Scientific A-msh, myocardial infarction and variable dosing

macgyver

Well-known member
Starting a thread for cardiac-related applications, namely myocardial infarction as outlined in the trademark description for Prenumbra. I recently spotted an article about a-msh and how it can influence different parts of the coronary vasculature through different dosage regimens which I will post here when I find it again, and hopefully elaborate on with other research. As Clinuvel has mentioned, Prenumbra will allow physicians to vary the dosing regimen to suit the circumstances. My initial thoughts on this were that it meant the physician can administer an increased amount of Prenumbra for a small sized oedema as an example to quickly reduce the swelling as opposed to Scenesse. But certain blood vessels will respond beneficially to varying levels of a-msh (level of dosage = amount of vessel dilation?). That’s a new aspect that hasn’t been discussed here or on other boards to the best of my knowledge.

Edit: This post has been updated.
 
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macgyver

Well-known member
This article mentions the possibility of extending the half-life of a-msh by binding it to transferrin for use in acute myocardial infarction. This article is from 2007 so it predates the concept of Prenumbra considerably. As Prenumbra is a liquid form that could be administered intravenously, having it constantly ‘on tap’ probably negates the need for an extended half-life but it’s good to know there are other methods of doing so.

α-Melanocyte Stimulating Hormone Fused to Transferrin: A Novel Adjunct to Reperfusion Therapy for Acute MI

 
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macgyver

Well-known member
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macgyver

Well-known member
The following excerpt from the above article is quite significant I think. In one of the other research threads I wrote about how a number of diseases can be traced to the vascular system and it’s performance of function. This excerpt alludes to that:

Administration of the hormone induced significant increases in CF by treated hearts versus controls. These outcomes reveal that α-MSH mediates an intensive dilatative effect on coronary vasculature, pointing to an additional physiologic effect that may be used by clinicians to design treatment strategies targeted specifically to pathological conditions that might be ameliorated by dilation of selected blood vessels. Such measures fall under the broad category of “biotherapeutic” interventions—which are strategies that target specific, root causes of a disease, ultimately resulting in true “cures” rather than providing only transitory palliative relief of symptoms.
 
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macgyver

Well-known member
I’ve been wondering how would you target specific blood vessels. Since all the vascular system is connected, as far as I’m aware you can only use embolization to close off a blood vessel for treatment, and even then you are not supposed to use aspirin or non-steroidal anti inflammatories, not to mention no blood flow in said blood vessel! Referring back to the first article in which a-msh can bind with transferrin thereby increasing its half-life, there are other proteins within blood that can deplete due to complications of a particular ailment. Perhaps binding with a quantity of the depleted protein would enable a-msh to reach the target area of the ailment that is causing the depletion of the protein in the first place.


 
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macgyver

Well-known member
This is the article:

Of particular significance was the specificity of dilatative effects on coronary vasculature, and similar outcomes of aortic ring experiments, which potentially allow different doses of the compound to be used to selectively target various portions of the vasculature for dilation.

Vascular disease in general can affect a number of organs. Vascular disease of the liver can cause cirrhosis, and kidney failure can result from damaged arteries supplying blood to the kidneys. Early diagnosis of vascular disease of the liver can improve the prognosis with a management plan, in which a-msh could play a role by facilitating vessel dilation within the liver itself. Given the size of the vessels contained within, perhaps micro-dosing could see a gradual improvement over time. In contrast, an elevated dosage of a-msh for extreme events such as heart attacks could be used to both improve dilation in larger arteries and fight reactive oxygen species etc. In this context the logic behind variable dosing becomes clearer.
 
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