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Effects of Clonidine and Isoflurane on the Myocardial Contractility Behavior of Isolated Rat Hearts
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Isoflurane is chosen as an anesthesia drug for cardiac surgeries, and its effectiveness and safety have been proved in countless clinical studies. Clonidine, a central -agonist, has recently been added to isoflurane to attenuate sympathetic hyperactivity by acting directly on its site of origin in the central nervous system. The ability of 2-adrenoceptor agonists to inhibit central sympathetic outflow may benefit patients at risk of myocardial damage by improving myocardial oxygen demand and the supply ratio and contributing to hemodynamic stability. We investigated the effects of clonidine and isoflurane, alone and in combination, on the myocardial contractility of isolated rat hearts and found that use of clonidine plus isoflurane decreased the systolic pressure somewhat, but use of the drugs separately did not exhibit this effect. Clonidine plus isoflurane did not affect +(dP/dt)max, but it did decrease -(dP/dt)max significantly compared with the use of isoflurane alone. These results indicate that clonidine and isoflurane have the capacity to interact with each other. The capacity of clonidine to decrease isoflurane's inotropic effect could theoretically contribute to improving the myocardial oxygen demand and the supply ratio, decreasing surgical stress, and benefiting patients at risk of myocardial damage.
Title: Effects of Clonidine and Isoflurane on the Myocardial Contractility Behavior of Isolated Rat Hearts
Description:
Isoflurane is chosen as an anesthesia drug for cardiac surgeries, and its effectiveness and safety have been proved in countless clinical studies.
Clonidine, a central -agonist, has recently been added to isoflurane to attenuate sympathetic hyperactivity by acting directly on its site of origin in the central nervous system.
The ability of 2-adrenoceptor agonists to inhibit central sympathetic outflow may benefit patients at risk of myocardial damage by improving myocardial oxygen demand and the supply ratio and contributing to hemodynamic stability.
We investigated the effects of clonidine and isoflurane, alone and in combination, on the myocardial contractility of isolated rat hearts and found that use of clonidine plus isoflurane decreased the systolic pressure somewhat, but use of the drugs separately did not exhibit this effect.
Clonidine plus isoflurane did not affect +(dP/dt)max, but it did decrease -(dP/dt)max significantly compared with the use of isoflurane alone.
These results indicate that clonidine and isoflurane have the capacity to interact with each other.
The capacity of clonidine to decrease isoflurane's inotropic effect could theoretically contribute to improving the myocardial oxygen demand and the supply ratio, decreasing surgical stress, and benefiting patients at risk of myocardial damage.
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