Monthly Affirmation

may I be I is the only prayer - not may I be great or good or beautiful or wise or strong. ~e.e. cummings

Sunday, December 13, 2009

I am trying to figure something out

In 2003 I was asked to start taking Niacin and before that a 5 grain Aspirin to stop the flushing side effects of the Niacin. Thus from 2003 I had been taking 325 mg of Aspirin a day. This was why I would bruise when a butterfly landed on my arm (well not that easy but you catch the thought). Now I do not bruise so much and am only taking 50 mg of Aspirin a day in the Aggrenox. The side effect of Aspirin as a constant is thinning the blood.

Aspirin prolongs the time that it takes for your blood to stop oozing (bleeding time). Aspirin does this by decreasing the ability of billions of tiny cells in the bloodstream to stick to each other. These cells are called platelets. Normally when there is an injury, platelets will adhere to the site of injury and stick to each other forming a plug or platelet aggregate, after which blood clotting is initiated. Blood will still clot when you take aspirin, but it will tend to ooze longer before it clots.

And in doing that little bit of research I just answered my own question. I was trying to determine why ... if I took that much Aspirin for so long did I have a clot that gave me a stroke. It is not that Aspirin does not create a clot it just takes more time. (So I could have had a stroke without this a lot earlier on in my life)

So how is less better? Good question let me take a look.

Dipyridamole inhibits the uptake of adenosine into platelets, endothelial cells and erythrocytes in vitro and in vivo; the inhibition occurs in a dose-dependent manner at therapeutic concentrations (0.5–1.9 μg/mL). This inhibition results in an increase in local concentrations of adenosine which acts on the platelet A2-receptor thereby stimulating platelet adenylate cyclase and increasing platelet cyclic-3',5'-adenosine monophosphate (cAMP) levels. Via this mechanism, platelet aggregation is inhibited in response to various stimuli such as platelet activating factor (PAF), collagen and adenosine diphosphate (ADP).

Dipyridamole inhibits phosphodiesterase (PDE) in various tissues. While the inhibition of cAMP-PDE is weak, therapeutic levels of dipyridamole inhibit cyclic-3',5'-guanosine monophosphate-PDE (cGMP-PDE), thereby augmenting the increase in cGMP produced by EDRF (endothelium-derived relaxing factor, now identified as nitric oxide).

Aspirin inhibits platelet aggregation by irreversible inhibition of platelet cyclooxygenase and thus inhibits the generation of thromboxane A2, a powerful inducer of platelet aggregation and vasoconstriction.

Whoa ... where are you going with the medical speak Philip. Well actually it helps me in giving me things to learn and that is what I love to do. Essentially Dipyridamole - the other part of Apprenox - is the extended part action that works with Aspirin to do the same thing but a different way. Dipyridamole keeps platelets in your blood from sticking together to form clots a little more aggressively than Aspirin does by itself. But in taking it in the form of medicine that I am there are beta and alpha half life factors involved in the Dipyridamole that have greater stability than the wonderful issues of Aspirin alone.

Plus I don't bruise when a butterfly flaps its wings in South Africa.

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"The secret of health for both mind and body is not to mourn for the past, worry about the future, or anticipate troubles but to live in the present moment wisely and earnestly." – Buddha