de Belder A, Moncada S
Department of Cardiology, King's College Hospital, London, UK.
Int J Cardiol. 1995 Jul;50(3):263-8. doi: 10.1016/0167-5273(95)02386-b.
The negative inotropism, myocardial dilatation and cytotoxicity in inflammatory heart disorders may be due to increased generation of nitric oxide (NO) by immunological induction of a high output NO pathway. This short review discusses the initial experiments which lead to this hypothesis, and evaluates data that this pathway exists in animal and human cardiomyopathic disorders. It is proposed that manipulation of this pathway may prove to be beneficial in patients with these disorders.
炎症性心脏疾病中的负性肌力作用、心肌扩张和细胞毒性可能是由于通过高输出一氧化氮(NO)途径的免疫诱导使一氧化氮生成增加所致。这篇简短综述讨论了导致该假说的初步实验,并评估了该途径存在于动物和人类心肌病中的数据。有人提出,对该途径进行调控可能对患有这些疾病的患者有益。