The autonomic control of the cardiovascular system plays an important role in maintaining the arterial pressure at the levels necessary for adequate tissue perfusion. In cardiovascular diseases, the impairment of the basic reflex mechanisms that are responsible for the moment-to-moment regulation could increase sympathetic activity and is correlated with an adverse outcome. The objective of the present review was to provide information about the methodological aspects exploring cardiopulmonary and chemoreceptor reflexes. Different techniques are available and all of them include assessment of reflexes through the activation or deactivation of either the cardiopulmonary baroreceptors or chemoreceptors. Intravenous saline load, head-down tilt, passive legs raising, head-out water immersion and the application of a lower body positive pressure are the principal methods utilized for activating cardiopulmonary baroreceptors; on the contrary deactivation could be achieved by acutely induced hypovolemia by furosemide or blood donation, inflation of a congestion cuff on the thighs or application of a negative pressure on the lower body. The transient exposure to a hypoxic or a hypercapnic gas mixture is frequently used to determine the peripheral and central chemoreflexes, respectively. The reflexes are quantified by the gain between output (i.e. heart rate, sympathetic activity, vascular resistance, ventilation) and input (oxygen saturation, end-tidal CO2 or changes in central venous pressure). One important limitation in assessing the cardiopulmonary baroreflex by using currently available techniques is that the involvement of the arterial baroreflex cannot be avoided. In addition, chemoreflexes cannot be interpreted unless the breathing rate is controlled. To date, several techniques are available for the quantification of cardiopulmonary baroreceptor and chemoreceptor reflexes and could provide new information on the abnormal autonomic mechanisms contributing to the pathophysiology of several cardiovascular diseases.

Sensibilità cardiopolmonare e chemosensibilità

Iacoviello M;
2001-01-01

Abstract

The autonomic control of the cardiovascular system plays an important role in maintaining the arterial pressure at the levels necessary for adequate tissue perfusion. In cardiovascular diseases, the impairment of the basic reflex mechanisms that are responsible for the moment-to-moment regulation could increase sympathetic activity and is correlated with an adverse outcome. The objective of the present review was to provide information about the methodological aspects exploring cardiopulmonary and chemoreceptor reflexes. Different techniques are available and all of them include assessment of reflexes through the activation or deactivation of either the cardiopulmonary baroreceptors or chemoreceptors. Intravenous saline load, head-down tilt, passive legs raising, head-out water immersion and the application of a lower body positive pressure are the principal methods utilized for activating cardiopulmonary baroreceptors; on the contrary deactivation could be achieved by acutely induced hypovolemia by furosemide or blood donation, inflation of a congestion cuff on the thighs or application of a negative pressure on the lower body. The transient exposure to a hypoxic or a hypercapnic gas mixture is frequently used to determine the peripheral and central chemoreflexes, respectively. The reflexes are quantified by the gain between output (i.e. heart rate, sympathetic activity, vascular resistance, ventilation) and input (oxygen saturation, end-tidal CO2 or changes in central venous pressure). One important limitation in assessing the cardiopulmonary baroreflex by using currently available techniques is that the involvement of the arterial baroreflex cannot be avoided. In addition, chemoreflexes cannot be interpreted unless the breathing rate is controlled. To date, several techniques are available for the quantification of cardiopulmonary baroreceptor and chemoreceptor reflexes and could provide new information on the abnormal autonomic mechanisms contributing to the pathophysiology of several cardiovascular diseases.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11369/390207
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