Sugden P H, Smith D M
Eur Heart J. 1984 Dec;5 Suppl F:147-53. doi: 10.1093/eurheartj/5.suppl_f.147.
We have examined the effects of various interventions on protein degradation and synthesis in the in vitro left side perfused working rat heart preparation of Taegtmeyer, Hems and Krebs. In the absence of insulin, we could not detect any effects of increased pressure workload or of increased volume workload on protein degradation. In the presence of insulin, increased pressure workload may inhibit protein degradation by about 30%. Hypoxia did not inhibit protein degradation when cardiac output was not deleteriously affected even though lactate output was greatly increased. A trebling of left atrial filling pressure stimulated protein synthesis in the left atrium by about 30%. This effect was observed when protein synthesis was expressed either relative to protein or relative to RNA. Right atrial protein synthesis was unaffected by the increased left atrial filling pressure and could be used as an internal control. We suggest that this acute effect of filling pressure on left atrial protein synthesis may be important in the development of left atrial hypertrophy which can occur in conditions where raised left atrial pressures are encountered, for example, in mitral stenosis.
我们研究了各种干预措施对泰格特迈尔、赫姆斯和克雷布斯体外左心灌注工作大鼠心脏标本中蛋白质降解和合成的影响。在没有胰岛素的情况下，我们未检测到压力负荷增加或容量负荷增加对蛋白质降解有任何影响。在有胰岛素的情况下，压力负荷增加可能会使蛋白质降解抑制约30%。即使乳酸产量大幅增加，但在心输出量未受到有害影响时，缺氧并不会抑制蛋白质降解。左心房充盈压增加两倍可使左心房蛋白质合成刺激约30%。当蛋白质合成以相对于蛋白质或相对于RNA表示时，均观察到这种效应。右心房蛋白质合成不受左心房充盈压增加的影响，可作为内部对照。我们认为，充盈压对左心房蛋白质合成的这种急性效应可能在左心房肥大的发展中起重要作用，左心房肥大可发生在遇到左心房压力升高的情况时，例如二尖瓣狭窄。
