ASPRIN
good find, dania.Effect of aspirin on coronary collateral blood flow
JD Altman, D Dulas, T Pavek and RJ Bache
Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.
BACKGROUND. Although aspirin exerts beneficial antiplatelet activity in patients with coronary artery disease, cyclooxygenase blockade produced by aspirin causes a potentially deleterious effect by interrupting endothelial production of prostacyclin. Collateral vessels that develop in response to coronary occlusion display prominent endothelial cell proliferation and undergo vasoconstriction in response to indomethacin. This study was performed to test the hypothesis that cyclooxygenase blockade with aspirin would cause constriction of coronary collateral vessels and that such vasoconstriction would be reversed with nitroglycerin. METHODS AND RESULTS. Collateral vessel growth was induced by embolic occlusion of the left anterior descending coronary artery in dogs. Four to 6 months later, coronary collateral flow was measured as retrograde flow from the cannulated collateral-dependent artery. Aspirin (1 mg/kg i.v.) caused 70 +/- 8% blockade of the increase in coronary blood flow produced by intra-arterial arachidonic acid and decreased retrograde flow from 37 +/- 7 to 28 +/- 7 ml/min (p < 0.03). Increasing the dose of aspirin to 15 mg/kg i.v. caused 91 +/- 3% blockade of the response to arachidonic acid and further decreased retrograde flow to 21 +/- 4 ml/min (p < 0.01). After aspirin administration, nitroglycerin (150 micrograms/min i.c.) reversed the collateral constriction and increased retrograde flow to 37 +/- 10 ml/min (p < 0.01). CONCLUSIONS. These data suggest that products of cyclooxygenase metabolism cause tonic vasodilation of well-developed coronary collateral vessels. Blockade of cyclooxygenase with even low- dose aspirin caused collateral vessel constriction with a decrease in collateral blood flow. However, nitroglycerin was able to fully reverse aspirin-induced collateral vasoconstriction and restore flow to the control level.
Cheer, any opinion on if aspirin is bad for the endothelium or for collaterals???
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Here: take this aspirin: it'll thin your blood and maybe prevent strokes or heart attacks. Oh, BTW we found out it causes collateral arteries to become constricted, and that might hurt a bit. But it's OK, just take a shot of nitro and you'll be all better. But BTW, stay away from the viagra while you're on the nitro. Lots to think about
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Not a doctor.
"I'm still here, how 'bout that? I may have lost my lunchbox, but I'm still here." John Cowan Hartford (December 30, 1937 – June 4, 2001)
BIG IDEA
Hey, maybe I am not the first one that thinks of this, but, could we put Bayer at our side?Cece wrote:Effect of aspirin on coronary collateral blood flow
JD Altman, D Dulas, T Pavek and RJ Bache
Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.
Bayer (aspirin patent holder) is a big pharma, but as far as I know, is behind the others in MS research. If aspirin is good for MS this could be a big boost to their shares and a powerful tool against their competitors. Maybe they could support a clinical trial for aspirin in CCSVI+MS conditions, or aspirin after angio in CCSVI.
Has anybody tried to contact Bayer responsibles? Anybody here is willing to do it?
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Old posting from Cheerleader xxxx
aspirin is not just about platelets/coagulation.
It also addresses endothelial dysfunction in oxidative stress and increases nitric oxide availability.
http://ajpheart.physiology.org/cgi/cont ... 94/4/H1562
Quote:
Aspirin preserves the integrity of the vascular wall through its free radical scavenging properties and its capacity to protect endothelial cells from the deleterious effects of hydrogen peroxide (16, 21, 40). The effects of aspirin in preventing cardiovascular events are attributed to its platelet-inhibitory function, which results from the irreversible inhibition of the activity of platelet cyclooxygenase and thromboxane B2, the major products of cyclooxygenase (COX-1) activity (39). Low-dose aspirin suppresses the age-related increase in oxidative stress via the modulation of NF-B (27). The acetyl group provides aspirin with the capacity to increase endothelial nitric oxide (NO) synthesis and bioavailability (14, 15, 24, 46, 53). Aspirin reduces monocyte chemoattractant protein-1 and soluble ICAM-1 levels in low-density lipoprotein (LDL) receptor-deficient mice (8, 9). This reduction in adherence molecule expression has a functional effect, since aspirin inhibits monocyte adhesion to LDL-stimulated endothelial cells (15). Evidence from explorative clinical trials suggests that treatment with low-dose aspirin increases EDR. In humans, low-dose aspirin administered over a 2-mo period has been found to improve endothelial function (34). In rats with vascular endothelial injury induced by an injection of native LDL, low-dose aspirin is able to reverse the EDR dysfunction (11).
ASPRIN.......
http://ajpheart.physiology.org/cgi/cont ... 94/4/H1562
Aspirin and the entire endothelial health program were not enough for Jeff to overcome his fatigue. He had such severe stenosis, he would fall asleep driving and had to stop after a fender bender.
Since angioplasty, he is awake full days, no naps, and back to working and driving. For some, aspirin can only do so much.
cheer
aspirin is not just about platelets/coagulation.
