Coronary blood flow question - USMLE Forums
USMLE Forums Logo
USMLE Forums         Your Reliable USMLE Online Community     Members     Posts
Home
USMLE Articles
USMLE News
USMLE Polls
USMLE Books
USMLE Apps
Go Back   USMLE Forums > USMLE Step 1 Forum

USMLE Step 1 Forum USMLE Step 1 Discussion Forum: Let's talk about anything related to USMLE Step 1 exam


Reply
 
Thread Tools Search this Thread Display Modes
  #1  
Old 02-08-2011
USMLE Forums Scout
 
Steps History: Step 1 Only
Posts: 48
Threads: 30
Thanked 37 Times in 14 Posts
Reputation: 47
Heart Coronary blood flow question

coronary blood flow is studies in an animal model of ischemic heart disease. in this model coronary blood flow is normal when the animal is at rest, but when the animal becomes active, coronary vasoconstriction occurs and coronary blood flow decreases. the most likely cause of the observed vasoconstriction is the action of which of the following on vascular smooth muscle?

a. adenosine
b. NO
c. NE
d. Oxygen
e. prostacyclin
Reply With Quote Quick reply to this message



  #2  
Old 02-08-2011
USMLE Forums Master
 
Steps History: 1+CK+CS+3
Posts: 1,175
Threads: 38
Thanked 852 Times in 478 Posts
Reputation: 862
Default

  1. Adenosine is used in PSVT, so can't be a vasoconstrictor
  2. NO is a potent Vasodilator
  3. NE alpha 1 & beta 1 actions could lead to a vasoconstrictive state in increased o2 demand states
  4. O2, has no direct actions on vascular smooth muscle
  5. Prostacylin is a vasodilator (opposite effects of TXA2)
Answer is NE
Reply With Quote Quick reply to this message
The above post was thanked by:
aktorque (02-09-2011), justfree (03-14-2012), Linc (10-16-2015), Mondoshawan (02-08-2011), Rawalian (02-08-2011), singapur_md (06-28-2011), sm3356 (06-14-2015)
  #3  
Old 02-09-2011
USMLE Forums Addict
 
Steps History: Not yet
Posts: 147
Threads: 18
Thanked 49 Times in 30 Posts
Reputation: 59
Default

in exercise there is symp stimulation leading to increase HR and cardiac contratility wh can cause coronary vasoconstriction,metabolites from exercising muscle eg adenosine,lactic acid cause vasodil,
so NE
Reply With Quote Quick reply to this message
The above post was thanked by:
aktorque (02-09-2011)
 
  #4  
Old 03-13-2012
Dr. Mexito's Avatar
USMLE Forums Master
 
Steps History: 1+CK+CS
Posts: 662
Threads: 72
Thanked 369 Times in 204 Posts
Reputation: 379
Default

Quote:
Originally Posted by dr tee View Post
in exercise there is symp stimulation leading to increase HR and cardiac contratility wh can cause coronary vasoconstriction,metabolites from exercising muscle eg adenosine,lactic acid cause vasodil,
so NE
but NE cause vasodilation in coronary art..
__________________
"Disease is very old, and nothing about it has changed. It is we who change as we learn to recognize what was formerly imperceptible." JMC
Reply With Quote Quick reply to this message
  #5  
Old 03-13-2012
patho2012's Avatar
USMLE Forums Veteran
 
Steps History: ---
Posts: 213
Threads: 13
Thanked 119 Times in 81 Posts
Reputation: 129
Default

Quote:
Originally Posted by Dr. Mexito View Post
but NE cause vasodilation in coronary art..
Are you sure?
Reply With Quote Quick reply to this message
  #6  
Old 03-13-2012
USMLE Forums Master
 
Steps History: 1+CK+CS
Posts: 1,406
Threads: 118
Thanked 644 Times in 408 Posts
Reputation: 654
Default

adenosine - vasodilates
NO - vasodilates
NE - vasoconstricts
Oxygen - dont know
prostacyclin - vasodilates

looks like NE is the answer.
__________________
"inflammable means flammable!? What a country."
Reply With Quote Quick reply to this message
  #7  
Old 03-13-2012
Dr. Mexito's Avatar
USMLE Forums Master
 
Steps History: 1+CK+CS
Posts: 662
Threads: 72
Thanked 369 Times in 204 Posts
Reputation: 379
Default

Quote:
Originally Posted by patho2012 View Post
Are you sure?
Yes... very sure...

