Nitric oxide modulates right ventricular flow and oxygen consumption during norepinephrine infusion.

@article{Setty2002NitricOM,
  title={Nitric oxide modulates right ventricular flow and oxygen consumption during norepinephrine infusion.},
  author={Srinath Setty and Johnathan D. Tune and H. Fred Downey},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2002},
  volume={282 2},
  pages={
          H696-703
        }
}
  • S. Setty, J. Tune, H. F. Downey
  • Published 1 February 2002
  • Medicine, Biology
  • American journal of physiology. Heart and circulatory physiology
This study was designed to test if nitric oxide (NO) contributes to norepinephrine-induced right coronary vasodilation and if NO blunts the norepinephrine-induced increase in myocardial oxygen consumption (MVO(2)) in the right ventricle. In five anesthetized, open-chest dogs, mean aortic pressure, heart rate, right ventricular rate of pressure development over time (dP/dt), right coronary blood flow, and right ventricular MVO(2) were measured before and during graded intracoronary infusions of… 
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15 Citations
Background Citations
7
Methods Citations
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Results Citations
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15 Citations

Citation Type

Citation Type

Nitric oxide contributes to oxygen demand-supply balance in hypoperfused right ventricle.
Endogenous nitric oxide regulates right coronary blood flow during acute pulmonary hypertension in conscious dogs
TLDR
No is required for the RC hyperemic response to acute pulmonary hypertension as well as for normal resting RC blood flow after blockade of NO synthesis, RV O 2 supply at rest and during pulmonary hypertension was sustained by increased RV O2 extraction.
Nitric oxide contributes to right coronary vasodilation during systemic hypoxia.
TLDR
It is concluded that NO contributes to RC vasodilation during systemic hypoxia, and increases in RV MVo(2) during Hypoxia are met normally by increasing RC blood flow.
Hypoxia-induced vasodilation in the right coronary circulation of conscious dogs: Role of adrenergic activation
α-Adrenergic Vasoconstrictor Tone Limits Right Coronary Blood Flow in Exercising Dogs
In exercising dogs, increased myocardial O2 consumption (MVO2) of the left ventricle is met primarily by hyperemia, whereas increased O2 extraction makes a greater contribution to right ventricular…
Mechanisms of Oxygen Demand/Supply Balance in the Right Ventricle
TLDR
Normal right ventricular external work and O2 demand/supply balance can be maintained during moderate coronary hypoperfusion, especially during poorly autoregulating right coronary circulation.
Right Ventricular Perfusion: Physiology and Clinical Implications
Regulation of blood flow to the right ventricle differs significantly from that to the left ventricle. The right ventricle develops a lower systolic pressure than the left ventricle, resulting in…
Phenotypic adaptation of the late preconditioned heart: myocardial oxygen consumption is reduced.
Norepinephrine increases tolerance to acute anemia*
TLDR
Application of norepinephrine can be judged a first-line intervention to bridge acute anemia via a stabilization of MAP and coronary perfusion pressure and its sole long-term use during extreme anemia without concomitant transfusion of erythrocytes is not advised.
Adaptation to acute pulmonary hypertension in pigs
TLDR
It is suggested that right ventricular compensation during acute pulmonary hypertension is strongly dependent on the individual capability to increase coronary flow and the cause for inter‐individual variability could be the dimension and reactivity of the coronary system.
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References

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TLDR
It is indicated that endogenous NO limits right ventricular MVO2 under controlled hemodynamic conditions, consistent with the greater shear stress-mediated release of NO.
Nitric oxide does not modulate the increases in blood flow, O2 consumption, or contractility during CaCl2 administration in canine hearts.
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TLDR
No causes a modest coronary vasodilation at rest and during exercise but does not act as a local metabolic vasodilator when NO synthesis is inhibited, and adenosine does not mediate a compensatory local metabolic coronary Vasodilation when NOhesis is inhibited.
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TLDR
The absence of NO in the coronary circulation of the conscious dog during exercise does not affect levels of CBF, because it shifts the relationship between cardiac work and myocardial oxygen consumption, suggesting that endogenous NO modulates myocardian metabolism.
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The contribution of the L-arginine/nitric oxide pathway to beta-adrenergic dilation of resistance coronary vessels was examined in conscious dogs instrumented for measuring coronary blood flow (CBF),…
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TLDR
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TLDR
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TLDR
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Endogenous Basal Nitric Oxide Production Does Not Control Myocardial Oxygen Consumption or Function
  • J. Sadoff, P. Scholz, H. Weiss
  • Medicine, Biology
    Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine
  • 1996
Abstract Previous studies from our laboratory have shown that an extrinsic nitric oxide (NO) donor (i.e., nitroprusside) caused vasodilatation and negative inotropy by activating guanylate cyclase…
Effect of inhibition of nitric oxide formation on coronary blood flow during exercise in the dog.
TLDR
Findings fail to support an essential role for nitric oxide in coronary resistance vessel dilatation during exercise in the dog.
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