Abstract
Even though hypoxia is known to depress the activity of many central nervous system neurons (11,12,18), CNS hypoxia increases ventilation and cardiovascular drive under some experimental and clinical conditions (1,5,8). Central hypoxia elicits the cerebral ischemic response which involves an increase in sympathetic nerve activity resulting in elevated arterial pressure, heart rate and ventricular contractility (1,8). Moreover, perfusion of hypoxic blood to the brain of the awake goat while maintaining the isolated carotid body circulation normoxic results in a tachypnea (2). In addition, hyperventilation is evoked by systemic hypoxia in the awake rat (15), cat (13), dog (3), pony (10) and goat (2) after peripheral chemoreceptor denervation. These studies suggest that central receptors exist which increase cardiorespiratory drive when stimulated by hypoxia. The recent focus of this laboratory has been to determine if hypoxia exerts a direct effect upon neurons in brain sites involved in control of the cardiovascular and respiratory systems. Our approach was to examine the in vivo and in vitro electrophysiological responses of single neurons to hypoxia (6,7,14). Our findings support the hypothesis that the inherent responses of neurons in the ventrolateral medulla (VLM) and caudal hypothalamus (CH) are involved in the coordinated response to hypoxia observed in the intact animal.
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Nolan, P.C., Dillon, G.H., Waldrop, T.G. (1995). Central Hypoxic Chemoreceptors in the Ventrolateral Medulla and Caudal Hypothalamus. In: Semple, S.J.G., Adams, L., Whipp, B.J. (eds) Modeling and Control of Ventilation. Advances in Experimental Medicine and Biology, vol 393. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1933-1_49
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DOI: https://doi.org/10.1007/978-1-4615-1933-1_49
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