In the coronary circulation, norepinephrine elicits vasodilation, due to the predominance of beta-adrenergic receptors in the coronary circulation. Agonists of alpha-receptors, such as phenylephrine, elicit very little constriction in the coronary circulation.

http://en.wikipedia.org/wiki/Coronary_circulation

Is also in UW...
__________________
"Disease is very old, and nothing about it has changed. It is we who change as we learn to recognize what was formerly imperceptible." JMC
Reply With Quote Quick reply to this message
  #8  
Old 03-13-2012
patho2012's Avatar
USMLE Forums Veteran
 
Steps History: ---
Posts: 213
Threads: 13
Thanked 119 Times in 81 Posts
Reputation: 129
Default

Quote:
Originally Posted by Dr. Mexito View Post
Yes... very sure...

Is also in UW...
Really confused...What does UW say?

For norepi, b1> a1=a2>>>b2 is favoured. Unless you make the poor animal totally relaxed, blocking a1 and infuse a huge amount of norepi into the coronary vessel, it won't dilate.

I think vasoconstriction of coronary vessels here is due to contraction of ventricular muscle that squeezes it. Correct me if I'm wrong. The Q makes you think that sympathetic nerves secrete Norepinephrine into the coronary vessel and provoke vasoconstriction. Coronary vasculature is under very minor effect of the sympathetic nervous system.
Reply With Quote Quick reply to this message
The above post was thanked by:
neha_subh (05-30-2013)
  #9  
Old 03-14-2012
Dr. Mexito's Avatar
USMLE Forums Master
 
Steps History: 1+CK+CS
Posts: 662
Threads: 72
Thanked 369 Times in 204 Posts
Reputation: 379
Default

Quote:
Originally Posted by patho2012 View Post
Really confused...What does UW say?

For norepi, b1> a1=a2>>>b2 is favoured. Unless you make the poor animal totally relaxed, blocking a1 and infuse a huge amount of norepi into the coronary vessel, it won't dilate.
I failed to find the Q in UW... but I found this:

http://ebm.rsmjournals.com/content/2....full.pdf+html

"...It is apparent that both alpha-vasoconstriction and beta-vasodilation occur simultaneously in the coronary circulation during sympathetic activation. These effects may not be as antagonistic as they at first appear. Alpha-Adrenoceptor vasoconstriction is predominantly a large vessel (>100 um) phenomenon, whereas small vessels only relax in response to norepinephrine (143–145). This may be explained by the distribution of alpha- and beta-adrenoceptors along the coronary arterial tree (160, 161).

This reciprocal gradient in adrenoceptors favors sympathetic vasodilation in resistance vessels and vasoconstriction in distribution vessels. Therefore, alpha-adrenoceptor vasoconstriction and beta-adrenoceptor vasodilation appear to be spatially distributed so as to increase coronary blood flow (beta) and at the same time improve transmural flow distribution (alpha). The feed-forward beta-adrenoceptor vasodilation accounts for ∼25% of the increase in coronary blood flow observed during exercise [...]

Feed-forward beta-adrenoceptor-mediated coronary vasodilation has been shown to account for ∼25% of coronary vasodilation observed during exercise.
This dilation is a direct effect of norepinephrine’s action on small coronary arterioles...."

So... going back to the question. It cannot be NO the one that is causing vasoconstriction in this dog.

I don't know the answer... but for sure is not NO.
__________________
"Disease is very old, and nothing about it has changed. It is we who change as we learn to recognize what was formerly imperceptible." JMC
Reply With Quote Quick reply to this message
  #10  
Old 03-14-2012
USMLE Forums Master
 
Steps History: ---
Posts: 530
Threads: 35
Thanked 291 Times in 207 Posts
Reputation: 301
Default oxygen is the answer

http://ajpheart.physiology.org/conte...1/H67.abstract - Hyperoxia causing vasoconstriction in rabbits

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941910/ - hyperoxia causing vasoconstriction in humans
Reply With Quote Quick reply to this message
The above post was thanked by:
Dr. Mexito (03-14-2012), Joanna (03-14-2012), patho2012 (03-14-2012)
  #11  
Old 03-14-2012
patho2012's Avatar
USMLE Forums Veteran
 
