• J. Auton. Nerv. Syst. · Jun 1997

    Temperature dependency of the vagal chronotropic response in the young puppy: an 'environmental-autonomic interaction'.

    • A S Pickoff, A Stolfi, and P Campbell.
    • Department of Pediatrics (Cardiology) SL-37, Tulane University School of Medicine, Tulane Hospital for Children, New Orleans, LA 70112, USA.
    • J. Auton. Nerv. Syst. 1997 Jun 6;64(2-3):107-14.

    AbstractWe investigated the effects of mild hypothermia (34.3 +/- 0.2 degrees C [mean +/- SD]), hyperthermia (40.8 +/- 0.2 degrees C) and hypoxia (PaO2 = 43 +/- 4 mmHg) on the response to heart rate to continuous right vagus nerve stimulation (the 'vagal chronotropic response') in young puppies, aged 5-22 days. Puppies were anesthetized with alpha-chloralose, vagotomized and pre-treated with propranolol (1 mg/kg i.v.) and phentolamine (1 mg/kg, 1-2 mg/kg/h i.v.). Hypoxia (n = 9) did not significantly alter the resting sinus cycle length and did not alter the response of sinus cycle to a 30 s train of 8 Hz right vagal stimulation. Mild hypothermia (n = 8) increased the resting sinus cycle length by 16 +/- 4% and greatly augmented the vagal chronotropic response (from 76 +/- 27% change in the sinus cycle length (normothermia) to 155 +/- 38% (hypothermia)). Both the sinus cycle length and the vagal chronotropic response turned towards pre-hypothermia values with rewarming. Mild hypothermia also increased the negative chronotropic response to 20 micrograms/kg/min i.v. of methacholine (12 +/- 2% change in the sinus cycle length (normothermia) versus 24 +/- 14% (hypothermia)), suggesting that a postsynaptic mechanism is involved in the hypothermia-induced augmentation of the cardiac vagal chronotropic response. In contrast to hypothermia, mild hyperthermia (n = 8) decreased the resting sinus cycle length slightly (-5 +/- 5% change) and significantly attenuated the cardiac vagal chronotropic response (from 88 +/- 28% change in sinus cycle length (normothermia) to 50 +/- 26% (hyperthermia)). These changes were also reversible with the re-establishment of normothermia. This demonstrates that clinically relevant, environmentally-induced changes in body temperature can directly and reversibly modify parasympathetic efferent responses.

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