I found this odd, in that I have never heard of this terminology before. Here's a bit, but there's more to read here:
[www.macses.ucsf.edu]

In mammals, two vagal components have evolved in the brainstem to regulate peripheral parasympathetic functions. The dorsal vagal complex (DVC), consisting of the dorsal motor nucleus (DMNX) and its connections, controls parasympathetic function below the level of the diaphragm, while the ventral vagal complex (VVC), comprised of nucleus ambiguus and nucleus retrofacial, controls functions above the diaphragm in organs such as the heart, thymus and lungs, as well as other glands and tissues of the neck and upper chest, and specialized muscles such as those of the esophageal complex.

Stephen Porges - Polyvagal theory and ways to test it through studies of infants and autistic children. In infants at 9 months of age, poor regulation of the vagal brake during tests of attention in a social situation predicted behavior problems at age 3. Underlying the individual variations in vagal tone is the question of plasticity vs. damage and reversibility of defects in the vagal brake and in reduced heart rate variability. He reported that autistic children could be made to be more attentive and responsive to human stimulation by training with a toned system of listening exercises. Increasing attention to phoneme range sounds is hypothesized to positively impact the disordered functioning of the VVC, deemed by him to be the substrate for autism. The maintenance of such behavioral changes was reported to be contingent, however, on modification of the living environment of the child to reduce sound over stimulation (e.g. exposure to a circus can "shut the child back down"). In a similar vein it was suggested that HRV may be decreased in lower SES individuals as they are exposed to greater noise and, as a result of their environment, have a greater need for vigilance—i.e., similar to "predator monitoring", and consequently are less "tuned-in" to voices and prosocial activities.

Here's another link about regulation of pacemaker activity.

"Sympathetic activation, which releases norepinephrine (NE), increases pacemaker rate by decreasing gK+ and increasing slow inward gCa++ and gNa+, all of which increase the slope of Phase 4. Parasympathetic (vagal) activation, which releases acetylcholine (ACh), decreases pacemaker rate by increasing gK+ which decreases the slope of Phase 4 thereby increasing the time to reach threshold. Vagal activity also hyperpolarizes the pacemaker cell during Phase 4 which results in a longer time to research threshold voltage."
[www.oucom.ohiou.edu]

Richard

Again you and PC are usually on the cutting edge of our medical understanding.

What to do with you two.....you send my mind spinning.

A quick cursory glance of the references availalbe to me show that there could indeed be not only a compeition between the ANS and CNS but also a competition between the two branhes of the parasympathetic systems as well (Up until I read your post, I didn't even know there was two!). Thus stating again...what you just posted.

"Physiological support for the hypothesis that DMNX can contribute to neurogenic bradycardia, independent of NA, is provided by lesion studies. Machado and Brody (1988) have reported that chronic bilateral lesions of NA reduced but did not totally block baroreceptor reflex-mediated bradycardia in conscious rats. Thus, DMNX contains vagal neurons capable of producing bradycardia with a response latency associated with the baroreceptor reflex. This is supported by Jerrell, Gentile, McCabe, & Schneiderman (1986), who argued that differential Pavlovian conditioning of bradycardia in rabbits, following sinoaortic denervation, was mediated via DMNX pathways. The results pose the possibility that vagal pathways, originating in both the DMNX and NA, have the potential to influence heart rate." (1)

....Apparantly, the measurement of RSA (Respitory Sinus Arrythmia) is a key factor in determining this competition. ...

"The Polyvagal Theory is introduced to explain the different functions of the two primary medullary source nuclei of the vague: the nucleus ambiguus (NA) and the dorsal motor nucleus (DMNX). Although vagal pathways from both nuclei terminate on the sinoatrial node, it is argued that the fibers originating in NA are uniquely responsible for respiratory sinus arrhythmia (RSA). Divergent shifts in RSA and heart rate are explained by independent actions of DMNX and NA. The theory emphasizes a phylogenetic perspective and speculates that mammalian, but not reptilian, brainstem organization is characterized by a ventral vagal complex (including NA) related to processes associated with attention, motion, emotion, and communication. " (2)

Ok Richard, it's not hard to see whay THE SA node would be affected by this contrary pulling between the fibers of the DMNX and the NA, but now we're going to have to immerse ourselves in the terminology of this new factor before we can attempt to synthesis it into our focus of understanding on the subjects....Great more work! Very interesting stuff and as I said, cutting edge....again.



