Mertes P M, Carteaux J P, Jaboin Y, Pinelli G, el Abassi K, Dopff C, Atkinson J, Villemot J P, Burlet C, Boulange M
Laboratoire de Chirurgie Experimentale, Faculté de Médecine de Nancy, Vandoeuvre-lès-Nancy, France.
Transplantation. 1994 Feb;57(3):371-7. doi: 10.1097/00007890-199402150-00010.
Brain death is a pathophysiological condition associated with major hemodynamic changes, temporary myocardial ischemia, and histological damage of the heart. These modifications could be related to a major local release of norepinephrine from myocardial sympathetic nerve endings leading to norepinephrine cardiotoxicity. This study was designed to evaluate the utility of cardiac microdialysis to measure interstitial myocardial norepinephrine release resulting from brain death. The dialysis probe consisted in a 10 x 0.20-mm dialysis fiber with a 18,000 mol wt cutoff. Dialysis probes were implanted into the right and left ventricular walls of the beating heart in anesthetized pigs and perfused with Ringer solution at 2 microliters/min. Dialysate norepinephrine concentration was measured using HPLC with electrochemical detection. The relative recovery rate of norepinephrine in vivo was 34 +/- 4%. Interstitial fluid concentrations were obtained using the following formula: [C]interstitium = [C]dialysate/Recovery in vivo. After brain death, a transient increase in interstitial norepinephrine concentration was observed (from 0.74 +/- 0.20 to 4.50 +/- 0.60 ng/ml and 0.76 +/- 0.20 to 6.2 +/- 0.9 ng/ml in left and right ventricle, respectively, P < 0.01) which far exceeded plasma level increase (from 0.50 +/- 0.10 ng/ml to 0.91 +/- 0.20 ng/ml, P < 0.05). This increase in myocardial norepinephrine was, moreover, biphasic, with a second peak occurring 40 min after brain death. The present study confirms the onset of a dramatic increase in cardiac norepinephrine release from myocardial nerve endings following brain death, and demonstrate the utility of the new cardiac microdialysis technique to assess changes in interstitial fluid content.
脑死亡是一种与主要血流动力学变化、短暂性心肌缺血及心脏组织学损伤相关的病理生理状态。这些改变可能与心肌交感神经末梢去甲肾上腺素大量局部释放导致去甲肾上腺素心脏毒性有关。本研究旨在评估心脏微透析在测量脑死亡所致心肌间质去甲肾上腺素释放方面的效用。透析探头由一根10×0.20毫米、截留分子量为18,000道尔顿的透析纤维组成。将透析探头植入麻醉猪跳动心脏的右心室壁和左心室壁，并以每分钟2微升的速度用林格溶液灌注。使用带电化学检测的高效液相色谱法测量透析液中去甲肾上腺素浓度。去甲肾上腺素在体内的相对回收率为34±4%。使用以下公式获得间质液浓度：[C]间质 = [C]透析液/体内回收率。脑死亡后，观察到间质去甲肾上腺素浓度短暂升高（左心室分别从0.74±0.20纳克/毫升升至4.50±0.60纳克/毫升，右心室从0.76±0.20纳克/毫升升至6.2±0.9纳克/毫升，P<0.01），这远远超过血浆水平的升高（从0.50±0.10纳克/毫升升至0.91±0.20纳克/毫升，P<0.05）。此外，心肌去甲肾上腺素的这种升高呈双相性，在脑死亡后40分钟出现第二个峰值。本研究证实了脑死亡后心肌神经末梢心脏去甲肾上腺素释放急剧增加的发生，并证明了新的心脏微透析技术在评估间质液含量变化方面的效用。
