Parasympathetic neurons in the cranial medial ventricular fat pad on the dog heart selectively decrease ventricular contractility
Parasympathetic neurons in the cranial medial ventricular fat pad on the dog heart selectively decrease ventricular contractility
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DOI：
10.1016/s0165-1838(98)00048-4
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发表时间：
1998-05-28
期刊：
影响因子：
--
通讯作者：
Gillis, RA
中科院分区：
文献类型：
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作者：
Dickerson, LW;Rodak, DJ;Gillis, RA
我们假设心室收缩力的选择性控制可能是由位于主动脉底部脂肪垫的颅内侧心室（CMV）神经节丛中的节后副交感神经元介导的。在双侧颈部迷走神经刺激（20-30 V，0.5 ms 脉冲。15-20 Hz）之前和期间，对八只氯醛糖麻醉的狗进行窦率、房室 (AV) 传导（心房起搏期间的心室率）和左心室收缩力（右心室起搏期间的 LV dP/dt）测量。其中七只狗在β-肾上腺素能阻断（普萘洛尔，0.8 mg kg(-1) 静脉注射）下进行了测试。对照反应包括窦房结心动过缓或自发节律期间停搏、高度房室传导阻滞或完全性心脏传导阻滞，以及收缩力从 2118 +/- 186 至 1526 +/- 187 mm Hg s(-1) 下降 30%（P < 0.05）。接下来，将神经节阻断剂三甲芬(0.3-1.0ml的50μgml(-1)溶液)注射到CMV脂肪垫中。然后重复迷走神经刺激，现在收缩力下降了相对较小的 5%（N.S.，P > 0.05），但仍然引起相同程度的窦性心动过缓和房室传导阻滞（N = 8，P < 0.05）。五只狗在注射曲美沙芬脂肪垫后 3 小时重新进行测试，此时迷走神经诱导的负性肌力的阻断被部分逆转，因为迷走神经刺激使 LV dP/dt 降低了 19%。局部给予其他脂肪垫（PVFP 或 IVC-ILA）或全身（静脉注射）相同剂量的三甲芬对迷走神经诱导的负性肌力没有影响。因此，位于 CMV 脂肪垫中的副交感神经节介导迷走神经刺激期间心室收缩力的降低。阻断 CMV 脂肪垫对迷走神经介导的窦率或 AV 传导减慢没有影响。 (C) 1998 年由 Elsevier Science B.V. 出版。保留所有权利。
We hypothesized that selective control of ventricular contractility might be mediated by postganglionic parasympathetic neurons in the cranial medial ventricular (CMV) ganglion plexus located in a fat pad at the base of the aorta. Sinus rate, atrioventricular (AV) conduction (ventricular rate during atrial pacing), and left ventricular contractile force (LV dP/dt during right Ventricular pacing) were measured in eight chloralose-anesthetized dogs both before and during bilateral cervical vagus stimulation (20-30 V, 0.5 ms pulses. 15-20 Hz). Seven of these dogs were tested under beta-adrenergic blockade (propranolol, 0.8 mg kg(-1) i.v.). Control responses included sinus node bradycardia or arrest during spontaneous rhythm, high grade AV block or complete heart block, and a 30% decrease in contractility from 2118 +/- 186 to 1526 +/- 187 mm Hg s(-1) (P < 0.05). Next, the ganglionic blocker trimethaphan (0.3-1.0 ml of a 50 mu g ml(-1) solution) was injected into the CMV fat pad. Then vagal stimulation was repeated, which now produced a relatively small 5% (N.S., P > 0.05) decrease in contractility but still elicited the same degree of sinus bradycardia and AV block (N = 8, P < 0.05). Five dogs were re-tested 3 h after trimethaphan fat pad injection, at which time blockade of vagally-induced negative inotropy was partially reversed, as vagal stimulation decreased LV dP/dt by 19%. The same dose of trimethaphan given either locally into other fat pads (PVFP or IVC-ILA) or systemically (i.v.) had no effect on vagally-induced negative inotropy. Thus, parasympathetic ganglia located in the CMV fat pad mediated a decrease in ventricular contractility during vagal stimulation. Blockade of the CMV fat pad had no effect on vagally-mediated slowing of sinus rate or AV conduction. (C) 1998 Published by Elsevier Science B.V. All rights reserved.