Lockwood Jennifer M, Wilkins Brad W, Halliwill John R
Department of Human Physiology, University of Oregon, Eugene, OR 97403-1240 USA.
J Physiol. 2005 Mar 1;563(Pt 2):633-42. doi: 10.1113/jphysiol.2004.080325. Epub 2004 Dec 23.
In normally active individuals, postexercise hypotension after a single bout of aerobic exercise is due to an unexplained peripheral vasodilatation. Histamine has been shown to be released during exercise and could contribute to postexercise vasodilatation via H1 receptors in the peripheral vasculature. The purpose of this study was to determine the potential contribution of an H1 receptor-mediated vasodilatation to postexercise hypotension. We studied 14 healthy normotensive men and women (ages 21.9 +/- 2.1 years) before and through to 90 min after a 60 min bout of cycling at 60% on randomized control and H1 receptor antagonist days (540 mg oral fexofenadine hydrochloride; Allegra). Arterial blood pressure (automated auscultation) and femoral blood flow (Doppler ultrasound) were measured in the supine position. Femoral vascular conductance was calculated as flow/pressure. Fexofenadine had no effect on pre-exercise femoral vascular conductance or mean arterial pressure (P > 0.5). At 30 min postexercise on the control day, femoral vascular conductance was increased (Delta+33.7 +/- 7.8%; P < 0.05 versus pre-exercise) while mean arterial pressure was reduced (Delta-6.5 +/- 1.6 mmHg; P < 0.05 versus pre-exercise). In contrast, at 30 min postexercise on the fexofenadine day, femoral vascular conductance was not elevated (Delta+10.7 +/- 9.8%; P = 0.7 versus pre-exercise) and mean arterial pressure was not reduced (Delta-1.7 +/- 1.2 mmHg; P = 0.2 versus pre-exercise). Thus, ingestion of an H1 receptor antagonist markedly reduces vasodilatation after exercise and blunts postexercise hypotension. These data suggest H1 receptor-mediated vasodilatation contributes to postexercise hypotension.
在正常活动的个体中，单次有氧运动后的运动后低血压是由于不明原因的外周血管扩张所致。研究表明，组胺在运动过程中会释放，并可能通过外周血管系统中的H1受体导致运动后血管扩张。本研究的目的是确定H1受体介导的血管扩张对运动后低血压的潜在作用。我们对14名健康的血压正常的男性和女性（年龄21.9±2.1岁）进行了研究，在随机对照日和H1受体拮抗剂日（口服540毫克盐酸非索非那定；阿莱格拉），让他们在60%的强度下进行60分钟的骑行运动，运动前、运动中及运动后90分钟均进行观察。在仰卧位测量动脉血压（自动听诊法）和股血流量（多普勒超声）。股血管传导率计算为血流量/血压。非索非那定对运动前股血管传导率或平均动脉压无影响（P>0.5）。在对照日运动后30分钟，股血管传导率增加（Δ+33.7±7.8%；与运动前相比，P<0.05），而平均动脉压降低（Δ-6.5±1.6 mmHg；与运动前相比，P<头0.05）。相比之下，在非索非那定日运动后30分钟，股血管传导率未升高（Δ+10.7±9.8%；与运动前相比，P=0.7），平均动脉压也未降低（Δ-1.7±1.2 mmHg；与运动前相比，P=0.2）。因此，摄入H1受体拮抗剂可显著降低运动后的血管扩张，并减轻运动后低血压。这些数据表明，H1受体介导的血管扩张与运动后低血压有关。