Steps History: ---
Posts: 213
Threads: 13
Thanked 119 Times in 81 Posts
Reputation: 129
Default

Quote:
Originally Posted by Sadde View Post
http://ajpheart.physiology.org/conte...1/H67.abstract - Hyperoxia causing vasoconstriction in rabbits

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941910/ - hyperoxia causing vasoconstriction in humans
You rock Sadde, but the question doesn't mention anything about therapy or treatment, why do you assume that it 's due to hyperoxia?
" in this model coronary blood flow is normal when the animal is at rest, but when the animal becomes active, coronary vasoconstriction occurs and coronary blood flow decreases"
Reply With Quote Quick reply to this message
The above post was thanked by:
Joanna (03-14-2012)
  #12  
Old 03-14-2012
Dr. Mexito's Avatar
USMLE Forums Master
 
Steps History: 1+CK+CS
Posts: 662
Threads: 72
Thanked 369 Times in 204 Posts
Reputation: 379
Default

Quote:
Originally Posted by patho2012 View Post
You rock Sadde, but the question doesn't mention anything about therapy or treatment, why do you assume that it 's due to hyperoxia?
" in this model coronary blood flow is normal when the animal is at rest, but when the animal becomes active, coronary vasoconstriction occurs and coronary blood flow decreases"

Exercise --> more O2 --> vasoconstriction.

Plus... by elimination... O2 is the only option.
__________________
"Disease is very old, and nothing about it has changed. It is we who change as we learn to recognize what was formerly imperceptible." JMC
Reply With Quote Quick reply to this message
The above post was thanked by:
Joanna (03-14-2012)
  #13  
Old 03-14-2012
patho2012's Avatar
USMLE Forums Veteran
 
Steps History: ---
Posts: 213
Threads: 13
Thanked 119 Times in 81 Posts
Reputation: 129
Default

you don't get hyperoxia by hyperventilation or increased blood flow to the lung...Hyperoxia is 100% O2 compressed in high pressure condition.
Reply With Quote Quick reply to this message
  #14  
Old 03-14-2012
Dr. Mexito's Avatar
USMLE Forums Master
 
Steps History: 1+CK+CS
Posts: 662
Threads: 72
Thanked 369 Times in 204 Posts
Reputation: 379
Default

Quote:
Originally Posted by patho2012 View Post
you don't get hyperoxia by hyperventilation or increased blood flow to the lung...Hyperoxia is 100% O2 compressed in high pressure condition.

But this is an experiment where they have a dog with cables and stuff all around there. So I'm thinking... they put the dog to walk, run or whatever... then, they add some extra O2 to the heart, sit down and see what happens.

That makes sense to me...
__________________
"Disease is very old, and nothing about it has changed. It is we who change as we learn to recognize what was formerly imperceptible." JMC
Reply With Quote Quick reply to this message
  #15  
Old 03-14-2012
USMLE Forums Master
 
Steps History: 1+CK+CS
Posts: 1,406
Threads: 118
Thanked 644 Times in 408 Posts
Reputation: 654
Default

But yo, isnt the heart always extracting maximum oxygen from the coronary blood flow? So whatever oxygen u give it it will take up. I cant see increased oxygen in the coronary blood causing vasoconstricton then as the heart welcomes as much oxygen as you want to give it.

I dont know, just a thought.
Correct me if my logic is wrong.
__________________
"inflammable means flammable!? What a country."
Reply With Quote Quick reply to this message



  #16  
Old 03-14-2012
Dr. Mexito's Avatar
USMLE Forums Master
 
Steps History: 1+CK+CS
Posts: 662
Threads: 72
Thanked 369 Times in 204 Posts
Reputation: 379
Default

Quote:
Originally Posted by patho2012 View Post
you don't get hyperoxia by hyperventilation or increased blood flow to the lung...Hyperoxia is 100% O2 compressed in high pressure condition.

"...Coronary diastolic blood velocity (CBV) and coronary vascular resistance (CVR) were measured breathing room air and after exposure to hyperoxia (100% O2) for 5 mins [...] indicating a direct vasoconstrictor effect of hyperoxia on the coronary circulation not mediated through autonomic reflexes."

