: | 10.1152/ajpheart.00256.2015 |
| Popis: | Seizures are associated with altered autonomic activity, which has been implicated in the development of cardiac dysfunction and structural damage. This study aimed to investigate the involvement of the autonomic nervous system in seizure-induced cardiomyopathy. Male Sprague-Dawley rats (320–350 g) were implanted with EEG/ECG electrodes to allow simultaneous telemetric recordings during seizures induced by intrahippocampal (2 nmol, 1 μl/min) kainic acid and monitored for 7 days. Seizure activity occurred in conjunction with increased heart rate (20%), blood pressure (25%), and QTc prolongation (15%). This increased sympathetic activity was confirmed by the presence of raised plasma noradrenaline levels at 3 h post-seizure induction. By 48 h post-seizure induction, sympathovagal balance was shifted in favor of sympathetic dominance, as indicated by both heart rate variability (LF/HF ratio of 3.5 ± 1.0) and pharmacological autonomic blockade. Functional cardiac deficits were evident at 7 and 28 days, as demonstrated by echocardiography showing a decreased ejection fraction (14% compared with control, P < 0.05) and dilated cardiomyopathy present at 28 days following seizure induction. Histological changes, including cardiomyocyte vacuolization, cardiac fibrosis, and inflammatory cell infiltration, were evident within 48 h of seizure induction and remained present for up to 28 days. These structural changes most probably contributed to an increased susceptibility to aconitine-induced arrhythmias. This study confirms that prolonged seizure activity results in acute and chronic alterations in cardiovascular control, leading to a deterioration in cardiac structure and function. This study further supports the need for modulation of sympathetic activity as a promising therapeutic approach in seizure-induced cardiomyopathy. |
| Databáze: | OpenAIRE |
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