School of Health Sciences, College of Health, Massey University, Wellington, New Zealand.
School of Sport, Exercise and Nutrition, College of Health, Massey University, Palmerston North, New Zealand.
Clin Physiol Funct Imaging. 2023 Nov;43(6):463-471. doi: 10.1111/cpf.12843. Epub 2023 Jun 25.
During hyperthermia, the perturbations in mean arterial blood pressure (MAP) produced by the Valsalva manoeuvre (VM) are more severe. However, whether these more severe VM-induced changes in MAP are translated to the cerebral circulation during hyperthermia is unclear.
Healthy participants (n = 12, 1 female, mean ± SD: age 24 ± 3 years) completed a 30 mmHg (mouth pressure) VM for 15 s whilst supine during normothermia and mild hyperthermia. Hyperthermia was induced passively using a liquid conditioning garment with core temperature measured via ingested temperature sensor. Middle cerebral artery blood velocity (MCAv) and MAP were recorded continuously during and post-VM. Tieck's autoregulatory index was calculated from the VM responses, with pulsatility index, an index of pulse velocity (pulse time) and mean MCAv (MCAv ) also calculated.
Passive heating significantly raised core temperature from baseline (37.9 ± 0.2 vs. 37.1 ± 0.1°C at rest, p < 0.01). MAP during phases I through III of the VM was lower during hyperthermia (interaction effect p < 0.01). Although an interaction effect was observed for MCAv (p = 0.02), post-hoc differences indicated only phase IIa was lower during hyperthermia (55 ± 12 vs. 49.3 ± 8 cm s for normothermia and hyperthermia, respectively, p = 0.03). Pulsatility index was increased 1-min post-VM in both conditions (0.71 ± 0.11 vs. 0.76 ± 0.11 for pre- and post-VM during normothermia, respectively, p = 0.02, and 0.86 ± 0.11 vs. 0.99 ± 0.09 for hyperthermia p < 0.01), although for pulse time only main effects of time (p < 0.01), and condition (p < 0.01) were apparent.
These data indicate that the cerebrovascular response to the VM is largely unchanged by mild hyperthermia.
在发热期间，瓦尔萨尔瓦动作（VM）引起的平均动脉血压（MAP）的波动更为剧烈。然而，在发热期间，这些更剧烈的 VM 引起的 MAP 变化是否会转化为脑循环尚不清楚。
12 名健康参与者（1 名女性，平均年龄±标准差：24±3 岁）在平卧位期间于正常体温和轻度发热时完成 30mmHg（口压）的 VM，持续 15 秒。使用液体调节服装被动地诱导发热，核心温度通过摄入式温度传感器测量。在 VM 期间和之后连续记录大脑中动脉血流速度（MCAv）和 MAP。从 VM 反应中计算泰克自动调节指数，还计算脉动指数，这是脉搏速度（脉冲时间）和平均 MCAv（MCAv）的指数。
被动加热使核心温度从基线显著升高（休息时为 37.9±0.2 与 37.1±0.1°C，p<0.01）。VM 期间 I 期至 III 期的 MAP 在发热时较低（交互效应 p<0.01）。尽管观察到 MCAv 的交互效应（p=0.02），但事后比较表明仅在发热时 IIa 期较低（分别为 55±12 与 49.3±8cm/s，p=0.03）。在两种情况下，VM 后 1 分钟时脉动指数均升高（正常体温下分别为 0.71±0.11 与 0.76±0.11，p=0.02，发热时分别为 0.86±0.11 与 0.99±0.09，p<0.01），尽管仅观察到时间的主要效应（p<0.01）和条件的主要效应（p<0.01）。
这些数据表明，VM 对脑血管的反应在轻度发热时基本不变。
