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Autonomic dysfunction in experimental autoimmune neuritis: heart rate.

N Wang¹, J Chapman, R Rabinowitz

¹Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.

Journal of the Neurological Sciences

|March 10, 2001

Summary

Autonomic nervous system dysfunction in Guillain-Barré syndrome (GBS) models shows altered heart rate variability. Experimental autoimmune neuritis (EAN) rats exhibited increased heart rate variation and impaired sympathetic response.

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Area of Science:

Neuroscience
Immunology
Cardiology

Background:

Autonomic nervous system (ANS) dysfunction is a critical complication in Guillain-Barré syndrome (GBS), contributing to mortality.
Investigating ANS dysfunction in GBS animal models is crucial for understanding disease mechanisms and developing treatments.

Purpose of the Study:

To evaluate heart rate (HR) changes in an animal model of GBS, experimental autoimmune neuritis (EAN).
To assess resting HR (rHR) and stress-induced HR (sHR) in EAN rats to identify autonomic impairments.

Main Methods:

EAN was induced in rats via immunization with bovine spinal root myelin.
Heart rate was measured at rest (rHR) and during stressful stimulation (sHR) in EAN rats and compared to baseline.
Statistical analysis (F-test) was used to determine the significance of HR variations.

Main Results:

EAN rats developed motor weakness, weight loss, and hypothermia.
While mean rHR did not significantly differ, EAN rats showed increased rHR variability, with instances of bradycardia and tachycardia (P<0.01).
Significantly lower sHR in EAN rats indicated sympathetic nervous system impairment (P<0.01).

Conclusions:

EAN serves as a relevant model for studying ANS dysfunction observed in GBS.
Increased heart rate variability and impaired sympathetic response in EAN rats highlight significant autonomic deficits.
These findings provide a foundation for therapeutic strategies targeting ANS dysfunction in GBS.