Parasympathetic neurons in the cranial medial ventricular fat pad on the dog heart selectively decrease ventricular contractility

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• 作者：Dickerson ; Linda W. ; Rodak ; David J. ; Fleming ; Terence J. ; Gatti ; Philip J. ; Massari ; V. John ; et. al.
• 关键词：Sinus rate ; SA node ; Atrioventricular conduction ; AV node ; Contractility ; Left ventricle ; Ganglionic blockade ; Dogs
• 刊名：Journal of the Autonomic Nervous System
• 出版年：1998
• 出版时间：May 28, 1998
• 年：1998
• 卷：70
• 期：1-2
• 页码：129-141
• 全文大小：928 K

文摘

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 μg 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.