Related Experiment Videos
Pulsation-induced dilation of subendocardial and subepicardial arterioles: effect on vasodilator sensitivity
Oana Sorop1, Jos A E Spaan, Ed VanBavel
1Department of Medical Physics, Academic Medical Center, University of Amsterdam, 1100 DE Amsterdam, The Netherlands.
Insights
Myocardial compression during systole impacts coronary blood flow. Pulsatile pressure in arteries causes dilation and increases sensitivity to vasodilators like bradykinin and adenosine, particularly in subendocardial vessels.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Myocardial Mechanics
Background:
- Coronary arteries experience mechanical compression during systole.
- This compression impedes blood flow, especially in the subendocardium.
- Understanding this effect is crucial for coronary circulation research.
Purpose of the Study:
- To investigate the impact of pulsatile pressure on isolated coronary resistance arteries.
- To determine if myocardial compression affects vasodilator responses.
- To elucidate the mechanisms behind pulsation-induced vasodilation.
Main Methods:
- Isolated subendocardial and subepicardial arteries were cannulated.
- Pulsatile transvascular pressure (0.5-2.5 Hz, 20-100 mmHg) was applied.
- Intracellular calcium and vasodilator sensitivity (bradykinin, adenosine) were measured.
Main Results:
- Pulsation induced vasodilation, more pronounced in subepicardial vessels.
- Pulsation caused a slight increase in intracellular calcium.
- Vasodilator sensitivity to bradykinin and adenosine significantly increased, especially in subendocardial vessels.
- Pulsation-induced dilation was independent of intracellular calcium reduction.
Conclusions:
- Pulsation-induced vasodilation occurs at physiological conditions in coronary arteries.
- This phenomenon enhances vasodilator sensitivity.
- The findings offer new insights into coronary blood flow regulation during cardiac cycles.
Abstract:
Coronary vessels are squeezed by the surrounding myocardium during systole, impeding blood flow specifically in the subendocardium. To study the myocardial compression effect, we applied pulsatile transvascular pressure to isolated, cannulated subendocardial (Endo) and subepicardial (Epi) resistance arteries. Pressure pulsation at 0.5 to 2.5 Hz between 20 and 100 mmHg induced dilation of preconstricted vessels that was somewhat larger in Epi arterioles. In four Epi and five Endo arterioles loaded with fura 2, pulsation led to a small increase in intracellular calcium. Pulsation induced a significant decrease in IC(50) for bradykinin (BK) (5.9 +/- 0.6 vs. 27.3 +/- 3.2 nM in Epi vessels and 7.6 +/- 0.3 vs. 302 +/- 9 nM in Endo vessels), compared with steady pressure. The adenosine (Ado) sensitivity was not significantly affected (2.21 +/- 0.08 vs. 3.76 +/- 0.4 microM) in Epi arteries but was enhanced during pulsations in Endo vessels (3.1 +/- 0.3 vs. 10.1 +/- 0.6 microM). When pulsation-induced dilation was compensated by a higher concentration of the preconstrictor (U-46619), a significantly larger dilation to BK or Ado was found during pulsations. In conclusion, pulsation-induced dilation occurs at physiologically relevant frequencies and amplitudes in Endo vessels. The process does not involve intracellular calcium reduction and increases vasodilator sensitivity.