Effects of propranolo, itramin tosylate and dipyridamole on myocardial phosphate metabolism in anoxic perfused rat hearts.
Effects of propranolo, itramin tosylate and dipyridamole on coronary flow, cardiac activity and phosphate metabolism were investigated in anoxic perfused rat hearts. During anoxia, heart contractions showed a transient increase followed by gradual declines in amplitude and frequency, while ATP and creatine phosphate (CP) contents strikingly decreased accompanying a pronounced increase in inorganic phosphate (Pi). Propranolol added to the anoxic perfusate attenuated the decrease in CP and increase in Pi, whereas heart contractions wre more markedly depressed than by anoxia alone. Similar effects were also seen in electrically paced anoxic hearts. Itramin decreased ATP contents in non-paced anoxic hearts, but did not in paced ones. Dipyridamole did not produce any significant effect on phosphate metabolism in anoxic myocardium. It was considered that propranolol prevented the anoxia-induced reduction in high-energy phosphates by antagonizing catecholamines released by anoxia and that itramin decreased ATP level by inhibiting ATP generation.
Effects of propranolo, itramin tosylate and dipyridamole on myocardial phosphate metabolism in anoxic perfused rat hearts. Effects of propranolo, itramin tosylate and dipyridamole on coronary flow, cardiac activity and phosphate metabolism were investigated in anoxic perfused rat hearts. During anoxia, heart contractions showed a transient increase followed by gradual declines in amplitude and frequency, while ATP and creatine phosphate (CP) contents strikingly decreased accompanying a pronounced increase in inorganic phosphate (Pi). Propranolol added to the anoxic perfusate attenuated the decrease in CP and increase in Pi, whereas heart contractions wre more markedly depressed than by anoxia alone. Similar effects were also seen in electrically paced anoxic hearts. Itramin decreased ATP contents in non-paced anoxic hearts, but did not in paced ones. Dipyridamole did not produce any significant effect on phosphate metabolism in anoxic myocardium. It was considered that propranolol prevented the anoxia-induced reduction in high-energy phosphates by antagonizing catecholamines released by anoxia and that itramin decreased ATP level by inhibiting ATP generation.