Torchiana D F, Love T R, Hendren W G, Geffin G A, Titus J S, Redonnett B E, O'Keefe D D, Daggett W M
Department of Surgery, Massachusetts General Hospital, Boston 02114.
J Thorac Cardiovasc Surg. 1987 Oct;94(4):606-13.
Cardiac arrest induced by hyperkalemic perfusion is generally considered to represent a state of complete electromechanical arrest. However, high-energy phosphate concentrations and ventricular function decrease with increasing cardioplegic calcium concentrations, possibly because of elevated resting muscle tone produced by calcium influx. We examined isolated rat hearts containing an isovolumic intraventricular balloon for the presence of contractile activity during the administration at 10 degrees C of a cardioplegic solution containing potassium, 20 mEq/L. Significant left ventricular pressure was developed (35.6% +/- 4.3% of prearrest systolic pressure) during administration of a solution containing a calcium concentration of 1.0 mmol/L and far less (9.7% +/- 1.6% of prearrest systolic pressure) with a calcium-free cardioplegic solution. The muscle contraction diminished with repeated doses, was increased by increasing cardioplegic calcium content, and was inhibited by magnesium. Adenosine triphosphate and creatine phosphate concentrations were 9.0 +/- 1.4 and 7.0 +/- 0.9 nmol/mg dry weight immediately after infusion of 15 ml of a hypoxic cardioplegic solution containing calcium, versus 13.3 +/- 1.3 (p less than 0.02) and 31.9 +/- 3.5 nmol/mg dry weight (p less than 0.0001) after a hypoxic acalcemic solution was given. When repeated doses of a hypoxic cardioplegic solution containing calcium in a concentration of 1.0 mmol/L were given at 15 minute intervals at 10 degrees C, ischemic contracture (a sustained development of ventricular pressure, mean 51% +/- 4% of prearrest systolic pressure) resulted within 1 hour. Coronary vascular resistance was increased during the muscle contractions induced by calcium-containing solutions, markedly so during contracture. Calcium-related mechanical activity was also observed during hypothermic cardioplegic arrest in five of six isolated isovolumic canine hearts. We conclude that hearts remain potentially active mechanically during cold hyperkalemic arrest and undergo energetically wasteful contraction when stimulated with calcium-containing hyperkalemic cardioplegic solutions.
高钾灌注诱发的心脏骤停通常被认为代表完全的电机械性停搏状态。然而，随着心脏停搏液中钙浓度的增加，高能磷酸盐浓度和心室功能会降低，这可能是由于钙内流导致静息肌张力升高所致。我们在10℃下给含有等容心室内球囊的离体大鼠心脏输注含20 mEq/L钾的心脏停搏液时，检查其是否存在收缩活动。在输注含1.0 mmol/L钙的溶液时，左心室产生了显著压力（为停搏前收缩压的35.6%±4.3%），而使用无钙心脏停搏液时压力则小得多（为停搏前收缩压的9.7%±1.6%）。肌肉收缩随着重复给药而减弱，随着心脏停搏液中钙含量的增加而增强，并受到镁的抑制。在输注15 ml含氯化钙的低氧心脏停搏液后，三磷酸腺苷和磷酸肌酸浓度分别为9.0±1.4和7.0±0.9 nmol/mg干重，而在给予低氧无钙溶液后分别为13.3±1.3（p<0.02）和31.9±3.5 nmol/mg干重（p<0.0001）。当在10℃下每隔15分钟重复给予含1.0 mmol/L钙的低氧心脏停搏液时，1小时内会出现缺血性挛缩（心室压力持续升高，平均为停搏前收缩压的51%±4%）。在含氯化钙溶液诱导的肌肉收缩过程中，冠状动脉血管阻力增加，在挛缩期间尤为明显。在六个离体等容犬心脏中的五个，在低温心脏停搏期间也观察到了与钙相关的机械活动。我们得出结论，在冷高钾停搏期间心脏仍具有潜在的机械活性，当用含氯化钙的高钾心脏停搏液刺激时会发生能量浪费的收缩。
