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Scientists, dentist, pharmacist and doctors
- Thread starter Sweet20s
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JackFTwist
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you ask very specific information and get pissed when you don;t get a reply in 26 minutes?
My father and grandfather were pharmicists so until someone who has the answer comes along how about this" I don't know
now if you want to post naked pics of yourself go ahead but don;t be pissed because no one with scientific expertise in this area has been on JUB in the last 26 minutes
My father and grandfather were pharmicists so until someone who has the answer comes along how about this" I don't know
now if you want to post naked pics of yourself go ahead but don;t be pissed because no one with scientific expertise in this area has been on JUB in the last 26 minutes
ixthrock
radical faerie
i have a friend who is a diagnostic sonographer specializing in the human heart; she would probably have a lot of interesting stuff to say about your question, even if there weren't a specific answer buried in her ruminations.
too bad i'm on the outs with her, right now, I'd call her up.
too bad i'm on the outs with her, right now, I'd call her up.
JackFTwist
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^ chill out yourself and post the nude pics, we want to discuss them and we don't need a scientist for that
i want it i want it i want it i want it but you can't have it: Peter Townsend
i want it i want it i want it i want it but you can't have it: Peter Townsend
ACE inhibitors are generally used on a more chronic basis to treat hypertension and heart failure. For an acute attack of angina, something fast acting (and more focused directly on the problem, like nitro) would be a better choice.
Won't take my cardio elective until May, so I'm sure someone who has already done that can give a more complete answer =P
Won't take my cardio elective until May, so I'm sure someone who has already done that can give a more complete answer =P
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Okay- here's the best explanation that I can give you without writing a book..
The renin-angiotensin-aldosterone system (RAAS) is how the kidneys manipulate peripheral resistance in the vascular system to raise blood pressure. When the kidneys perceive that they are underperfused, they release renin which triggers the RAAS. RAAS does a lot of things including increasing the resistance in arterioles aka peripheral vascular resistance (PVR).
Angiotensin converting enzyme (ACE) inhibitors block a step in the activation of the RAAS system. It prevents the cascade of things that happen when RAAS is activated including prevention of the action of Angiotensin II on the arterioles.
So, who would benefit from an ACE inhibitor (ACEI)? Technically, anyone with high blood pressure. The studies show that patients with hypertension do benefit from ACEI therapy but the response is very individualized. In clinical practice, the population that seems to benefit from ACEI therapy are diabetes, patients with renal artery stenosis and patients for whom other antihypertensives have not been as effective.
The important thing to keep in mind is that the mechanism of ACEI is slow and the clinical response is dependent upon the underlying pathology that is causing the hypertension.
In contrast, the mechanism of angina has two components- decreased flow through the coronary artery or increased oxygen demand by the myocardium (MV02). Angina is an ACUTE not chronic event. The drugs that are given for angina are drugs with rapid onset. This is why the drug of choice for angina was nitroglycerin. The nitrates in the NTG tablets have an immediate vasodilatory effect upon the vascular system INCLUDING the coronary arteries. This increases the perfursion in the coronary artery which increases available oxygen in transported to the myocardium.
ACEI therapy will reduce overall incidence of anginal attacks by reducing MV02. How? Over time, as PVR decreases the workload on the ventricles is decreased due to the positive effects on both afterload and preload. Ideally, with time this will reduce ventricular hypertrophy and cardiac workload which will reduce MV02. The problem is that the affects of ACEI therapy are gradual and the positive effects on MV02 are not seen immediately.
In the acute anginal event, time is of the essence so you want to immediately increase cardiac perfusion dramatically which can only occur through immediate dilation of the coronary aterry either through medications such as NTG which has an immediate effect or through mechanical means such as PTCA.
Hopefully you'll get this in time to help complete whatever homework you're working on.
The renin-angiotensin-aldosterone system (RAAS) is how the kidneys manipulate peripheral resistance in the vascular system to raise blood pressure. When the kidneys perceive that they are underperfused, they release renin which triggers the RAAS. RAAS does a lot of things including increasing the resistance in arterioles aka peripheral vascular resistance (PVR).
Angiotensin converting enzyme (ACE) inhibitors block a step in the activation of the RAAS system. It prevents the cascade of things that happen when RAAS is activated including prevention of the action of Angiotensin II on the arterioles.
So, who would benefit from an ACE inhibitor (ACEI)? Technically, anyone with high blood pressure. The studies show that patients with hypertension do benefit from ACEI therapy but the response is very individualized. In clinical practice, the population that seems to benefit from ACEI therapy are diabetes, patients with renal artery stenosis and patients for whom other antihypertensives have not been as effective.
