Henning R J, Feliciano L, Coers C M
University of South Florida College of Medicine, Division of Cardiology, Tampa, FL, USA.
Cardiovasc Res. 1996 Nov;32(5):846-53.
To determine the effects of vasoactive intestinal peptide, released from the right and left vagal nerves, on ventricular contraction, relaxation, and heart rate.
The muscarinic and beta-adrenergic receptors were blocked with atropine and propranolol, and afterload was controlled in 48 anesthetized, open-chest mongrel dogs. Experiments were performed in the absence (Series 1, 10 dogs) and in the presence (Series 2, 22 dogs) of a controlled heart rate and prior to and after the administration of a sensitive and selective vasoactive intestinal peptide antagonist (Series 3, 16 dogs).
Right ventricular contraction (+dp/dtmax), relaxation (-dp/dtmin) and heart rate increased significantly during 20 Hz vagal nerve stimulation for 5 min. Vagal nerve stimulation in Series 1 increased right ventricular +dp/dtmax by 28% from a control value of 480 +/- 11 (P < 0.001) and right ventricular -dp/dtmin by 23% from a control value of 341 +/- 11 (P < 0.002). Left ventricular +dp/dtmax and -dp/dtmin increased slightly but not significantly. Vagal nerve stimulation also increased the heart rate by 29% from a control value of 149 +/- 2 (P < 0.001). During controlled heart rate in Series 2, vagal nerve stimulation at 20 Hz consistently increased right ventricular +dp/dtmax and -dp/dtmin comparable to Series 1 experiments but did not increase left ventricular +dp/dtmax or -dp/dtmin. Injection of the vasoactive intestinal peptide antagonist [4Cl-DPhe6, Leu17]VIP into the right coronary artery of 16 dogs in Series 3 did not affect right ventricular +dp/dtmax, -dp/dtmin, or heart rate. However, this antagonist substantially decreased the vagal-induced increases in right ventricular +dp/dtmax, -dp/dtmin, and heart rate by 85, 63, and 71% (P < 0.005), respectively.
The present experiments suggest that vagal nerve stimulation releases vasoactive intestinal peptide (VIP) or a "VIP-like substance' that significantly increases right ventricular contraction, relaxation, and heart rate.
确定左右迷走神经释放的血管活性肠肽对心室收缩、舒张及心率的影响。
用阿托品和普萘洛尔阻断毒蕈碱能和β-肾上腺素能受体,并对48只麻醉开胸杂种犬的后负荷进行控制。实验在无控制心率(系列1,10只犬)和有控制心率(系列2,22只犬)的情况下进行,且在给予敏感且选择性的血管活性肠肽拮抗剂之前和之后(系列3,16只犬)进行。
在20Hz迷走神经刺激5分钟期间,右心室收缩(+dp/dtmax)、舒张(-dp/dtmin)和心率显著增加。系列1中的迷走神经刺激使右心室+dp/dtmax较480±11的对照值增加28%(P<0.001),右心室-dp/dtmin较341±11的对照值增加23%(P<0.002)。左心室+dp/dtmax和-dp/dtmin略有增加但不显著。迷走神经刺激还使心率较149±2的对照值增加29%(P<0.001)。在系列2的控制心率期间,20Hz的迷走神经刺激持续增加右心室+dp/dtmax和-dp/dtmin,与系列1实验相当,但未增加左心室+dp/dtmax或-dp/dtmin。向系列3中的16只犬的右冠状动脉注射血管活性肠肽拮抗剂[4Cl-DPhe6,Leu17]VIP,未影响右心室+dp/dtmax、-dp/dtmin或心率。然而,该拮抗剂分别使迷走神经诱导的右心室+dp/dtmax、-dp/dtmin和心率增加显著降低85%、63%和71%(P<0.005)。
本实验提示迷走神经刺激释放血管活性肠肽(VIP)或一种“VIP样物质”,其可显著增加右心室收缩、舒张及心率。