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Vagal inhibition of cardiovascular activity in the decerebrate cat

RICHARD L. GLASSER

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Abstract

Cardiovascular responses after decerebration at three levels of the central neuraxis and subsequent vagotomy were studied in the cat. Midpontile decerebration produced a marked, transient depression in heart rate and arterial blood pressure, from which recovery to and sometimes above pretransection levels usually occurred within 30 min. Subsequent vagotomy in the midpontile decerebrate animals produced marked tachycardia and hypertension. This cardiovascular hyperactivity, particularly hypertension, was conspicuously diminished by stimulation of the central ends of the sectioned vagi. In distinct contrast to the dramatic augmentation of cardiovascular activity after vagotomy in the midpontile animals, vagotomy in midmesencephalic and medullary animals typically produced moderate and transient elevations in heart rate and blood pressure. These data support the concept of a cardiovascular-augmenter area in the caudal pons and a cardiovascular-depressor area in a more rostral portion of the brain stem. These data suggest that the vagal system antagonizes and masks a potential cardiovascular hyperactivity in the midpontile decerebrate animal.

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Cardiovascular responses after decerebration at three levels of the central neuraxis and subsequent vagotomy were studied in the cat. Midpontile decerebration produced a marked, transient depression in heart rate and arterial blood pressure, from which recovery to and sometimes above pretransection levels usually occurred within 30 min. Subsequent vagotomy in the midpontile decerebrate animals produced marked tachycardia and hypertension. This cardiovascular hyperactivity, particularly hypertension, was conspicuously diminished by stimulation of the central ends of the sectioned vagi. In distinct contrast to the dramatic augmentation of cardiovascular activity after vagotomy in the midpontile animals, vagotomy in midmesencephalic and medullary animals typically produced moderate and transient elevations in heart rate and blood pressure. These data support the concept of a cardiovascular-augmenter area in the caudal pons and a cardiovascular-depressor area in a more rostral portion of the brain stem. These data suggest that the vagal system antagonizes and masks a potential cardiovascular hyperactivity in the midpontile decerebrate animal.

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Available abstract

Cardiovascular responses after decerebration at three levels of the central neuraxis and subsequent vagotomy were studied in the cat. Midpontile decerebration produced a marked, transient depression in heart rate and arterial blood pressure, from which recovery to and sometimes above pretransection levels usually occurred within 30 min. Subsequent vagotomy in the midpontile decerebrate animals produced marked tachycardia and hypertension. This cardiovascular hyperactivity, particularly hypertension, was conspicuously diminished by stimulation of the central ends of the sectioned vagi. In distinct contrast to the dramatic augmentation of cardiovascular activity after vagotomy in the midpontile animals, vagotomy in midmesencephalic and medullary animals typically produced moderate and transient elevations in heart rate and blood pressure. These data support the concept of a cardiovascular-augmenter area in the caudal pons and a cardiovascular-depressor area in a more rostral portion of the brain stem. These data suggest that the vagal system antagonizes and masks a potential cardiovascular hyperactivity in the midpontile decerebrate animal.

Key concepts: Decerebration, Vagotomy, Heart rate, Medicine, Blood pressure, Anesthesia, Internal medicine, Decerebrate State

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