Dickerson L W, Rodak D J, Fleming T J, Gatti P J, Massari V J, McKenzie J C, Gillis R A
Department of Pharmacology, Georgetown University School of Medicine, Washington, DC 20007, USA.
J Auton Nerv Syst. 1998 May 28;70(1-2):129-41. doi: 10.1016/s0165-1838(98)00048-4.
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 microg 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.
我们推测，心室收缩性的选择性控制可能由位于主动脉根部脂肪垫内的颅内侧心室（CMV）神经节丛中的节后副交感神经元介导。在8只氯醛糖麻醉的犬中，分别于双侧颈迷走神经刺激前及刺激期间（20 - 30 V，0.5 ms脉冲，15 - 20 Hz）测量窦性心率、房室（AV）传导（心房起搏时的心室率）和左心室收缩力（右心室起搏时的LV dP/dt）。其中7只犬在β - 肾上腺素能阻断（普萘洛尔，0.8 mg kg⁻¹静脉注射）下进行测试。对照反应包括自发节律时的窦性心动过缓或停搏、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降至1526±187 mmHg s⁻¹，下降30%（P < 0.05）。接下来，将神经节阻滞剂三甲噻方（50 μg ml⁻¹溶液0.3 - 1.0 ml）注入CMV脂肪垫。然后重复迷走神经刺激，此时收缩力仅产生相对较小的5%下降（无统计学意义，P > 0.05），但仍引发相同程度的窦性心动过缓和房室传导阻滞（N = 8，P < 0.05）。5只犬在三甲噻方脂肪垫注射3小时后重新测试，此时迷走神经诱导的负性肌力作用的阻断部分逆转，因为迷走神经刺激使LV dP/dt降低了19%。将相同剂量的三甲噻方局部注入其他脂肪垫（PVFP或IVC - ILA）或全身给药（静脉注射）对迷走神经诱导的负性肌力作用无影响。因此，位于CMV脂肪垫的副交感神经节介导了迷走神经刺激期间心室收缩力的下降。阻断CMV脂肪垫对迷走神经介导的窦性心率减慢或房室传导无影响。
