The effects of .BETA.-blocking agents on mitochondrial function in ischemic myocardium.

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Abstract
The protective effects of .beta.-adrenergic blocking agents on ischemia-induced mitochondrial dysfunction were investigated in 42 anesthetized mongrel dogs. The animals, divided into 6 groups of 7 dogs each, were premedicated with either saline for the controls, or D, L-propranolol (0.5 mg/kg), D-propranolol (0.5 mg/kg), D-L-acebutolol (2.5 mg/kg), D, L-pindolol (0.1 mg/kg) or L-isoproterenol (0.2 .mu.g/kg per min, for 10 min). Myocardial mitochondria were prepared from both the normal and the ischemic areas after 30 min of coronary ligation. The concentration of long-chain acyl-CoA [acyl-coenzyme A] was measured enzymatically. Respiratory control index, ADP/O, and the rate of O2 consumption in State II of mitochondria were also measured. In the control group, acyl-CoA in ischemic mitochondria increased significantly compared with that in normal mitochondria, and mitochondrial dysfunction was observed. Administration of L-isoproterenol further increased acyl-CoA level and accelerated the dysfunction, whereas premedication with .beta.-blocking agents reduced the elevation of acyl-CoA level and prevented the dysfunction. Premedication with D-propranolol had no effect on mitochondria. Since the accumulation of acyl-COA interferes with normal mitochondrial function, these results suggest that the protective effects of .beta.-blocking agents are based, at least in part, on the prevention of the accumulation of acyl-CoA esters.

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