Ferguson D W, Abboud F M, Mark A L
J Clin Invest. 1985 Dec;76(6):2265-74. doi: 10.1172/JCI112236.
We studied the contribution of carotid vs. extracarotid baroreceptors in control of heart rate in normal humans. We measured heart interval (HI) and arterial pressure during steady-state infusion of phenylephrine (PE). PE increased mean arterial pressure (MAP) by 13 +/- 2 mmHg (mean +/- SEM; n = 10) and thus stimulated both carotid and aortic baroreceptors. Neck pressure (NP) was applied during PE infusion to counter the increase in transmural carotid sinus pressure, thus leaving only aortic baroreceptors stimulated by the increase in arterial pressure. PE infusion alone prolonged HI by 230 +/- 24 ms (P less than 0.05). Application of NP attenuated the HI response to 65 +/- 22 ms above control (P less than 0.05 vs. PE alone). During these steady-state increases in arterial pressure, elimination of the carotid baroreflex contribution reduced the HI prolongation by 41-70% in five subjects and by greater than 93% in five subjects. We also measured the HI response to dynamic ramp elevation of systolic arterial pressure (SAP) using bolus administrations of PE. Baroreflex control was calculated from the slope of the regression correlating SAP to succeeding HI for PE alone (carotid and aortic baroreceptor activation) and for PE plus superimposed dynamic NP at levels equal to the increases in SAP (aortic baroreceptor activation). During PE alone, the baroreflex slope was 20.2 +/- 2.9 ms/mmHg (n = 10). During PE plus NP, the baroreflex slope was reduced by 30% to 14.1 +/- 2.8 ms/mmHg (P less than 0.02 vs. during PE alone). Thus, during dynamic increases in arterial pressure, eliminating the carotid baroreflex contribution reduced the HI response by 30%. These studies indicate that extracarotid (presumably aortic) and carotid baroreflexes both participate in control of heart rate in humans. Extracarotid (aortic) baroreflexes appear to have the greater role in control of heart rate during dynamic increases in arterial pressure.
我们研究了在正常人体中，颈动脉与颈外动脉压力感受器对心率控制的贡献。我们在持续输注去氧肾上腺素（PE）期间测量了心搏间期（HI）和动脉压。PE使平均动脉压（MAP）升高了13±2 mmHg（平均值±标准误；n = 10），从而刺激了颈动脉和主动脉压力感受器。在输注PE期间施加颈部压力（NP）以抵消跨壁颈动脉窦压力的升高，因此仅主动脉压力感受器受到动脉压升高的刺激。单独输注PE使HI延长了230±24 ms（P<0.05）。施加NP使HI反应减弱至比对照高65±22 ms（与单独使用PE相比，P<0.05）。在这些动脉压的稳态升高期间，消除颈动脉压力反射的贡献使五名受试者的HI延长减少了41%-70%，使另外五名受试者的HI延长减少了超过9
3%。我们还使用PE推注测量了对收缩期动脉压（SAP）动态斜坡升高的HI反应。压力反射控制是根据单独使用PE（颈动脉和主动脉压力感受器激活）以及PE加与SAP升高水平相等的叠加动态NP（主动脉压力感受器激活）时，将SAP与随后的HI相关联的回归斜率计算得出的。单独使用PE时，压力反射斜率为20.2±2.9 ms/mmHg（n = 10）。在PE加NP期间，压力反射斜率降低了30%，至14.1±2.8 ms/mmHg（与单独使用PE期间相比，P<0.02）。因此，在动脉压动态升高期间，消除颈动脉压力反射的贡献使HI反应降低了30%。这些研究表明，颈外动脉（可能是主动脉）和颈动脉压力反射均参与人体心率的控制。在动脉压动态升高期间，颈外动脉（主动脉）压力反射似乎在心率控制中发挥更大作用。
