Related Experiment Videos
Endothelium-dependent contraction of canine coronary artery is enhanced by crystalloid cardioplegic solution
1Division of Thoracic and Cardiovascular Surgery, Chang Gung Memorial Hospital, Chang Gung Medical College, Taipei, Taiwan, Republic of China.
Insights
Hyperkalemic cardioplegic solution significantly increases endothelium-dependent coronary artery contraction after preservation. This L-arginine-dependent pathway may promote coronary vasospasm post-cardiac surgery.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Surgical Preservation
Background:
- Coronary artery function is critical during and after cardiac surgery.
- Preservation solutions can impact vascular reactivity.
- Endothelium-dependent contractions play a role in coronary blood flow regulation.
Purpose of the Study:
- To investigate the effect of hyperkalemic crystalloid cardioplegic solution on canine coronary artery contraction.
- To determine if this solution enhances endothelium-dependent responses to hypoxia.
- To elucidate the underlying pathway of enhanced contraction.
Main Methods:
- Canine coronary artery segments were preserved in cardioplegic or physiologic solutions.
- Isometric force measurements were used to assess vascular contraction.
- Hypoxia was induced, and responses were modulated by nitric oxide synthesis inhibitors and amino acids.
Main Results:
- Arteries preserved in cardioplegic solution showed significantly greater hypoxic, endothelium-dependent contraction compared to controls.
- This enhanced contraction was mediated by an L-arginine-dependent pathway.
- NG-monomethyl-L-arginine (a nitric oxide synthesis inhibitor) attenuated the contraction, which was reversed by L-arginine.
Conclusions:
- Hyperkalemic crystalloid cardioplegic solution augments endothelium-dependent coronary artery contraction.
- This effect is mediated via an L-arginine-dependent pathway.
- This phenomenon may contribute to coronary vasospasm following cardiac operations.
Abstract:
Experiments were designed to determine whether hyperkalemic crystalloid cardioplegic solution enhances endothelium-dependent contraction of coronary arteries. Segments of canine coronary arteries (n = 8 in each group) were preserved in cold (4 degrees C) crystalloid cardioplegic solution (group 1) and physiologic solution (group 2) for 60 minutes. Segments of preserved and control (group 3) coronary arteries with or without endothelium were suspended in organ chambers to measure isometric force. Perfusate hypoxia (oxygen tension 35 +/- 5 mm Hg) caused endothelium-dependent contraction in the arteries of all three groups. However, vascular segments with endothelium of group 1 exhibited hypoxic contraction (68.5% +/- 15.3% of the initial tension contracted by prostaglandin F2 alpha 2 x 10(-6) mol/L, p < 0.05) that was significantly greater than contraction of the group 2 and group 3 segments with endothelium (26.6% +/- 5.6% and 20.6 +/- 4.4%). The hypoxic contraction in arteries of group 1 could be attenuated by NG-monomethyl-L-arginine, the blocker of endothelial cell synthesis of the nitric oxide from L-arginine. The action of NG-monomethyl-L-arginine could be reversed by L-arginine but not D-arginine. Thus after preservation with cardioplegic solution, augmented endothelium-dependent contraction, occurs by L-arginine-dependent pathway, would favor coronary vasospasm after cardiac operation.