Caspi J, Coles J G, Benson L N, Wilson G J
Department of Pathology, The Hospital for Sick Children, Toronto, Ontario, Canada.
Ann Thorac Surg. 1998 Jun;65(6):1730-6. doi: 10.1016/s0003-4975(98)00196-9.
Brain damage is associated with myocardial dysfunction resulting from excessive release of endogenous catecholamines and Ca2+ overload. Magnesium ion, a natural Ca2+ blocker, has recently been recognized as a myoprotective agent.
Myocardial function was assessed in 3- to 7-day-old piglets from pressure-volume data (obtained by the conductance catheter/micromanometer technique) before and for 4 hours after ligation of the aortic arch vessels and was correlated with ultrastructural changes. Group a (n = 6) received MgSO4 immediately after induction of brain damage for 4 hours, whereas group b (n = 6) did not receive MgSO4 and served as control.
In both groups after induction of brain damage, there was a significant (p < 0.05) increase in end-systolic elastance and preload-recruitable stroke work that persisted for 1 hour. However, after 2 and 4 hours, there was a significant (p < 0.05) reduction in both variables in group b (end-systolic elastance, 74% +/- 5% and 59% +/- 6%, respectively, and preload-recruitable stroke work, 77% +/- 4% and 64% +/- 3%, respectively, compared with baseline), and in group a, the values returned to baseline. The chamber stiffness index rose significantly (p < 0.05) in group b 15 minutes after induction of brain damage and remained significantly (p < 0.05) higher for 4 hours versus no significant change in group a. Plasma levels of epinephrine and norepinephrine were similar in the groups before and after brain damage. Electron microscopic study showed severe ultrastructural changes in group b and significantly milder changes in group a.
We conclude that MgSO4 may protect the neonatal myocardium when administered immediately after brain damage.
脑损伤与内源性儿茶酚胺过度释放及钙超载导致的心肌功能障碍有关。镁离子作为一种天然的钙阻滞剂，近来被认为是一种心肌保护剂。
通过电导导管/微测压技术获取压力-容积数据，对3至7日龄仔猪在结扎主动脉弓血管前及结扎后4小时的心肌功能进行评估，并将其与超微结构变化相关联。a组（n = 6）在脑损伤诱导后立即给予硫酸镁4小时，而b组（n = 6）未给予硫酸镁，作为对照。
在两组脑损伤诱导后，收缩末期弹性和可通过增加前负荷增加的每搏功均显著（p < 0.05）增加，并持续1小时。然而，在2小时和4小时后，b组这两个变量均显著（p < 0.05）降低（收缩末期弹性分别为基线的74% ± 5%和59% ± 6%，可通过增加前负荷增加的每搏功分别为基线的77% ± 4%和64% ± 3%），而a组的值恢复至基线水平。脑损伤诱导后15分钟，b组的心室僵硬度指数显著（p < 0.05）升高，并在4小时内一直显著（p < 0.05）高于a组，而a组无显著变化。两组脑损伤前后血浆肾上腺素和去甲肾上腺素水平相似。电子显微镜研究显示，b组有严重的超微结构变化，而a组变化明显较轻。
我们得出结论，脑损伤后立即给予硫酸镁可能对新生心肌起到保护作用。