The important thing to keep in mind is that the mechanism of ACEI is slow and the clinical response is dependent upon the underlying pathology that is causing the hypertension.
In contrast, the mechanism of angina has two components- decreased flow through the coronary artery or increased oxygen demand by the myocardium (MV02). Angina is an ACUTE not chronic event. The drugs that are given for angina are drugs with rapid onset. This is why the drug of choice for angina was nitroglycerin. The nitrates in the NTG tablets have an immediate vasodilatory effect upon the vascular system INCLUDING the coronary arteries. This increases the perfursion in the coronary artery which increases available oxygen in transported to the myocardium.
ACEI therapy will reduce overall incidence of anginal attacks by reducing MV02. How? Over time, as PVR decreases the workload on the ventricles is decreased due to the positive effects on both afterload and preload. Ideally, with time this will reduce ventricular hypertrophy and cardiac workload which will reduce MV02. The problem is that the affects of ACEI therapy are gradual and the positive effects on MV02 are not seen immediately.
In the acute anginal event, time is of the essence so you want to immediately increase cardiac perfusion dramatically which can only occur through immediate dilation of the coronary aterry either through medications such as NTG which has an immediate effect or through mechanical means such as PTCA.
Hopefully you'll get this in time to help complete whatever homework you're working on.
AdmiraalW238
JUB Addict
Okay- here's the best explanation that I can give you without writing a book..
Hopefully you'll get this in time to help complete whatever homework you're working on.
And I hope you cite Karabulut when you have finished your homework.
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Quoting Sweet20s: "okay, is someone intelligent going to help me and answer my question or do I need to take all of my clothes off and post some pics before someone answer my question."
You can still post those nekkid pics, by the way.
You can still post those nekkid pics, by the way.
Nur melden falls du hilfe brauchst.... die fotos müssten aber von dir seinsoon we will be the only homwework-help forum where you can pay with nude pics
hmm i have a paper on software agents due to sunday
Karabulut is right on... thanks.
Wrong forum, we can't help you here.... try technology. Although I don't know if they accept nude photos as payment... so you can post those here instead as gratitude
Wrong forum, we can't help you here.... try technology. Although I don't know if they accept nude photos as payment... so you can post those here instead as gratitude
In angina, the heart is functioning fine by itself (except during anginal attacks), there is no problem with preload or afterload. The problem lies within the coronary arteries which are clogged with fat. The majority of anginal treatment therefore lies in fixing the problematic arteries (statins, aspirin, CABG, PTCA, nitrates).
A blood-pressure controlling drug is used in angina, which is a beta-blocker. This is because some beta-blockers are cardioselective and will only exert its effects on the heart (which is useful, as angina is only a heart disease), and are also cardioprotective (a property which ACE-I don't have).
Also, ACE-I have side-effects that can worsen or complicate angina; hypotension, and hyperkalaemia (can cause dysrhytmias in an already compromised heart).
ACE-I are amazing antihypertensives, and are first line treatment in other blood-pressure diseases though!
A blood-pressure controlling drug is used in angina, which is a beta-blocker. This is because some beta-blockers are cardioselective and will only exert its effects on the heart (which is useful, as angina is only a heart disease), and are also cardioprotective (a property which ACE-I don't have).
Also, ACE-I have side-effects that can worsen or complicate angina; hypotension, and hyperkalaemia (can cause dysrhytmias in an already compromised heart).
ACE-I are amazing antihypertensives, and are first line treatment in other blood-pressure diseases though!
confused01
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I see I'm too late to give the answer... That's a shame Maybe I can make it up to you guys with a fun anecdote: The nitroglycerin talked about by KaraBulut is indeed a vasodillatator. It has this effect because it releases nitric oxide (NO).
NO is also used by the body as a vasodillatator in the process of ... the penis erection (NO causes cGMP to be formed in the body which is the actual vasodillatator and relaxes the smooth muscle tissue).
Other anecdote: Viagra works by blocking the break down of cGMP (cyclic guanidine monophosphate)
That was my contribution to this forum today
Maybe I can make it up to you guys with a fun anecdote: The nitroglycerin talked about by KaraBulut is indeed a vasodillatator. It has this effect because it releases nitric oxide (NO). NO is also used by the body as a vasodillatator in the process of ... the penis erection
(NO causes cGMP to be formed in the body which is the actual vasodillatator and relaxes the smooth muscle tissue). Other anecdote: Viagra works by blocking the break down of cGMP (cyclic guanidine monophosphate)
That was my contribution to this forum today
