This preclinical study demonstrates that respiratory changes, specifically reflexly induced apnoea, differentially modulate the cardiovascular reflexes elicited by cardiac receptor and carotid chemoreceptor stimulation in cats.
Apnoea enhances cardio-inhibitory but not vasodilator responses to cardiac receptor stimulation in cats; leaves open relevance to human reflex control.
In cats anaesthetized with a mixture of chloralose and urethane, stimulation of cardiac receptors by left atrial injections of veratridine had little or no effect on pulmonary ventilation but caused bradycardia, systemic hypotension and hindlimb vasodilation with a latency of 3.3 s. 2. The hindlimb vasodilatation was due largely, if not entirely, to a reduction in sympathetic vasoconstrictor activity. 3. Similar cardiovascular responses occurred when the arterial blood pressure was maintained constant and also in artificially ventilated animals. 4. When the cardiac receptors were excited during a period of apnoea which was induced reflexly by electrical stimulation of the central cut end of a superior laryngeal nerve, the cardio-inhibitory response to left atrial injections of veratridine was enhanced but the size of the vasodilator response was unaffected. 5. In contrast, the cardiovascular effects of stimulation of the carotid body chemoreceptors, bradycardia and hindlimb vasoconstriction were enhanced by the laryngeal input. 6. The possible central mechanism responsible for the differential modulation of cardiac receptor and carotid chemoreceptor reflexes by respiration are discussed.
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Daly et al. (1988) studied this question.
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