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Cardiac mast cell stabilization and cardioprotective effect of ischemic preconditioning in isolated rat heart
1Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, India.
Insights
Disodium cromoglycate (DSCG) appears to block the heart-protective benefits of ischemic preconditioning. This mast cell stabilizer may abolish cardioprotection by stabilizing cardiac mast cells during preconditioning.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Ischemic preconditioning (IP) offers cardioprotection against ischemia-reperfusion injury.
- Mast cells are implicated in the mechanisms of IP.
Purpose of the Study:
- To investigate the effect of disodium cromoglycate (DSCG), a mast cell stabilizer, on the cardioprotective effects of IP.
- To determine if DSCG modulates mast cell degranulation during IP.
Main Methods:
- Isolated rat hearts were subjected to global ischemia and reperfusion.
- IP was induced using brief cycles of ischemia and reperfusion.
- Hearts were treated with DSCG (10 and 100 microM) during IP or reperfusion.
- Lactate dehydrogenase (LDH), creatine kinase (CK), and mast cell peroxidase (MPO) release were measured.
Main Results:
- IP and DSCG treatment reduced LDH, CK release, and arrhythmias during reperfusion.
- Both IP and DSCG treatment reduced ischemia/reperfusion-induced MPO release.
- However, DSCG administered *during* IP attenuated the cardioprotective and antiarrhythmic effects of IP.
- DSCG given during IP did not significantly affect MPO release.
Conclusions:
- DSCG administered during ischemic preconditioning abolishes its cardioprotective and antiarrhythmic effects.
- This effect may be due to DSCG stabilizing cardiac mast cells, thereby interfering with IP signaling pathways.
Abstract:
This study was designed to investigate the effect of disodium cromoglycate (DSCG), a mast cell stabilizer, on cardioprotective effect of ischemic preconditioning. Isolated rat heart was subjected to 30 min of global ischemia followed by 30 min of reperfusion. Ischemic preconditioning was provided by four episodes of 5-min global ischemia followed by 5 min of reperfusion before sustained ischemia. Ischemic preconditioning and DSCG (10 and 100 microM) treatment markedly decreased the release of lactate dehydrogenase (LDH) and creatine kinase (CK) in coronary effluent and percentage incidence of ventricular premature beats (VPBs) and ventricular tachycardia/fibrillation (VT/VF) during reperfusion. Ischemic preconditioning and DSCG treatment also significantly reduced ischemia/reperfusion-induced mast cell peroxidase (MPO) release, a marker of mast cell degranulation. A significant increase in MPO release was observed immediately after ischemic preconditioning, and the release was found to be inhibited in hearts perfused with DSCG (10 and 100 microM) during ischemic preconditioning. DSCG administered during ischemic preconditioning (DSCG in ischemic preconditioning) attenuated the cardioprotective and antiarrhythmic effects of ischemic preconditioning. DSCG in ischemic preconditioning produced no marked effect on ischemia/reperfusion-induced MPO release. These findings tentatively suggest that DSCG administration during ischemic preconditioning abolishes its cardioprotective effect, perhaps by stabilizing resident cardiac mast cells.
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