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Procaine in cardioplegia: the effect on EDHF-mediated function in porcine coronary arteries
Qin Yang1, Anthony P C Yim, Ahmed A Arifi
1Division of Cardiothoracic Surgery, Department of Surgery, The Chinese University of Hong Kong, Hong Kong SAR, China..
Insights
Procaine enhances endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation in coronary arteries, despite a depolarizing effect. However, adding procaine to cardioplegia did not alter EDHF-mediated endothelial function.
Area of Science:
- Cardiovascular Physiology
- Endothelial Function
- Pharmacology
Background:
- Hyperkalemia during cardioplegia can impair endothelium-derived hyperpolarizing factor (EDHF)-mediated function.
- Understanding interventions to preserve EDHF function during cardiac procedures is crucial.
Purpose of the Study:
- To investigate the effect of procaine on EDHF-mediated responses in porcine coronary arteries.
- To determine if procaine can mitigate the negative effects of hyperkalemia on EDHF function.
Main Methods:
- Isometric force studies using myography on porcine coronary artery rings.
- Incubation with Krebs solution or high potassium (20 mM K+) with or without procaine (1 mM).
- Measurement of EDHF-mediated relaxation induced by bradykinin (BK) and single smooth muscle cell membrane potential.
Main Results:
- Procaine significantly enhanced EDHF-mediated relaxation in coronary arteries.
- Procaine exhibited a depolarizing effect on smooth muscle cells, reducing bradykinin-induced hyperpolarization.
- Procaine did not alter EDHF-mediated relaxation in arteries exposed to high potassium (20 mM K+).
Conclusions:
- Procaine enhances EDHF-mediated relaxation in coronary arteries via a mechanism independent of high potassium.
- Despite its depolarizing effect, procaine's addition to cardioplegia did not improve EDHF-mediated endothelial function in this model.
Objectives:
Hyperkalemia in cardioplegia impairs the endothelium-derived hyperpolarizing factor (EDHF)-mediated function. This study examined the effect of procaine in cardioplegia on the EDHF-mediated response in porcine coronary arteries.
Methods:
An isometric force study was performed in a myograph. Two rings taken from the same artery (diameter 200-450 microm) were incubated with Krebs solution (group I) or 20 mM K+ (group II) with/without procaine (1 mM) at 37 degrees C for 1 hour. The EDHF-mediated relaxation was induced by bradykinin (BK, -10 approximately -6.5 log M) after U46619 (-8 log M, in group I) or K+-precontraction (in group II) in the presence of indomethacin (7 microM), NG-nitro-L-arginine (300 microM), and hemoglobin (20 microM). The membrane potential of a single smooth muscle cell was measured by a microelectrode after superfusion with Krebs solution with/without procaine for 1 hour.
Results:
The EDHF-mediated relaxation was increased by the treatment with procaine with the EC50 shifted leftward (97.3 +/- 0.6% vs. 83.0 +/- 5.1% at -7 log M and 99.4 +/- 0.6% vs. 96.7 +/- 1.6% at -6.5 log M, p < 0.05; EC50: -8.57 +/- 0.24 vs. -7.92 +/- 0.23 log M, p < 0.05). Procaine decreased the BK-induced hyperpolarization from -72.3 +/- 0.7 mV to -68.8 +/- 0.8 mV (-6.5 log M, p < 0.01). The EDHF-mediated relaxation in arteries exposed to 20 mM K+ was not altered by procaine (49.9 +/- 7.4% vs. 55.8 +/- 7.6%, p > 0.05).
Conclusions:
In the coronary arteries, procaine has a depolarizing effect but it enhances EDHF-mediated relaxation. Addition of procaine in cardioplegia did not change the EDHF-mediated endothelial function.
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