It also addresses endothelial dysfunction in oxidative stress and increases nitric oxide availability.
http://ajpheart.physiology.org/cgi/cont ... 94/4/H1562
Quote:
Aspirin preserves the integrity of the vascular wall through its free radical scavenging properties and its capacity to protect endothelial cells from the deleterious effects of hydrogen peroxide (16, 21, 40). The effects of aspirin in preventing cardiovascular events are attributed to its platelet-inhibitory function, which results from the irreversible inhibition of the activity of platelet cyclooxygenase and thromboxane B2, the major products of cyclooxygenase (COX-1) activity (39). Low-dose aspirin suppresses the age-related increase in oxidative stress via the modulation of NF-B (27). The acetyl group provides aspirin with the capacity to increase endothelial nitric oxide (NO) synthesis and bioavailability (14, 15, 24, 46, 53). Aspirin reduces monocyte chemoattractant protein-1 and soluble ICAM-1 levels in low-density lipoprotein (LDL) receptor-deficient mice (8, 9). This reduction in adherence molecule expression has a functional effect, since aspirin inhibits monocyte adhesion to LDL-stimulated endothelial cells (15). Evidence from explorative clinical trials suggests that treatment with low-dose aspirin increases EDR. In humans, low-dose aspirin administered over a 2-mo period has been found to improve endothelial function (34). In rats with vascular endothelial injury induced by an injection of native LDL, low-dose aspirin is able to reverse the EDR dysfunction (11).
ASPRIN.......
http://ajpheart.physiology.org/cgi/cont ... 94/4/H1562
Aspirin and the entire endothelial health program were not enough for Jeff to overcome his fatigue. He had such severe stenosis, he would fall asleep driving and had to stop after a fender bender.
Since angioplasty, he is awake full days, no naps, and back to working and driving. For some, aspirin can only do so much.
cheer
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Re: BIG IDEA
According to the timeline listed at the Aspirin Foundation's website, Bayer's patent on aspirin ran out in the 1930s.frodo wrote: Bayer (aspirin patent holder) is a big pharma, but as far as I know, is behind the others in MS research. If aspirin is good for MS this could be a big boost to their shares and a powerful tool against their competitors. Maybe they could support a clinical trial for aspirin in CCSVI+MS conditions, or aspirin after angio in CCSVI.
Has anybody tried to contact Bayer responsibles? Anybody here is willing to do it?
http://www.aspirin-foundation.com/what/timeline.html
1930s Bayer's patent on acetyl salicylic acid runs out. It becomes a generic drug.
Dx'd with MS & HNPP (hereditary peripheral neuropathy) 7/03 but must have had MS for 30 yrs before that. I've never taken meds for MS except 1 yr experiment on LDN. (I found diet, exercise, sleep, humor, music help me the most.)
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JOHNNYMACJohnnymac wrote:I've been wondering about this as well since Court is supposed to start taking low dose asprin daily after we finish with her arixtra.
I CONSIDER THIS A FAILURE IN MY COMMUNICATION WITH YOU.
Courtney should now be on aspirin in addition to anticoagulation. Platelet adherence to intimal damage caused by angioplasty can result in thrombosis.
Please have courtney begin aspirin immediately.
The paper that is reported relates to arteries, not veins. Arterial collaterals are different from venous collaterals. With the main IJV open we actually want more blood through it. Be careful what you read. There are big differences between arterial and venous angioplastgy, stenting, endothelial integrity, collaterals, damage, etc etc etc.
Often a direct comparison is unhealthy.
I appreciate you all discussing things but i beg my patients not to act on internet chatter without discussion with me.
Thanks
DrS
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- drsclafani
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i have revised my approach. there is no reason to delay the aspirinRompers wrote:DrS ...should all of your patients begin taking the low dose aspirin immediately following our procedures, as I confess that Gene and I both thought the use was to commence following Arixtra as well.
Rhonda
5/3/11
With a penny in my pocket!
- silverbirch
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Dr S
I put myself on low aspirin 0.75 when I read Dr Z's theory so about 15mts ago. I had my procedure and I still continue to take it - surgeon said at the time it may do me some good ....
I must say that I am not on any meds nor have I ever been... DX 2009 CCSVI 2010.
My GP /Neuro know I’m on aspirin - I plan on staying on it... unless told differently or illness dictates I’m mindful of what I understand its effects
I take a coated aspirin and with probiotic drink
Your opinion would be very much welcomed
I put myself on low aspirin 0.75 when I read Dr Z's theory so about 15mts ago. I had my procedure and I still continue to take it - surgeon said at the time it may do me some good ....
I must say that I am not on any meds nor have I ever been... DX 2009 CCSVI 2010.
My GP /Neuro know I’m on aspirin - I plan on staying on it... unless told differently or illness dictates I’m mindful of what I understand its effects
I take a coated aspirin and with probiotic drink
Your opinion would be very much welcomed
- drsclafani
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i have taken a baby aspirin daily for 25 years.silverbirch wrote:Dr S
I put myself on low aspirin 0.75 when I read Dr Z's theory so about 15mts ago. I had my procedure and I still continue to take it - surgeon said at the time it may do me some good ....
I must say that I am not on any meds nor have I ever been... DX 2009 CCSVI 2010.
My GP /Neuro know I’m on aspirin - I plan on staying on it... unless told differently or illness dictates I’m mindful of what I understand its effects
I take a coated aspirin and with probiotic drink
Your opinion would be very much welcomed