"... the hypothesis that hyperoxia leads to the generation of reactive oxygen species, which in turn decreases the bioavailability of nitric oxide and results in vasoconstriction"
__________________
"Disease is very old, and nothing about it has changed. It is we who change as we learn to recognize what was formerly imperceptible." JMC
Reply With Quote Quick reply to this message
  #17  
Old 03-14-2012
Joanna's Avatar
USMLE Forums Scout
 
Steps History: Step 1 Only
Posts: 51
Threads: 0
Thanked 21 Times in 19 Posts
Reputation: 31
Default

"coronary blood flow is studies in an animal model of ischemic heart disease"

vasospastic angina is due to a reversible decrease in coronary blood flow ...

decrease in coronary blood flow ---> decrease oxygen uptake ( don't forget the dog is already ischemic )

the case is O2 yes ... but decrease not increase .. my answer will be D
Reply With Quote Quick reply to this message
The above post was thanked by:
Dr. Mexito (03-14-2012)
  #18  
Old 03-14-2012
Dr. Mexito's Avatar
USMLE Forums Master
 
Steps History: 1+CK+CS
Posts: 662
Threads: 72
Thanked 369 Times in 204 Posts
Reputation: 379
Default

Quote:
Originally Posted by Dr.NickRiviera View Post
But yo, isnt the heart always extracting maximum oxygen from the coronary blood flow? So whatever oxygen u give it it will take up. I cant see increased oxygen in the coronary blood causing vasoconstricton then as the heart welcomes as much oxygen as you want to give it.

I dont know, just a thought.
Correct me if my logic is wrong.
Myocardial Oxygen Consumption during Hyperoxia
One could speculate that an increase in oxygen extraction in ACS might compensate for the decreased CBF seen with oxygen. Animal studies suggest that a high PO2 decreases myocardial oxygen consumption independent of heart rate, cardiac performance and metabolic requirements. [...] high flow oxygen therapy causes a misdistribution of microcirculatory blood flow with increased functional O2 shunting and a reduction in total body oxygen consumption [...] Thus high flow oxygen, despite improving oxygenation may not improve organ specific oxygen delivery.
  1. Hyperoxia leads to the generation of reactive oxygen species
  2. K+ATP channels in hyperoxia induced vasoconstriction
  3. Hyperoxia can induce vasoconstriction by acting directly on L-type Ca2+ channels
  4. Hyperoxia may affect the release of angiotensin II with subsequent changes in endothelin-1 levels
  5. Hyperoxia increases the production of potent vasoconstrictor 20-HETE
So... going back to the question. The correct answer is O2

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941910/

P.S. thanks Sadde for the link
__________________
"Disease is very old, and nothing about it has changed. It is we who change as we learn to recognize what was formerly imperceptible." JMC
Reply With Quote Quick reply to this message
The above post was thanked by:
justfree (03-14-2012)
  #19  
Old 03-14-2012
USMLE Forums Scout
 
Steps History: Not yet
Posts: 36
Threads: 14
Thanked 11 Times in 10 Posts
Reputation: 21
Default

Quote:
Originally Posted by Dr.NickRiviera View Post
But yo, isnt the heart always extracting maximum oxygen from the coronary blood flow? So whatever oxygen u give it it will take up. I cant see increased oxygen in the coronary blood causing vasoconstricton then as the heart welcomes as much oxygen as you want to give it.

I dont know, just a thought.
Correct me if my logic is wrong.
This is what it says in BRS physio.....the most important local metabolic factors for coronary circulation (in autoregulation) are hypoxia and adenosine. For example, increases in myocardial contractility are accompanies by an increased demand for O2. To meet this demand, compensatory vasodilation of coronary vessels occurs and, accordingly, both blood flow and O2 delivery to the contracting heart muscle increase.

Since flow increases adenosine will not locally accumulate to cause vasodilation. Does that contribute to vasoconstrictive effect as in the question? Just a thought.
Reply With Quote Quick reply to this message
  #20  
Old 03-14-2012
USMLE Forums Addict
 
Steps History: Not yet
Posts: 191
Threads: 8
Thanked 121 Times in 76 Posts
Reputation: 131
Default

Quote:
Originally Posted by justfree View Post
This is what it says in BRS physio.....the most important local metabolic factors for coronary circulation (in autoregulation) are hypoxia and adenosine. For example, increases in myocardial contractility are accompanies by an increased demand for O2. To meet this demand, compensatory vasodilation of coronary vessels occurs and, accordingly, both blood flow and O2 delivery to the contracting heart muscle increase.

