Why the study?
It is unclear whether anticipatory cardiovascular responses occur before pain stimulation after repetitive pain experiences and how nitrous oxide/oxygen inhalation affects these responses.
Does 40% nitrous oxide/oxygen inhalation attenuate anticipatory cardiovascular responses to repetitive pain experiences in young adults?
Does 40% nitrous oxide/oxygen inhalation attenuate anticipatory cardiovascular responses to repetitive pain experiences in young adults?
Repetitive pain induces a feedforward heart rate increase, and while 40% nitrous oxide decreases vascular stiffness, it only attenuates anticipatory pressor responses when this feedforward heart rate increase is absent.
Repetitive pain may evoke anticipatory HR rises attenuated by N2O; leaves open relevance to procedural sedation or pain management.
Background Repetitive experiences of certain stresses evoke feedforward cardiovascular responses via central command (CC)--central signals from the higher brain. However, it is unclear whether the anticipatory cardiovascular responses before pain stimulation occur after repetitive pain experiences and how nitrous oxide/oxygen inhalation (N 2 O), a sedative widely used in dentistry, affects the responses. We tested the hypothesis that the repetitive cold pressor test (CPT) alters the anticipatory cardiovascular responses, which are attenuated by N 2 O. Materials and methods Beat-to-beat systolic (SBP) and diastolic blood pressure (DBP), heart rate (HR), and finger arterial stiffness ( β -stiffness) were measured during the 5-min rest, 30-s countdown (CD) before CPT, 2-min CPT, and 3-min recovery (CPT [1st] ) in 15 young adults [age, 28 ± 4 years]. The same protocols were repeated randomly with the second CPT (CPT + CC) or placebo test (PLCB + CC). Results SBP and DBP increased from baseline in CPT [1st] and CPT + CC under room air (RA) and 40 % N 2 O, while SBP was lower under N 2 O than under RA in CPT [1st] . HR in CPT [1st] was lower under N 2 O than under RA. The change (Δ) in HR was smaller during CPT [1st] than during CPT + CC under N 2 O, and a similar trend was observed under RA. ΔSBP by CD was lower under N 2 O than under RA in CPT [1st] but not in CPT + CC. HR increased with CD in CPT + CC but not in CPT [1st] under both RA and N 2 O. β -stiffness increased by CD regardless of the pain experience, while it was lower under N 2 O. Conclusion Repetitive pain experiences induce a feedforward HR increase. 40 % N 2 O decreases vascular stiffness, which may attenuate the anticipatory pressor response only when the feedforward HR increase does not exist.
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Miyazaki et al. (2023) studied this question.
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