Carter Y M, Jia C X, Soto P F, Starr J P, Rabkin D G, Hsu D T, Fisher P E, Spotnitz H M
Department of Surgery, Columbia University College of Physicians & Surgeons, New York, New York 10032, USA.
J Heart Lung Transplant. 1998 Feb;17(2):140-9.
Although myocardial edema is known to impair diastolic filling of the left ventricle, the interrelation of edema, histologic condition, and function has not been quantitated sufficiently for extrapolation to studies of multifactorial influences on diastolic properties.
Accordingly, ACI rat hearts arrested at 4 degrees C underwent coronary artery perfusion with a cardioplegia solution that was either unaltered (288 mOsm/L, P288 group, n = 6), diluted (144 mOsm/L, P144 group, n = 6), or concentrated (380 mOsm/L, P380 group, n = 6). Postmortem left ventricular pressure-volume curves and myocardial water content were measured. Myocardial samples were fixed in varying dilutions of glutaraldehyde. After dehydration and paraffin embedding, edema was graded subjectively (0 to 5), and myocardial interstitial spaces were determined by use of a semiquantitative method.
Mean normalized left ventricular filling volume at 20 mm Hg filling pressure in the P144 group, 189 +/- 16 microliters (SEM), was reduced versus both the P288 (278 +/- 26 microliters) and the P380 (332 +/- 18 microliters) groups (p < 0.05, ANOVA). Mean myocardial water content in the P144 group, 80.7% +/- 1%, was increased versus the P380 (76.7% +/- 0.4%, p < 0.05) but not versus the P288 group (78.4% +/- 0.8%). In hearts preserved with 2.5% glutaraldehyde, mean edema grade and interstitial space in the P144 group (4.0 +/- 0.3) were increased versus the P380 (1.8 +/- 0.3, p < 0.05) but not the P288 group (2.7 +/- 0.5). Derived linear regressions relate water content to filling volume and histologic condition.
Coronary perfusate osmolarity is thus associated with predictable changes in myocardial water content, left ventricular filling volume, and edema. These correlations allow definition of new hypotheses for the study of cardiac allograft rejection in patients and experimental animals.
尽管已知心肌水肿会损害左心室的舒张充盈，但水肿、组织学状况和功能之间的相互关系尚未得到充分量化，无法外推至对舒张特性的多因素影响研究。
因此，将4℃停跳的急性心肌梗死（ACI）大鼠心脏用未改变的（288 mOsm/L，P288组，n = 6）、稀释的（144 mOsm/L，P144组，n = 6）或浓缩的（380 mOsm/L，P380组，n = 6）心脏停搏液进行冠状动脉灌注。测量死后左心室压力-容积曲线和心肌含水量。心肌样本用不同稀释度的戊二醛固定。脱水和石蜡包埋后，主观对水肿进行分级（0至5级），并使用半定量方法测定心肌间质间隙。
P144组在20 mmHg充盈压下的平均标准化左心室充盈容积为189±16微升（SEM），与P288组（278±26微升）和P380组（332±18微升）相比均降低（p < 0.05，方差分析）。P144组的平均心肌含水量为80.7%±1%，与P380组（76.7%±0.4%，p < 0.05）相比增加，但与P288组（78.4%±0.8%）相比无差异。在用2.5%戊二醛保存的心脏中，P144组的平均水肿分级和间质间隙（4.0±0.3）与P380组（1.8±0.3，p < 0.05）相比增加，但与P288组（2.7±0.5）相比无差异。得出的线性回归将含水量与充盈容积和组织学状况相关联。
冠状动脉灌注液渗透压因此与心肌含水量、左心室充盈容积和水肿的可预测变化相关。这些相关性为研究患者和实验动物的心脏移植排斥反应定义了新的假设。
