Brunson Charlie E, Abbud Eliyya, Osman Khidir, Skelton Thomas N, Markov Angel K
Division of Cardiovascular Diseases, University of Mississippi Medical Center, Jackson, MS 39216, USA.
J Investig Med. 2005 Dec;53(8):434-7. doi: 10.2310/6650.2005.53807.
The genesis of the J wave during hypothermia has been attributed to injury current, delayed ventricular depolarization and early repolarization, tissue anoxia, and acidosis. To our knowledge, no studies have addressed the appearance of the J wave in relation to the myocardial K+ transfer and metabolism during hypothermia. Dogs (n = 9) were progressively cooled, blood samples were taken from the aorta and coronary sinus, and myocardial tissue samples were obtained for adenosine triphosphate (ATP), creatine phosphate (CP), and glycolytic intermediate determination. In every instance, the appearance of the J wave was preceded by a net loss of K+ from the myocardium. In one dog, there was no myocardial K+ loss and the J wave was absent. The J wave appeared when the esophageal temperature was between 27 degrees and 24 degrees C (26.6 +/- 0.73 degrees C). At that temperature, the animals were hypotensive and bradycardic, but arterial oxygen partial pressure, carbon dioxide partial pressure, and pH were within the physiologic range at that temperature. The myocardial ATP and CP from the hypothermic dogs was lower compared with the value obtained from dogs at 37 degrees C (p < .025 and p < .005, respectively). The levels of the glycolytic intermediates, fructose-1,6-diphosphate, dihydroxyacetone phosphate, and pyruvate, were lower and the level of lactate was higher compared with those from the normothermic dogs (not significant; p < .007, p < .02, p < .001, respectively). These findings suggest that the appearance of the J wave on electrocardiography during cooling is a result of depression of the metabolic process concerned with maintenance of the partition of ions across the cell membrane, as evidenced by decreased myocardial energy content and K+ loss during the hypothermic state.
低温时J波的产生归因于损伤电流、心室去极化延迟和早期复极化、组织缺氧及酸中毒。据我们所知,尚无研究探讨低温时J波的出现与心肌钾离子转运及代谢的关系。选取9只犬,使其逐渐降温,从主动脉和冠状窦采集血样,并获取心肌组织样本以测定三磷酸腺苷(ATP)、磷酸肌酸(CP)及糖酵解中间产物。在每种情况下,J波出现之前心肌钾离子均有净丢失。在1只犬中,心肌无钾离子丢失且未出现J波。当食管温度在27℃至24℃之间(26.6±0.73℃)时出现J波。在该温度下,动物血压降低、心率减慢,但动脉血氧分压、二氧化碳分压及pH值在该温度下的生理范围内。与37℃犬相比,低温犬的心肌ATP和CP较低(分别为p<0.025和p<0.005)。与正常体温犬相比,糖酵解中间产物1,6-二磷酸果糖、磷酸二羟丙酮和丙酮酸的水平较低,而乳酸水平较高(差异无统计学意义;分别为p<0.007、p<0.02、p<0.001)。这些发现表明,降温期间心电图上J波的出现是与维持细胞膜离子分布有关的代谢过程受抑制的结果,低温状态下心肌能量含量降低及钾离子丢失证明了这一点。