Thanks for that, Qadgop. I can’t emulate your cardiac lab experience, so I must accept your input at face value.
However, all the info I have accessed since reading your post place reasonable emphasis on the reduction on left ventricular diastolic pressure (and the consequent reduction in workload), as well as coronary vasodilation, to explain the relief of angina pectoris from glyceryl trinitrate (GTN).
Also, your post refers to direct administration to the site of action via a catheter, so of course an instant coronary effect is achieved. I am more accustomed to the familiar sub-lingual or dermal administration of GTN, where the effect is seen in peripheral vessels upon absorption, prior to moving to the heart via venous return.
Assuming your thoughts reflect the current thinking on this issue, why hasn’t the pharmacology information as supplied by drug companies been updated?
"The vascular endothelium, once thought to be merely a passive barrier that separates the lumen from the vessel wall, is actively involved in the response to noxious environmental stimuli. These defense mechanisms include release of endothelium-derived relaxing factor (EDRF), which is now known to be nitric oxide.2 Nitric oxide relaxes vascular smooth muscle and also inhibits platelet aggregation and adhesion. The various forms of nitrate therapy provide an exogenous source of nitric oxide.
Nitrates are potent venodilators and, at higher doses, they are also arterial dilators. Nitrate-induced venodilation causes a decrease in venous return to the heart, thereby reducing left ventricular wall stress, which leads to a decrease in myocardial oxygen demand. Dilatation of the stenotic vessel, as well as dilatation of the intracoronary collateral arteries, increases blood flow to ischemic myocardium. Nitrates have also been shown to relieve coronary spasm."
I dunno Deev, I guess a lot of the nitric oxide actions aren’t fully understood yet. They did award the Nobel Prize for Medicine to the guy who figured out that Nitric Oxide was involved in this whole process, but there’s still a lot of ground to be covered. After all, Viagra was designed as an anti-anginal med, working by futzing with NO2, and look how that actually played out. But examining the above cite tends to support both of our claims, so maybe we should just chalk up the effects to synergy. Two points for both of us!
nor a med student, for that matter. And now you say it,I DO remember seeing Billy Rubin in Silence, but I didn’t intentionally hijack it from there.
And I saw my newborn under a bilirubin light, I’m not sure anyone would look good in that light.
And saying it was “handy” was a bad pun at Handy, who made a comment about the handle, as if to say, “boy, what a totally non-original handle”. Took mild offense but since I thought I might be reading it wrong, I just made the comment about it being “handy” rather than being confrontational, as I dislike confrontation, or for that matter, pissing anyone off. And you guys totally lost me with all that medical stuff- whooooooo- I’m glad i’m not a doctor OR play one on TV.