Nitrous oxide inhalation was reported to suppress pressor response to pain stimulation, while an increase in heart rate (HR) remained unchanged. We evaluated whether nitrous oxide inhalation attenuates an increase in muscle sympathetic nerve activity (MSNA) during cold stress. MSNA (microneurography), arm cuff and beat‐to‐beat blood pressure (BP), and HR were measured during 5‐min baseline, 2‐min cold pressor test (CPT) in 12 young men [30±1 (SE) yrs] after they receive room air, 100% oxygen, 30%, and 40% nitrous oxide for 20 min through a mask, respectively. BP increased during CPT in all conditions, while the increase of systolic BP tended to be smaller during inhalation of 40% nitrous oxide than room air (26±5 vs 15±4 mmHg, P=0.081). HR also increased during CPT without any difference the increase between the conditions. MSNA burst frequency increased during CPT, while the increase was smaller during the inhalation of 40% nitrous oxide than room air (21±4 vs 12±3 burst/min, P=0.045). Change (Δ) in systolic BP during CPT was correlated with ΔMSNA burst frequency (r=0.40), but not ΔHR (r=0.06) in all conditions. These results suggest that suppressed pressor response to pain stimuli by inhalation of nitrous oxide is attributable to the attenuation of increase in muscle sympathetic nerve activity.Supported by JSPSKAKENHI70566661.
Background Procedural sedation with propofol is widely used to reduce stress and suppress cardiovascular responses to anxiety and fear during medical and dental treatments. A well‐known adverse event of propofol is a decrease in peripheral vascular resistance resulting in hypotension; however, the effects on intravascular pressure at the central arteries are unknown. Intravascular pressure is formed by the synthesis of reflected waves from the periphery with forward pulse waves produced during ejection, and the augmented pressure by the reflected waves is one of the determinants of the systolic blood pressure (BP) at the central arteries and is known to be related to cardiovascular events. We tested the hypotheses that propofol reduces the augmentation index (AIx) in the carotid artery and that the reduction is caused by a delay in the arrival time of the reflected wave (Tr). Methods Beat‐by‐beat finger BP and heart rate (HR) were continuously recorded in seven healthy young men (Age: 30 ± 2 years). Central BP, AIx, Tr of the carotid artery, and carotid‐to‐femoral pulse wave velocity (cfPWV) were measured using applanation tonometry during supine rest before (BL) and 20 min after the onset of continuous administration of propofol (PRO). This study was approved by the Institutional Review Board of Matsumoto Dental University. Results Systolic BP was lower in PRO than in BL (P < 0.001) in both peripheral and central arteries, while it was lower in the central artery than in the peripheral artery in PRO (80 ± 5 and 96 ± 6 mmHg, P < 0.001). HR in PRO remained unchanged from BL. AIx was decreased (−40.9 ± 10.3 vs −11.8 ± 11.3%, P < 0.001), and Tr was prolonged (199 ± 14 vs 173 ± 8 ms, P < 0.001) in PRO than in BL at the carotid artery. A negative correlation was found between AIx and Tr (r = −0.91, P < 0.001). Furthermore, Tr was negatively correlated with cfPWV (r = −0.72, P = 0.004), but not with the effective reflected length (P = 0.291). Conclusions Since propofol delayed the time when the reflected wave reached the large vessels, the interval between the peaks of the forward wave and the reflected wave widened, resulting in a decreased peak value of the augmented pressure. These results suggest that the carotid artery pressure is decreased by propofol‐induced reduction in augmentation pressure, which is dependent on the delay in the arrival time of the reflected wave to the central arteries.
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