Mild dehydration modifies the cerebrovascular response to the cold pressor test

• Published in: Experimental physiology 2016-01, Vol.101 (1), p.135-142
• Main Authors: Perry, Blake G., Bear, Tracey L. K., Lucas, Samuel J. E., Mündel, Toby
• Format: Article
• Language: English
• Subjects: Adult; Arterial Pressure; Blood Flow Velocity - physiology; Cerebrovascular Circulation; Cold Temperature; Dehydration - physiopathology; Heart Rate; Humans; Immersion - physiopathology; Male; Pain Perception; Pressure; Young Adult
• ISSN: 0958-0670; 1469-445X
• DOI: 10.1113/EP085449

New Findings What is the central question of this study? The cold pressor test (CPT) is commonly used to investigate cerebrovascular regulation. Despite blood viscosity per se being able to modulate cerebral blood flow, it is unknown whether hydration status alters this response, nor is it commonly reported. We investigated the effects of mild dehydration on the cerebrovascular response to the CPT. What is the main finding and its importance? The main finding from this study is that when compared with euhydration, mild dehydration reduced cerebral blood flow via a decrease in the partial pressure of end‐tidal CO2. This demonstrates that hydration status is an important modulator of the cerebrovascular response to the CPT and should be reported and controlled for. The cold pressor test (CPT) is widely used in clinical practice and physiological research. It is characterized by a robust autonomic response, with associated increases in heart rate (HR), mean arterial pressure (MAP) and mean middle cerebral artery blood flow velocity (MCAvmean). Hydration status is not commonly reported when conducting this test, yet blood viscosity alone can modulate MCAvmean, potentially modifying the MCAvmean response to the CPT. We investigated the effect of mild dehydration on the physiological response to the CPT in 10 healthy men (mean ± SD: age 28 ± 5 years; body mass 83 ± 5 kg). All participants completed two CPTs, cold water (0°C) immersion of both feet for 90 s, with the order of the euhydration and dehydration trials counterbalanced. Beat‐to‐beat MCAv, MAP, HR and breath‐by‐breath partial pressure of end‐tidal CO2 (P ET ,CO2) were measured continuously. Participants’ pain perception was measured 1 min into the CPT using a visual analog scale (no pain = 0; maximal pain = 10). Dehydration significantly elevated plasma osmolality and urine specific gravity and reduced body mass (all P  0.05). After 90 s of immersion, the change in MCAvmean from baseline was less in the dehydration compared with the euhydration trial (change 0 ± 5 versus 7 ± 7 cm s−1, P = 0.01), as was P ET ,CO2 (change −3 ± 2 versus 0 ± 3 mmHg, P = 0.02). Dehydration was associated with greater relative pain sensation during the CPT (7.0 ± 1.3 vs 5.8 ± 1.8, P = 0.02). Our results demonstrate that mild dehydration can modify the cerebrovascular response to the CPT, with dehydration increasing perceived pain, lowering P ET ,