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Abstract

This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.

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Most cited references 36

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Human sinus arrhythmia as an index of vagal cardiac outflow.

Dwain Eckberg (1983)

Since changes of heart period follow changes of cardiac vagal efferent activity quantitatively with nearly fixed latencies, measurements of respiratory sinus arrhythmia may provide insights into human central vagal mechanisms. Accordingly, I measured intervals between heartbeats during controlled breathing (at breathing intervals of 2.5-10 s and nominal tidal volumes of 1,000 and 1,500 ml) in six healthy young men and women. As breathing interval increased, the longest heart periods became longer, the shortest heart periods became shorter, and the peak-valley P-P intervals increased asymptotically. Peak-valley P-P intervals also increased in proportion to tidal volume. However, this influence was small: a 50% increase of tidal volume increased the average peak-valley P-P interval by only about 15%. The phase angles between heart period changes and respiration varied as linear functions of breathing interval. Heart period shortening (cardioacceleration) began in inspiration at short breathing intervals and in expiration at long breathing intervals. Heart period lengthening, however, began in early expiration at all breathing intervals studied. These results point toward a close relationship between variations of respiratory depth and interval and the quantity, periodicity, and timing of vagal cardiac outflow in conscious humans. They suggest that, at usual breathing rates, phasic respiration-related changes of vagal motoneuron activity began in expiration, progress slowly, and are incompletely expressed at fast breathing rates.