[Rawalian]

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

 

[patelMD]

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

 

[dr tee]

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

 

[Dr. Mexito]

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..

 

[patho2012]

but NE cause vasodilation in coronary art..

Are you sure?

 

[Dr.NickRiviera]

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

looks like NE is the answer.

 

[Dr. Mexito]

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...

 

[patho2012]

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.

 

[Dr. Mexito]

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/227/4/238.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.

 

[Sadde]

oxygen is the answer

http://ajpheart.physiology.org/content/272/1/H67.abstract - Hyperoxia causing vasoconstriction in rabbits

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941910/ - hyperoxia causing vasoconstriction in humans

 

[patho2012]

http://ajpheart.physiology.org/content/272/1/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"

 

[Dr. Mexito]

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.

 

[patho2012]

you don't get hyperoxia by hyperventilation or increased blood flow to the lung...Hyperoxia is 100% O2 compressed in high pressure condition.

 

[Dr. Mexito]

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...

 

[Dr.NickRiviera]

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.

 

[Dr. Mexito]

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"

 

[Joanna]

"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

 

[Dr. Mexito]

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

 

[justfree]

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.

 

[mohitkmc]

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