Recovery of Function and Adenosine Triphosphate Metabolism Following Myocardial Ischemia Induced in the Presence of Volatile Anesthetics

Abstract

Using a normothermic isolated working rabbit heart model, experiments were performed to determine whether exposure to halothane or isoflurane prior to ischemia improved postischemic recovery of myocardial function and the preservation of myocardial high energy phosphates. After 30 min of Langendorff perfusion, hearts were perfused for 30 min in the working mode. Three groups were studied: 1) the blank undergoing no pretreatment during an additional 15 min of working mode; 2) hearts exposed to 1.5% halothane; and 3) hearts exposed to 2.3% isoflurane during the additional 15 min of working mode. Subsequently, all hearts underwent 15 min of global normothermic ischemia, followed by 5 min of Langendorff reperfusion and 15 min of working heart mode using a perfusate devoid of volatile anesthetic. Adenosine triphosphate (ATP) and catabolites were determined after 15 min exposure to volatile anesthetics or blank, after 15 min global ischemia and at the end of the recovery phase. Myocardial function was determined after 30 min of working mode, after exposure to volatile anesthetics, and at the end of the recovery phase. In nonischemic hearts, 15-min treatment with 1.5% halothane or 2.3% isoflurane resulted in a significant decrease in positive LVdP/dt, from 1858 +/- 286 to 1316 +/- 180 mm Hg.s-1 and from 1888 +/- 304 to 1541 +/- 226 mm Hg.s-1, respectively. Coronary flow was increased significantly after isoflurane but not after halothane.(ABSTRACT TRUNCATED AT 250 WORDS)

Sevoflurane reduces dysrhythmias during reperfusion in the working rat heart

“…In these experiments, volatile anesthetics were delivered before ischemia, during ischemia, and during the reperfusion period. In contrast to the above studies, Mattheussen et al [9] showed that exposure to halothane or isoflurane only prior to ischemia had no effect on functional and metabolic indices of recovery after myocardial stunning. In addition, Belo et al [10] demonstrated that subsequent administration of halothane or isoflurane after reperfusion did not improve contractile function in stunned myocardium.…”

Hydroxyl radical formation during inhalation anesthesia in the reperfused working rat heart

“…Coetzee et al 7 suggested that the beneficial effects of inhalation anesthetics after cardioplegic arrest might be related to the prevention of the reperfusion injury and could not be ascribed to depression of global myocardial contractile function. Mattheussen et al 19 have assessed the effect of inhalation anesthetics on myocardial metabolism using the ischemic working heart preparation. Although they employed the same experimental model as we did, inhalation anesthetics were administered only during the pre-ischemic period and they did not affect myocardial high energy phosphates at the end of reperfusion.…”

Inflammatory response and cardioprotection during open‐heart surgery: the importance of anaesthetics

“…Volatile anaesthetics to various degrees have been shown to decrease myocardial contractility and myocardial oxygen demand, a property that has been suggested to explain cardioprotection against ischaemia and reperfusion ( Coetzee et al , 1993 ; Mattheussen et al , 1993 ; Schlack et al , 1998 ). However, these anaesthetics were also found to induce cardioprotection via mechanisms that are similar to pathways involved in ischaemic preconditioning ( Cope et al , 1997 ).…”