Mild dehydration modifies the cerebrovascular response to the cold pressor test

Abstract

New Findings r 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. r 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 CO 2 . 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 (MCAv mean ). Hydration status is not commonly reported when conducting this test, yet blood viscosity alone can modulate MCAv mean , potentially modifying the MCAv mean 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 CO 2 (P ET,CO 2 ) 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 < 0.01). The MAP and HR responses were not different between treatments (both P > 0.05). After 90 s of immersion, the change in MCAv mean 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,CO 2 (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,CO 2 and, ultimately, blunting the MCAv mean response.

Cerebrovascular response to the cold pressor test – the critical role of carbon dioxide

“…A recent study investigated the effects of hydration status on the middle cerebral artery mean blood velocity (MCAv) response to CPT and found that MCAv increased during CPT, but this response was attenuated in dehydrated individuals (Perry et al . ). The authors speculated that their results were attributed to a hyperventilation‐related reduction in , probably because of an elevated pain response in the dehydrated individuals (Perry et al .…”

“…The authors speculated that their results were attributed to a hyperventilation‐related reduction in , probably because of an elevated pain response in the dehydrated individuals (Perry et al . ). However, their assessment of CBF was only done in the middle cerebral artery (MCA) using transcranial Doppler ultrasound (TCD) and was not controlled, and emerging evidence suggests that TCD may not be a valid measurement of CBF during increased MAP and SNA (Verbree et al .…”

“…; Perry et al . ), which was probably associated with the high degrees of pain some individuals experience in the submerged limb (Duranti et al . ; Di Piero et al .…”

Pain Perception in Unresponsive Wakefulness Syndrome May Challenge the Interruption of Artificial Nutrition and Hydration: Neuroethics in Action

“…With respect to the latter, Ogino and collaborators (59) demonstrated that dehydration, in control subjects, leads to increased brain activity in the anatomical structures involved in pain perception (ACC, insula, and thalamus). Thus, dehydration may per se constitute a source of pain in healthy subjects (60). Furthermore, Perry et al (60) reported that hydration status is an important modulator of the cerebrovascular response to cold pressor tests, which are commonly used to investigate cerebrovascular regulation.…”

“…Thus, dehydration may per se constitute a source of pain in healthy subjects (60). Furthermore, Perry et al (60) reported that hydration status is an important modulator of the cerebrovascular response to cold pressor tests, which are commonly used to investigate cerebrovascular regulation. Therefore, dehydration may not only constitute a source of pain but also interfere with the ability to assess a nociceptive response in the patient.…”