(1) Psychophysiology, 32 (1995), 301-318. Cambridge University Press. Printed in the USA. Orienting in a defensive world: Mammalian modifications of our evolutionary heritage. A Polyvagal Theory

Joe,

I don't have near the understanding of the body as does PC. This article sent my mind spinning, as well. I just keep searching and hoping to find something that helps spur the better intelligence here. What I had not heard of was the ventral vagal complex, but it all still confuses me. I just keep plugging along, and hoping to stimulate thoughts with what I find and try to learn something as I go, and I have a very long way to go.

Richard

Richard and Joe,

Good work. Simple (?!) things that struck a chord with me:

From Richard's post:

'ventral vagal complex (VVC), comprised of nucleus ambiguus and nucleus retrofacial, controls functions above the diaphragm in organs such as the heart, thymus and lungs, as well as other glands and tissues of the neck and upper chest, and specialized muscles such as those of the esophageal complex.

Esophagal complex. And cardiologists still in the main will not acknowledge a link between upper digestive tract problems and vagally mediated AF. Jackie has also mentioned her diaphragm problems here. Maybe the involvement of the VVC with the lungs gives some AFrs the unpleasant breathing sensations whilst in AF.

Also:

'Increasing attention to phoneme range sounds is hypothesized to positively impact the disordered functioning of the VVC, deemed by him to be the substrate for autism.'

One of the characteristics of autism is obsessive behaviour..... People who know me well say I display signs of autism as regards my obsessiveness - diagnosed OCD as an adult. And many of you will have thought I'm sure that I'm a bit obsessed with this forum!!

From Joe's post:

'The theory emphasizes a phylogenetic perspective and speculates that mammalian, but not reptilian, brainstem organization is characterized by a ventral vagal complex (including NA) related to processes associated with attention, motion, emotion, and communication.'

Mmmm...... emotion..... Looks like we really ARE what we feel.

Interesting stuff fellas.

For me in particular, I think that my traumatic childhood and the anxious adulthood have precipitated biochemical inbalances which have led on one hand to above normal levels of ectopy, and on the other to a faulty and/or over-compensatory vagal system which, when charging hardest in the wee small hours, and when combined with the aforementioned ectopy, can result in VMAF.

Mike F.

This is very interesting stuff and ties in with what I have been studying recently (I am a graduate student in counseling psychology) about experiences in early life and the development of various neurological disorders such as hypervigilence and a low startle threshold. Incidentally, similar kinds of neurological dysfunction can occur in adults under severely traumatic conditions (as in soldiers in combat or in victims of violence) which produce a syndrome called Post Traumatic Stress Disorder.

THis summer when my prior cardio was running a Dobutamine stress test and nuclear imaging in the hospital to see if I could tolerate Flecainide (my heart is as health as a horse as it turns out). He couldn't get my HR high enough with the dobutamine and so he injected a dose of atropine which immediately sent my blood pressure north of 210 over 115 and I got a splitting headache (which I still feel at times) and caused him to panic and terminate the test and order a CT scan of my head for fear of a cerebral aneurysm ( couldn't use an MRI due to my pacemaker). Anyway, the CT didn't show any problems that are large enough to be seen with that technology.

However, after I switched to my new EP -cardio who is much more with it, he said what had happend was that in all likelihood the dobutamine stimluated my vagal tone which put a lid on my blood pressure and heart rate and when they hit me with the atropine to riase my HR more, I had a "vagal rebound" and the atropine immediately blocked the vagal tone enhancement of the dobutamine and my blood pressure spiked.

He also speculated that since polio, which I had, caused damage to the parasympathetic nervous system, that this could have predisposed me to not only having that reaction in the test, but also to being vagally mediated in my AFIB.

Michael,

Put me down for hypervigilance and a low startle threshold too. Sometimes the phone starting to ring will make me JUMP out of my seat........... but a near auto miss??? Hardly bothers me at all - I just measure up my avoidance options and do whatever I can as cool as you like. Sorta like my adrenaline system is on overload for the small all-the-time regular things..... and then under-reacts when it really SHOULD get going!

Mike F.