Middle cerebral artery blood flow velocity in response to lower body positive pressure

Abstract

Lower body positive pressure (LBPP) has been used in the treatment of haemorrhagic shock and in offsetting g-force induced fluid shifts. However, the middle cerebral artery blood flow velocity (MCAv) response to supine LBPP is unknown. Fifteen healthy volunteers (mean ± SD: age, 26 ± 5 year; body mass, 79 ± 10 kg; height, 174 ± 9 cm) completed 5 minutes of 20 and 40 mm Hg LBPP, in a randomized order, separated by 5 minutes rest (baseline). Beat-to-beat MCAv and blood pressure, partial pressure of end-tidal carbon dioxide (PET CO2 ) and heart rate were recorded and presented as the change from the preceding baseline. All measures were similar between baseline periods (all P>0·30). Mean arterial pressure (MAP) increased by 7 ± 6 (8 ± 7%) and 13 ± 7 mm Hg (19 ± 11%) from baseline during 20 and 40 mm Hg (P<0·01), respectively. The greater MAP increase at 40 mm Hg (P<0·01 versus 20 mm Hg) was mediated via a greater increase in total peripheral resistance (P<0·01), with heart rate, cardiac output (Model flow) and PET CO2 remaining unchanged (all P>0·05) throughout. MCAv increased from baseline by 3 ± 4 cm s(-1) (5 ± 5%) during 20 mm Hg (P = 0·003), whilst no change (P = 0·18) was observed during 40 mm Hg. Our results indicate a divergent response, in that 20 mm Hg LBPP-induced modest increases in both MCAv and MAP, yet no change in MCAv was observed at the higher LBPP of 40 mm Hg despite a further increase in MAP.

Steady‐state tilt has no effect on cerebrovascular CO2 reactivity in anterior and posterior cerebral circulations

“…; intravenous phenylephrine injection) and non‐pharmacological manipulations of MAP (Perry et al . and , lower‐body positive pressure in supine position; Ogoh et al . , intravenous volume loading), it appears that tilt has differential effects on cerebrovascular regulation compared with other stressors, probably through effects on sympathetic nervous system activation or through a balanced cerebrovascular transmural pressure in HDT.…”

High-Intensity Interval Exercise and Cerebrovascular Health: Curiosity, Cause, and Consequence

“…111 The asymmetrical CBF changes in response to acute hypertension compared with acute hypotension have been attributed, in part, 112 to a SNA-mediated role in CBF regulation. 108,113,114 Such a role may be vital in limiting hyperperfusion injury during HIT before CA is effective, particularly in populations with autonomic dysfunction who display impaired CBF regulation. 115 With this knowledge at hand, a graduated increase in exercise intensity over the first 10 seconds may limit this hyperperfusion risk by 'priming' the cerebrovasculature.…”

The effects of superimposed tilt and lower body negative pressure on anterior and posterior cerebral circulations

“…; Perry et al. ), nor on cerebrovascular reactivity to increasing and decreasing partial pressure of arterial CO 2 (PaCO 2 ) (Tymko et al. ), likely due to compensatory changes in intracranial pressure, and thus cerebral perfusion pressure (Macias et al.…”

“…These reflexes are critical for rapid regulation of heart rate and vascular resistance in humans in order to maintain mean arterial pressure (MAP), and subsequently, cerebral perfusion pressure. Recent studies have demonstrated that changes in MAP associated with steady-state tilt and lower body positive pressure (90°HUT; 90°HDT), are within the autoregulatory capacity of the brain, and thus have no effect on steady-state CBF (Gelinas et al 2012;Perry et al 2013), nor on cerebrovascular reactivity to increasing and decreasing partial pressure of arterial CO 2 (PaCO 2 ) (Tymko et al 2015), likely due to compensatory changes in intracranial pressure, and thus cerebral perfusion pressure (Macias et al 2015;Tymko et al 2015). To date, however, only one study compared regional CBF regulation during LBNP stress in supine and HUT (Deegan et al 2010), and none during HDT positions when central blood volume, intracranial pressure, and MAP are likely elevated.…”