I believe they would, because when you cut axons they do not necessarily die immediately, but still are able to release neurotransmitters for many hours if not days. Plus you have the intracardiac ganglia that sits on top the heart. I have worked on intracardiac ganglion neurons and they definately survive for a long time after dissection. And one would expect them to have at least some, even small, modulatory effect.
I believe they would, because when you cut axons they do not necessarily die immediately, but still are able to release neurotransmitters for many hours if not days. Plus you have the intracardiac ganglia that sits on top the heart. I have worked on intracardiac ganglion neurons and they definately survive for a long time after dissection. And one would expect them to have at least some, even small, modulatory effect.
Despite what Refik said above, the obvious answer is no. Yes, axons can still release neurotransmitters, but unless they have Bluetooth, it is not the ANS that is controlling them.
I also agree that isolated heart's cannot have modulation by the A.N.S as it has been denervated. In fact, as we know that HRV is a reflection of arterial baroreflex function mediated through the A.N.S and so if the heart is isolated HRV will not exist.
Yes, the Autonomic Nervous System still has an effect on the Heart Rate Variability of isolated hearts on Langerdoff setup. Nor-epinephrine and acetylcholine are the major neurotransmitters of ANS and their receptors present on the heart ex-vivo experiment. Perfusion of heart with Krebs-Henseleit buffer containign Ach leads to bradycardia in response result. Conversely, addition of NA induce tachycardia. Further, washout o f these transmitters from heart through buffer show normal HR.
There is residual heart rate variability (HRV) in the patients 1-2 years after heart transplantation surgery, but the role of ANS in the residual heart rate variability is not clear yet. Please see my research article in the following link:
About Dr. Cheng-Deng Kuo comment, I would like to add that since 1930 when Bainbridge proposed that a proportion of the HRV occurs as a consequence of the mechanical events (due to stretch o the atria that results from both changes in cardiac filling and the changing thoracic pressure that occur during respiration), HRV data should be interpreted with appropriate caution. This conclusion is supported by the observation that heart transplant patients,despite the absence of cardiac nerves, still exhibit small change in R–R interval associated with the respiratory cycle, as described by Bernardi in 1989. And about Sita Sharan Patel comment. The fact that adrenal receptors still work in a isolated heart does not mean that stimulation comes from an autonomic nervous system influence. The case you exposed in your comment is a pharmacologycal effect of adrenergic and cholinergic agonist on this receptors.
The heart rate variability (HRV) signal is a useful and non-invasive tool for the evaluation of cardiovascular system and Autonomic Nervous System(ANS) so if The separation between the sympathetic and parasympathetic nerves system from heart and lack of Bluetooth,therefore it is not the (ANS) that is controlling them.
can be added Autonomic nervous system (ANS) is a part of central nervous system (CNS). The pumping power of heart is greatly controlled by sympathetic and parasympathetic (vagal) and go to heart in great numbers
I think it seems to be an unsolved puzzle. I am not sure and I am not convinced either way. I suggest you do a simple experiment and give us an answer. The experiment I suggest you do is, can be summarized as below. Dissect the heart, do a control measurement when it is stable, and then you perfuse the heart with the adrenergic and cholinergic receptor blockers (separately), and tell us what happens or anything changes at all? This experiment relies on the presumption that all the adrenergic and cholinergic input to the heart is via neural pathways. What do you think?
it all depends on what you mean by 'the autonomic nervous system'. Obviously, the Langendorff preparation is separated from its CNS. However, the nerve terminals and the cardiac ganglia are still present. Depending on the interventions that you do it is very conceivable (and even likely) that you activate those nerves and find their effects in your results. Addition of well-chosen blockers might prevent that, however, some are known to have a direct effect on the myocardial membrane, which might give yet another interference with what you are after.
John Karemaker is right as usual ! you may look into the literature under Bernardi. he has done interesting things on transplanted hearts, which is not exactly the "in vitro" question you may have in mind.