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Cholinergic blockade and the mesenteric artery response to head‐up tilt‐induced central hypovolaemia

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The influence of muscarinic blockade on the superior mesenteric artery (SMA) response to head‐up tilt (HUT) was assessed by Doppler ultrasound in eight healthy adults pretreated with i.v. glycopyrron. During supine rest, cholinergic blockade increased heart rate from 58 ± 3 to 106 ± 6 beats min−1 (mean ± SE) and mean arterial pressure from 81 ± 3 to 97 ± 4 mmHg (P<0·01) and it reduced the cardiac stroke volume from 89 ± 6 to 59 ± 7 ml (P<0·01) with no significant effect on the SMA diameter and blood flow velocities. HUT provoked a further increase in heart rate to 134 ± 5 beats min−1(P<0·01) and a reduction in stroke volume to 45 ± 4 ml (P<0·01). The early diastolic velocity increased from −51 ± 4 to 6 ± 8 cm s−1 during the normotensive stage of HUT and further to 21 ± 9 cm s−1 during the hypotensive stage with a reduction in mean arterial pressure from 97 ± 4 to 73 ± 7 mmHg (P<0·01) but, in contrast to control HUT (without cholinergic blockade), the end‐diastolic velocity did not change significantly. Maintenance of blood velocity and diameter in spite of an increase in arterial pressure at rest indicates increased SMA impedance. Likewise, during hypovolaemia, a glycopyrron‐induced inhibition in diastolic velocity supports an increase in SMA impedance. The results indicate cholinergic vasorelaxing influence on the superior mesenteric artery both at rest and during normotensive central hypovolaemia.
Title: Cholinergic blockade and the mesenteric artery response to head‐up tilt‐induced central hypovolaemia
Description:
The influence of muscarinic blockade on the superior mesenteric artery (SMA) response to head‐up tilt (HUT) was assessed by Doppler ultrasound in eight healthy adults pretreated with i.
v.
glycopyrron.
During supine rest, cholinergic blockade increased heart rate from 58 ± 3 to 106 ± 6 beats min−1 (mean ± SE) and mean arterial pressure from 81 ± 3 to 97 ± 4 mmHg (P<0·01) and it reduced the cardiac stroke volume from 89 ± 6 to 59 ± 7 ml (P<0·01) with no significant effect on the SMA diameter and blood flow velocities.
HUT provoked a further increase in heart rate to 134 ± 5 beats min−1(P<0·01) and a reduction in stroke volume to 45 ± 4 ml (P<0·01).
The early diastolic velocity increased from −51 ± 4 to 6 ± 8 cm s−1 during the normotensive stage of HUT and further to 21 ± 9 cm s−1 during the hypotensive stage with a reduction in mean arterial pressure from 97 ± 4 to 73 ± 7 mmHg (P<0·01) but, in contrast to control HUT (without cholinergic blockade), the end‐diastolic velocity did not change significantly.
Maintenance of blood velocity and diameter in spite of an increase in arterial pressure at rest indicates increased SMA impedance.
Likewise, during hypovolaemia, a glycopyrron‐induced inhibition in diastolic velocity supports an increase in SMA impedance.
The results indicate cholinergic vasorelaxing influence on the superior mesenteric artery both at rest and during normotensive central hypovolaemia.

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