Since flow increases adenosine will not locally accumulate to cause vasodilation. Does that contribute to vasoconstrictive effect as in the question? Just a thought.
Agree with you on this..Definitely exercise results in increase O2 demand of the cardiac muscle all the vessels in the body ecxept pulmonary vessels cause vasodilation to meet the requires O2 demand...During exercise the blood flow in the coronary vessels increases resulting in washing away of adenosine which is the most important mechanism of locally causing vasodilation in the coronary vessels...so it can be responsible here
Answer is A
Hypoxia should hv caused coronary vasodilation
Good question made all of us think...
@Rawalian cn u pls tell the answer
Reply With Quote Quick reply to this message
  #21  
Old 03-14-2012
XpaezX's Avatar
USMLE Forums Master
 
Steps History: 1+CK+CS+3
Posts: 1,216
Threads: 41
Thanked 1,327 Times in 711 Posts
Reputation: 1342
Default

Quote:
Originally Posted by mohitkmc View Post
Agree with you on this..Definitely exercise results in increase O2 demand of the cardiac muscle all the vessels in the body ecxept pulmonary vessels cause vasodilation to meet the requires O2 demand...During exercise the blood flow in the coronary vessels increases resulting in washing away of adenosine which is the most important mechanism of locally causing vasodilation in the coronary vessels...so it can be responsible here
Answer is A
Hypoxia should hv caused coronary vasodilation
Good question made all of us think...
@Rawalian cn u pls tell the answer
Adenosine causes vasodilation, there they specify what caused the VASOCONSTRICTION not vasodilation, it has to be O2
Reply With Quote Quick reply to this message
  #22  
Old 03-14-2012
patho2012's Avatar
USMLE Forums Veteran
 
Steps History: ---
Posts: 213
Threads: 13
Thanked 119 Times in 81 Posts
Reputation: 129
Default

Guys, you have taken this too far.
Norepinephrine is a vasoconstrictor because it has greater sensitivity for a1 Rs much more than for b2 Rs, and where there are b2 Rs, there are also a1 Rs. B2 Rs are reserved for Epinephrine, secreted by Adrenal gland. (Kaplan Pharm note and Dr Raymond 's lecture).

This animal studies is an analogy for exertional angina in ischemic patients, ie pain increases with activity and disappears at rest. There is no injection of Norepi or Hyperbaric O2 therapy or it must be a super hard Q.
Reply With Quote Quick reply to this message
The above post was thanked by:
Joanna (03-14-2012)
  #23  
Old 01-27-2013
USMLE Forums Scout
 
Steps History: Not yet
Posts: 28
Threads: 2
Thanked 1 Time in 1 Post
Reputation: 11
Default plz post answer

plz post answer correct
Reply With Quote Quick reply to this message
  #24  
Old 01-27-2013
neha_subh's Avatar
USMLE Forums Veteran
 
Steps History: 1 + CS
Posts: 209
Threads: 18
Thanked 112 Times in 75 Posts
Reputation: 122
Default

coronary blood flow is studies in an animal model of ischemic heart disease. in this model coronary blood flow is normal when the animal is at rest, but when the animal becomes active, coronary vasoconstriction occurs and coronary blood flow decreases. the most likely cause of the observed vasoconstriction is the action of which of the following on vascular smooth muscle?

a. adenosine (vasodilatory metabolite increased during exercise)
b. NO (vasodilator)
c. NE (vasoconstriction)
d. Oxygen (no role in constriction or dilatation)
e. prostacyclin (vasodilator)
__________________
lets kick some doors open and help each other to reach our destinies
To view links or images in signatures your post count must be 10 or greater. You currently have 0 posts.
Reply With Quote Quick reply to this message
  #25  
Old 05-25-2013
USMLE Forums Newbie
 
Steps History: Not yet
Posts: 3
Threads: 0
Thanked 5 Times in 1 Post
Reputation: 15
Default

