Halejcio-Delophont P, Siaghy E M, Devaux Y, Ungureanu-Longrois D, Richoux J P, Beck B, Burlet C, Villemot J P, Mertes P M
Laboratoire de Chirurgie Experimentale, UPRES 971068, Faculté de Médecine de Nancy, Université Henri Poincaré, France.
Transplantation. 1998 Nov 27;66(10):1278-84. doi: 10.1097/00007890-199811270-00003.
Brain death-related cardiovascular dysfunction has been documented; however, its mechanisms remain poorly understood. We investigated changes in myocardial function and metabolism in brain-dead and control pigs.
Heart rate, systolic (SAP) and mean (MAP) arterial pressure, left ventricular (LV) dP/dtmax, rate-pressure product, cardiac output (CO), left anterior descending coronary artery blood flow, lactate metabolism, and interstitial myocardial purine metabolite concentrations, monitored by cardiac microdialysis, were studied. A volume expansion protocol was performed at the end of the study.
After brain death, a transient increase in heart rate (from 90 [67-120] to 158 [120-200] beats/min) (median, with range in brackets), MAP (82 [74-103] to 117 [85-142] mmHg), LV dP/dtmax (1750 [1100-2100] to 5150 [4000-62,000] mmHg x sec(-1), rate-pressure product (9100 [7700-9700] beats mmHg/min to 22,750 [20,000-26,000] beats mmHg/min), CO (2.2 [2.0-4.0] to 3.3 [3.0-6.0] L/min), and a limited increase in left anterior descending coronary artery blood flow (40 [30-60] to 72 [50-85] ml/min) were observed. Net myocardial lactate production occurred (27 [4-40] to -22 [-28, -11] mg/L, P<0.05) and persisted for 2 hr. A 6-7-fold increase in adenosine dialysate concentration was observed after brain death induction (2.9 [1.0-5.8] to 15.8 [7.0-50.7] micromol/L), followed by a slow decline. Volume expansion significantly increased MAP, CO, and LV dP/dtmax in control animals, but decreased LV dP/dtmax and slightly increased CO in brain-dead animals. A significant increase in adenosine concentration was observed in both groups, with higher levels (P<0.05) in brain-dead animals.
Brain death increased oxygen demand in the presence of a limited increase in coronary blood flow, resulting in net myocardial lactate production and increased interstitial adenosine concentration consistent with an imbalance between myocardial oxygen demand and supply. This may have contributed to the early impairment of cardiac function in brain-dead animals revealed by rapid volume infusion.
脑死亡相关的心血管功能障碍已有文献记载；然而，其机制仍知之甚少。我们研究了脑死亡猪和对照猪心肌功能和代谢的变化。
研究了心率、收缩压（SAP）和平均动脉压（MAP）、左心室（LV）dP/dtmax、速率-压力乘积、心输出量（CO）、左前降支冠状动脉血流量、乳酸代谢以及通过心脏微透析监测的心肌间质嘌呤代谢物浓度。在研究结束时进行了容量扩充方案。
脑死亡后，心率（从90[67 - 120]次/分钟短暂增加至158[120 - 200]次/分钟）（中位数，括号内为范围）、MAP（从82[74 - 103]mmHg增加至117[85 - 142]mmHg）、LV dP/dtmax（从1750[1100 - 2100]mmHg·sec⁻¹增加至5150[4000 - 62000]mmHg·sec⁻¹）、速率-压力乘积（从9100[7700 - 9700]次·mmHg/分钟增加至22750[20000 - 26000]次·mmHg/分钟）、CO（从2.2[2.0 - 4.0]L/分钟增加至3.3[3.0 - 6.0]L/分钟），左前降支冠状动脉血流量有有限增加（从40[30 - 60]ml/分钟增加至72[50 - 85]ml/分钟）。出现了心肌乳酸净生成（从27[4 - 40]mg/L变为 - 22[-28, - 11]mg/L，P<0.05）并持续2小时。诱导脑死亡后，腺苷透析液浓度增加了6 - 7倍（从2.9[1.0 - 5.8]μmol/L增加至15.8[7.0 - 50.7]μmol/L），随后缓慢下降。容量扩充使对照动物的MAP、CO和LV dP/dtmax显著增加，但使脑死亡动物的LV dP/dtmax降低且CO略有增加。两组腺苷浓度均显著增加，脑死亡动物中的水平更高（P<0.05）。
脑死亡在冠状动脉血流量有限增加的情况下增加了氧需求，导致心肌乳酸净生成以及间质腺苷浓度增加，这与心肌氧需求和供应之间的不平衡一致。这可能导致了快速容量输注所揭示的脑死亡动物早期心脏功能损害。
