期刊
CLINICAL SCIENCE
卷 106, 期 1, 页码 75-82出版社
PORTLAND PRESS
DOI: 10.1042/CS20030174
关键词
adenosine; carotid artery; chemoreceptor; chemoreflex; sympathetic nervous system
The direct vasodilatory and negative chronotropic effects of adenosine in humans are counterbalanced by a reflex increase in sympathetic nerve traffic. A suggested mechanism for this reflex includes peripheral chemoreceptor activation. We, therefore, assessed the contribution of carotid chemoreceptors to sympatho-excitation by adenosine. Muscle sympathetic nerve activity was recorded during adenosine infusion (140 mug.kg(-1).min(-1) for 5 min) in five patients lacking carotid chemoreceptors after bilateral carotid body tumour resection (one male and four female, mean age 51+/-11 years) and in six healthy controls (two male and four female, mean age 50+/-7 years). Sympathetic responses to sodium nitroprusside injections were assessed to measure baroreceptor-mediated sympathetic activation. In response to adenosine, controls showed no change in blood pressure, an increase in heart rate (+48.2+/-3.2%; P<0.003) and an increase in sympathetic nerve activity (+195&PLUSMN;103%; P<0.022). In contrast, patients showed a decrease in blood pressure (-14.6+/-4.9/-17.6+/-6.0%; P<0.05), an increase in heart rate (+25.3&PLUSMN;8.4%; P<0.032) and no significant change in sympathetic activity. Adenosine-induced hypotension in individual patients elicited less sympathetic activation than equihypotensive sodium nitroprusside injections. In humans lacking carotid chemoreceptors, adenosine infusion elicits hypotension due to the absence of significant sympatho-excitation. Chemoreceptor activation is essential for counterbalancing the direct vasodilation by adenosine. In addition, blunting of the baroreflex sympathetic response to adenosine-induced hypotension may indicate a direct sympatho-inhibitory effect of adenosine.
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