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Updated: Sep 20, 2026
Acute Myocardial Infarction in Rats
Published on: February 16, 2011
Cardioprotective effects of morphine on rat heart suffering from ischemia and reperfusion
Enyi Shi1, Xiaojing Jiang, Han Bai
1Department of Cardiac Surgery, the First Affiliated Hospital, China Medical University, Shenyang 110001, China.
Objective:
To investigate the cardioprotective effects of morphine on ischemic reperfused rat heart in vitro and its mechanism.
Methods:
The isolated rat heart was perfused in a Langendorff apparatus. Infarct myocardium was determined by TTC. Coronary flow (CF), heart rate (HR), left ventricular pressure (LVP), the first derivative of ventricular pressure (LVP/dtmax) and infarct size after ischemia and reperfusion in rat heart given 0.3 micro mol/L morphine were observed. The effects of naloxone and glibenclamide on the cardioprotection of morphine were also measured.
Results:
After ischemia and reperfusion, CF, HR, LVP and LVP/dtmax of isolated rat hearts decreased significantly (P < 0.01). After morphine preconditioning, HR, LVP and LVP/dtmax increased (P < 0.01) and infarct size was reduced significantly (P < 0.01), while no significant change in CF (P > 0.05). The cardioprotective effects of morphine were abolished by naloxone or glibenclamide completely.
Conclusions:
Morphine can reduce ischemia-reperfusion injuries in isolated rat heart. The cardioprotective effects of morphine are mediated by a local opioid receptor-K(ATP) channel linked mechanism in rat hearts.
Insights
Morphine preconditioning protects isolated rat hearts from ischemia-reperfusion injury. This cardioprotective effect is mediated by opioid receptors and K(ATP) channels, reducing infarct size.
Area of Science:
- Cardiovascular Science
- Pharmacology
- Cellular Physiology
Background:
- Ischemia-reperfusion injury is a significant cause of myocardial damage.
- Understanding protective mechanisms is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the cardioprotective effects of morphine on isolated rat hearts subjected to ischemia-reperfusion.
- To elucidate the underlying mechanism involving opioid receptors and K(ATP) channels.
Main Methods:
- Isolated rat hearts were perfused using the Langendorff apparatus.
- Infarct size was quantified using triphenyltetrazolium chloride (TTC) staining.
- Hemodynamic parameters (coronary flow, heart rate, left ventricular pressure) and infarct size were measured after morphine administration, with and without naloxone or glibenclamide.
Main Results:
- Ischemia-reperfusion significantly reduced heart rate, left ventricular pressure, and its first derivative, while increasing infarct size.
- Morphine preconditioning significantly improved these hemodynamic parameters and reduced infarct size.
- The protective effects of morphine were completely blocked by naloxone and glibenclamide.
Conclusions:
- Morphine exhibits significant cardioprotective effects against ischemia-reperfusion injury in isolated rat hearts.
- These protective effects are mediated through a mechanism involving local opioid receptors and K(ATP) channels.
