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d-Propranolol prevents adenosine formation associated with myocardial hypoperfusion
R D Wangler1, W P Peterson, H V Sparks
1Department of Physiology, Michigan State University, East Lansing 48824.
The American Journal of Physiology
|March 1, 1989
Summary
d-Propranolol prevents increased adenosine release from hypoperfused hearts by blocking nucleoside formation. This occurs by reducing oxygen demand, preventing oxygen supply reduction from stimulating adenosine production.
Area of Science:
- Cardiovascular Physiology
- Biochemistry
Background:
- Hypoperfusion in the heart increases adenine nucleoside release.
- d-Propranolol has been shown to eliminate this increased release.
Purpose of the Study:
- To determine if d-propranolol reduces adenosine formation or its release into the vascular compartment.
- To investigate the mechanism by which d-propranolol affects adenosine nucleoside release during hypoperfusion.
Main Methods:
- Measurement of myocardial tissue adenosine (TADO) and nucleoside release.
- Induction of hypoperfusion by reducing perfusion pressure by 50% and 75%.
- Administration of d-propranolol during hypoperfusion and assessment of its effects on coronary flow (CF), venous oxygen tension (PVO2), myocardial oxygen consumption (MVO2), and adenosine/inosine release.
Main Results:
- Hypoperfusion significantly increased TADO and adenosine/inosine release.
- d-Propranolol administration during hypoperfusion eliminated the increase in adenosine and inosine release.
- TADO remained significantly lower in hypoperfused hearts treated with d-propranolol compared to untreated hypoperfused hearts.
- d-Propranolol maintained a normal oxygen supply-to-consumption ratio despite severe hypoperfusion.
Conclusions:
- d-Propranolol blocks cardiac nucleoside formation during hypoperfusion.
- This blockade is achieved by reducing myocardial oxygen demand.
- Consequently, reduced oxygen supply does not stimulate adenosine formation in the presence of d-propranolol.