What does this research mean for the field?

Static carotid baroreceptor stimulation combined with water immersion is insufficient to fully replicate the decreases in mean arterial pressure and heart rate seen during a seated-to-supine posture change, indicating that increased pulse pressure and low-pressure receptor stimulation also contribute to these cardiovascular responses. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

June 1, 2001

Cardiovascular effects of static carotid baroreceptor stimulation during water immersion in humans

Structured PICO

Does static carotid baroreceptor stimulation during water immersion replicate the hypotensive and bradycardic effects of a seated to supine posture change in healthy males?

Population

10 seated healthy males

Intervention

Five 15-minute interventions: posture change to supine, seated water immersion to the Xiphoid process (WI), seated neck suction (NS), WI with simultaneous neck suction (-22 mmHg) (WI + NS)

Comparator

Seated control

Outcome

Mean arterial pressure (MAP) and heart rate (HR)surrogate

Static carotid baroreceptor stimulation combined with water immersion is insufficient to fully replicate the decreases in mean arterial pressure and heart rate seen during a seated to supine posture change.

Abstract

We hypothesized that the more-pronounced hypotensive and bradycardic effects of an antiorthostatic posture change from seated to supine than water immersion are caused by hydrostatic carotid baroreceptor stimulation. Ten seated healthy males underwent five interventions of 15-min each of 1) posture change to supine, 2) seated water immersion to the Xiphoid process (WI), 3) seated neck suction (NS), 4) WI with simultaneous neck suction (-22 mmHg) adjusted to simulate the carotid hydrostatic pressure increase during supine (WI + NS), and 5) seated control. Left atrial diameter increased similarly during supine, WI + NS, and WI and was unchanged during control and NS. Mean arterial pressure (MAP) decreased the most during supine (7 +/- 1 mmHg, P < 0.05) and less during WI + NS (4 +/- 1 mmHg) and NS (3 +/- 1 mmHg). The decrease in heart rate (HR) by 13 +/- 1 beats/min (P < 0.05) and the increase in arterial pulse pressure (PP) by 17 +/- 4 mmHg (P < 0.05) during supine was more pronounced (P < 0.05) than during WI + NS (10 +/- 2 beats/min and 7 +/- 2 mmHg, respectively) and WI (8 +/- 2 beats/min and 6 +/- 1 mmHg, respectively, P < 0.05). Plasma vasopressin decreased only during supine and WI, and plasma norepinephrine, in addition, decreased during WI + NS (P < 0.05). In conclusion, WI + NS is not sufficient to decrease MAP and HR to a similar extent as a 15-min seated to supine posture change. We suggest that not only static carotid baroreceptor stimulation but also the increase in PP combined with low-pressure receptor stimulation is a possible mechanism for the more-pronounced decrease in MAP and HR during the posture change.

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