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Direct effects of oxygenated crystalloid or blood cardioplegia on isolated myocyte contractile function
J R Handy1, B H Dorman, M J Cavallo
1Department of Surgery, Medical University of South Carolina, Charleston 29425, USA.
Insights
Both oxygenated crystalloid and blood cardioplegia equally impacted myocyte contractile function and cell volume during hypothermic arrest. This study compared their effects in an isolated myocyte model, finding similar outcomes for myocardial protection.
Area of Science:
- Cardiology
- Cell Biology
- Biochemistry
Background:
- Myocardial protection during surgery often uses hypothermic, hyperkalemic cardioplegia.
- A direct comparison between oxygenated crystalloid and blood cardioplegia in isolated myocytes is lacking.
- This study investigates contractile function and cell swelling in myocytes under these conditions.
Purpose of the Study:
- To compare the effects of oxygenated crystalloid versus blood cardioplegia on isolated myocyte contractile function.
- To assess myocyte swelling as an indicator of intracellular volume changes after cardioplegic arrest.
- To evaluate myocardial protective techniques in a controlled cellular model.
Main Methods:
- Isolated pig left ventricular myocytes underwent 2-hour cardioplegic arrest at 4°C using either oxygenated crystalloid or blood cardioplegia.
- Contractile function (velocity of shortening) was measured at baseline and after beta-adrenergic stimulation (isoproterenol).
- Myocyte profile surface area was measured to assess cell volume changes.
Main Results:
- Both cardioplegia types equally reduced myocyte velocity of shortening from baseline.
- Beta-adrenergic stimulation increased shortening velocity, but less effectively in both cardioplegia groups compared to controls.
- Myocyte surface area increased significantly and equally in both cardioplegia groups post-arrest, indicating cell swelling.
Conclusions:
- Oxygenated crystalloid and blood cardioplegia demonstrate equivalent effects on myocyte contractile function.
- Both methods similarly impact inotropic responsiveness and intracellular volume regulation.
- Findings suggest comparable efficacy of these cardioplegic solutions at the cellular level.
Unlabelled:
The majority of myocardial protective techniques performed in the United States incorporate hypothermic, hyperkalemic blood or crystalloid cardioplegia. Oxygenated blood cardioplegia has not been compared with oxygenated crystalloid cardioplegia in an isolated myocyte model of hypothermic, hyperkalemic cardioplegic arrest in which direct measurements of contractile function and myocyte swelling can be made. Accordingly, isolated myocyte contractile function and myocyte profile surface area were examined after hypothermic arrest with oxygenated crystalloid or blood cardioplegia.
Methods:
Isolated left ventricular pig myocytes were randomly assigned to undergo cardioplegic arrest for 2 hours at 4 degrees C. Either oxygenated crystalloid or blood cardioplegia was used. After 2 hours, myocytes were reperfused with standard cell medium at 37 degrees C and contractile function was examined. A control group of myocytes was maintained in cell medium at 37 degrees C for 2 hours. Myocyte velocity of shortening (micrometers per second) was examined at baseline and after beta-adrenergic stimulation (isoproterenol, 25 nmol/L). Velocity of shortening declined equally from baseline control values (65 +/- 2 micron n/sec) in the groups subjected to oxygenated crystalloid cardioplegia and blood cardioplegia (37 +/- 2 micron n/sec and 42 +/- 1 micron n/sec, respectively; p < 0.05).
Results:
Although beta-adrenergic stimulation caused a significant increase in velocity of shortening in all myocyte groups, the increase was less pronounced in myocytes subjected to crystalloid cardioplegia (157 +/- 6 micron n/sec) and blood cardioplegia (159 +/- 6 micron n/sec) than in normothermic control myocytes (205 +/- microm/sec; p < 0.05). Myocyte profile surface area, an index of cell volume, was measured in all myocyte groups. Myocyte surface area increased equally after cardioplegic arrest and rewarming in both cardioplegia groups (crystalloid 4119 +/- 53 micron2; blood 3924 +/- 48 micron2); surface areas in both cardioplegia groups were significantly greater than in the normothermic control group (3158 +/- 39 micron2, p < 0.05).
Conclusion:
Equivalent effects of oxygenated crystalloid and blood cardioplegia were observed with respect to myocyte contractile function, inotropic responsiveness, and intracellular volume regulatory processes.
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