HI
BHALVERS:My answer would be "yes but only in the context of present-understanding which is totally incomplete". In the most general sense the neurochemical pathway (cholinergic) stimuli that produce the gut evacuation produces an opposite effect if applied to the heart. There are multiple pathways that regulate the tone and motility of the GIT, but the basic physiology is one of "cholinergic stimulation increases gut motility but when applied to the heart would reduce heartrate and stroke volume". And the various other mechanisms that can be invoked in IBS via neurochemical mediator release just have not been examined in this context...and what is known does not appear to support that these 2 symptoms would share the same mechanism. Again, that does not mean I am saying it does not happen, because it does if people experience it. Only that there are probably 2 separate mechanisms, and they are related (in simplest possible terms, such as a stress-response producing adrenergic stimulation of the heart may result from the feeling your gut is about to explode and the fear that goes with it...so they are related).On the other hand, the research immunologist I work with has pointed out vehemently and more than once the fundamental mechanism which is seen in the IBS symptom set of loss of integrity of circulating polymorphoneuclear cells. This allows direct release of intracellular contents into the plasma of the microvasuclature of the small intestine on exposure to a trigger substance, and these mediators released then enter the systemic circulation as a result and are distributed throughout the body.The chemicals that can be released from granulocytic cells include (but are not limited to) not only preformed mediators within granulocytic cells, but potentially synthesized mediators as the reactions occurs (chemokines, cytolkines, prostaglandins and leukotrienes). Even platelet-activiating-factor is clearly released in some patients, as platelet aggregation is seen in the response. Leukotrienes in particular are extremely "strong" at low concentrations compared to histamine. Each of these intracellular chemicals has an entire chemical action-reponse matrix that goes with it in the context of normal immunologic reactions. But whose effects are not well understood systemically when they are just dumped into the systemic circulation as is seen in these toxic-responses to food additives and foods in sensitive individuals. These are not "textbook" hypersensitivity reactions, and what hapens to the granulocytes and lymphocytic reactions elicited are not textbook either.There may very well emerge a mechanism of action-response directly related to the presence of one or more of these mediators within the systemic circulation in the near future as work progresses.A protocol defining a means of quantifying exactly which mediators are most frequently released, what the extracellular concentrations can become ,etc. must be established first, then the investigators will know which path to follow in assessing tissue and neurologic effects.Apparently this is tough to do as their relative concentrations are minute, especially in the in vitro environment created to simulate the in vivo concentrations of allergen. I sat in on a meeting about this last night...over my head.None of that is actually being looked at in other research at this time...mostly functions within the neurotransmission system are being scrutinized, seeking chemical interventional methods.This is one of those things where it is easy to fall victim to the "flat earth" thought process, and that would be a mistake.Gotta run...Have a Tachycardia-free eveningMNL_____________
www.leapallergy.com [This message has been edited by Mike NoLomotil (edited 11-21-2000).]
