Autonomic mechanisms associated with heart rate and vasoconstrictor reserves

Hemorrhage is accompanied by baroreflex-mediated tachycardia and vasoconstriction. The difference between baseline and maximum responses is defined as the heart rate (HR) and vasoconstrictor 'reserve'.

To test the hypothesis that higher HR and vasoconstrictor reserves in subjects with high tolerance (HT) to central hypovolemia is associated with greater reserve for sympathoexcitation and vagal withdrawal compared with low tolerant (LT) subjects.

R-R intervals (RRI), systolic arterial pressure (SAP), estimated stroke volume, and muscle sympathetic nerve activity (MSNA) were measured during lower body negative pressure (LBNP) designed to induce pre-syncope. Subjects with tolerance ≤ 60 mmHg LBNP were classified as LT (n = 22) while subjects who tolerated LBNP levels >60 mmHg were classified as HT (n = 56). Spontaneous cardiac baroreflex sensitivity (BRS) was assessed via RRI-SAP down-down sequences.

HR reserve in HT subjects (+52 ± 2 bpm) was twofold greater (P < 0.001) than that in LT subjects (+27 ± 3 bpm). Vasoconstrictor reserve in the HT group (+3.4 ± 0.5 pru) was greater (P = 0.04) than that of the LT group (+1.9 ± 0.3 pru). HT subjects demonstrated greater (P ≤ 0.03) BRS reserve (-14.2 ± 1.8 ms/mmHg) and MSNA reserve (+41 ± 2 bursts/min) compared with LT subjects (-7.4 ± 1.7 ms/mmHg and +26 ± 7 bursts/min).

Our data support the hypothesis that greater physiological reserve capacity for tachycardia and vasoconstriction related to high tolerance to central hypovolemia is associated with greater reserves for sympathoexcitation and cardiac vagal withdrawal.