Q is a bit confusing.
Exercise--sympathetic activation--Increased HR + contractility -- Coronary vasodilation to provide proper blood flow.
For increased O2 demand , increased O2 supply is needed.
How there is exercise and coronary vasoconstriction at the same time...!
Reply With Quote Quick reply to this message



  #26  
Old 05-25-2013
USMLE Forums Addict
 
Steps History: Not yet
Posts: 198
Threads: 19
Thanked 47 Times in 43 Posts
Reputation: 57
Default

"Normal coronary arteries show coronary vasodilation of the proximal (+20%) and distal (+40%) vessel segments during supine bicycle exercise. However, patients with coronary artery disease show exercise-induced vasoconstriction of the stenotic vessel segments. The exact mechanism of exercise-induced stenosis narrowing is not clear but might be related to a passive collapse of the disease-free vessel wall (Venturi mechanism), elevated plasma levels of circulating catecholamines, an insufficient production of the endothelium-derived vasorelaxing factor or increased platelet aggregation due to turbulent blood flow with release of thromboxane A2 and serotonin. "
Reply With Quote Quick reply to this message
The above post was thanked by:
mohdkhan (05-31-2013)
  #27  
Old 05-31-2013
USMLE Forums Newbie
 
Steps History: Not yet
Posts: 3
Threads: 0
Thanked 5 Times in 1 Post
Reputation: 15
Post

Quote:
Originally Posted by mk09 View Post
"Normal coronary arteries show coronary vasodilation of the proximal (+20%) and distal (+40%) vessel segments during supine bicycle exercise. However, patients with coronary artery disease show exercise-induced vasoconstriction of the stenotic vessel segments. The exact mechanism of exercise-induced stenosis narrowing is not clear but might be related to a passive collapse of the disease-free vessel wall (Venturi mechanism), elevated plasma levels of circulating catecholamines, an insufficient production of the endothelium-derived vasorelaxing factor or increased platelet aggregation due to turbulent blood flow with release of thromboxane A2 and serotonin. "
@mk09 thank you for your convincing explanation.
Reply With Quote Quick reply to this message



Reply

Tags
Cardiovascular-, Physiology-, Step-1-Questions

Quick Reply
Message:
Options

Register Now

In order to be able to post messages on the USMLE Forums forums, you must first register.
Please enter your desired user name, your email address and other required details in the form below.
User Name:
Password
Please enter a password for your user account. Note that passwords are case-sensitive.
Password:
Confirm Password:
Email Address
Please enter a valid email address for yourself.
Email Address:
Medical School
Choose "---" if you don't want to tell. AMG for US & Canadian medical schools. IMG for all other medical schools.
USMLE Steps History
What steps finished! Example: 1+CK+CS+3 = Passed Step 1, Step 2 CK, Step 2 CS, and Step 3.

Choose "---" if you don't want to tell.

Favorite USMLE Books
What USMLE books you really think are useful. Leave blank if you don't want to tell.
Location
Where you live. Leave blank if you don't want to tell.

Log-in

Human Verification

In order to verify that you are a human and not a spam bot, please enter the answer into the following box below based on the instructions contained in the graphic.



Thread Tools Search this Thread
Search this Thread:

Advanced Search
Display Modes


Similar Threads
Thread Thread Starter Forum Replies Last Post
Autoregulation of Coronary Blood Flow Rawalian USMLE Step 1 Forum 1 02-14-2011 04:20 PM
50% Decreased Flow in the Coronary Artery kemoo USMLE Step 1 Forum 6 01-27-2011 12:18 PM
blood flow in vessel? kemoo USMLE Step 1 Forum 2 01-27-2011 10:37 AM
Increased coronary blood flow in aortic stenosis ecgram USMLE Step 1 Forum 2 05-22-2010 01:16 PM
Blood film question DrLANC USMLE Step 1 Forum 6 12-14-2009 11:59 AM

RSS Feed
Find Us on Facebook
vBulletin Security provided by vBSecurity v2.2.2 (Pro) - vBulletin Mods & Addons Copyright © 2017 DragonByte Technologies Ltd.

USMLE® & other trade marks belong to their respective owners, read full disclaimer
USMLE Forums created under Creative Commons 3.0 License. (2009-2014)