Song D, O'Regan M H, Phillis J W
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Neurosci Lett. 1996 Dec 6;220(1):1-4. doi: 10.1016/s0304-3940(96)13228-6.
An isolated rat Langendorff heart preparation has been developed as a model in which to study the release of glutamate, aspartate and other amino acids during ischemia, anoxia and hypoglycemia. 15 min periods of ischemia resulted in large increases in perfusate levels of glutamate, aspartate, glycine, phosphoethanolamine, serine, alanine, taurine and glutamine. Amino acid levels returned towards pre-ischemic levels in subsequent perfusate collections. Anoxia (15 min duration) increased perfusate levels of most of the measured amino acids, with glutamate and aspartate being particularly affected. In contrast to ischemia, glutamate and aspartate levels declined slowly following reoxygenation. Hypoglycemia (15 min) resulted in small but significantly elevated levels of glutamate and glycine in heart perfusates. As the effects of ischemia or anoxia on glutamate and aspartate release from the heart appear to be comparable to those observed in the brain, it is proposed that the heart preparation may be a suitable model in which to study the ischemia-evoked release of these amino acids in the absence of complications arising from their depolarizing and excitotoxic actions on central neurons.
已开发出一种离体大鼠Langendorff心脏制备模型，用于研究缺血、缺氧和低血糖期间谷氨酸、天冬氨酸及其他氨基酸的释放情况。15分钟的缺血导致灌注液中谷氨酸、天冬氨酸、甘氨酸、磷酸乙醇胺、丝氨酸、丙氨酸、牛磺酸和谷氨酰胺水平大幅升高。在随后收集的灌注液中，氨基酸水平恢复到缺血前水平。缺氧（持续15分钟）使大多数被测氨基酸的灌注液水平升高，谷氨酸和天冬氨酸受影响尤为明显。与缺血不同，复氧后谷氨酸和天冬氨酸水平缓慢下降。低血糖（15分钟）导致心脏灌注液中谷氨酸和甘氨酸水平小幅但显著升高。由于缺血或缺氧对心脏谷氨酸和天冬氨酸释放的影响似乎与在大脑中观察到的影响相当，因此有人提出，该心脏制备模型可能是一个合适的模型，用于在不存在因这些氨基酸对中枢神经元的去极化和兴奋毒性作用而产生并发症的情况下，研究缺血诱发的这些氨基酸的释放。
