Fluck D S, Etherington P J, Sheridan D J, Winlove C P
Academic Cardiology Unit, St. Mary's Hospital Medical School, London, United Kingdom.
Basic Res Cardiol. 1998 Oct;93(5):354-60. doi: 10.1007/s003950050103.
Coronary occlusion in the rabbit reduces the delivery of particulate tracers to close to zero, but exchange of diffusible solutes, derived from non-arterial sources, continues at a significant level. We investigated the relationships between the exchange of diffusible solutes during coronary occlusion and the extent of myocardial necrosis and between duration of ischaemia and the extent of recovery of solute exchange during reflow.
In an anaesthetised rabbit model of regional ischaemia and reflow, solute exchange is measured using the voltammetric hydrogen clearance technique. The area at risk and infarct size are determined ex vivo with monastral blue and nitroblue tetrazolium staining, respectively. Three groups are studied: control perfusion for 130 minutes (group A); 30 minutes coronary ligation followed by 90 minutes reflow (group B) and 40 minutes coronary ligation followed by 90 minutes reflow (group C).
There was no significant difference in area at risk between the groups B and C (50 +/- 2% and 45 +/- 5%; p = ns) or in infarct size when expressed relative to the area at risk (42 +/- 7% and 55 +/- 5%; p = ns). During coronary ligation hydrogen clearance remained constant at 22 +/- 4% of the control region in group B and 32 +/- 4% in group C, at the same time period in group A it was 87 +/- 2% (ANOVA = p < 0.05, with a significant non-linear trend). Although the duration of ischaemia and the level of solute exchange during ischaemia did not correlate individually with the extent of myocardial necrosis, together they showed a significant correlation (ANOVA; p < 0.05). Following coronary occlusion, hydrogen clearance recovered to 72 +/- 9% after 30 minutes ischaemia but only to 57 +/- 5% following 40 minutes ischaemia and was 95 +/- 2% in the control group (ANOVA between the three groups p < 0.05 with a significant linear trend). Myocardial hydration fell in the apical region following coronary ligation by 27 +/- 5% in group B and by 25 +/- 5% in group C, and rose on reperfusion but only to 80 +/- 3% in group B and 83 +/- 3% in group C of their preligation values.
In collateral deficient myocardium, the extent of myocardial necrosis is dependent on the level of solute exchange occurring during ischaemia. The level of solute exchange during reflow is dependent on the duration of ischaemia.
兔冠状动脉闭塞可使颗粒示踪剂的输送降至接近零，但来自非动脉源的可扩散溶质的交换仍在显著水平持续进行。我们研究了冠状动脉闭塞期间可扩散溶质交换与心肌坏死程度之间的关系，以及缺血持续时间与再灌注期间溶质交换恢复程度之间的关系。
在麻醉兔的局部缺血和再灌注模型中，使用伏安氢清除技术测量溶质交换。分别用亚甲蓝和硝基四氮唑蓝染色在体外确定危险区域和梗死面积。研究三组：对照组灌注130分钟（A组）；冠状动脉结扎30分钟后再灌注90分钟（B组）和冠状动脉结扎40分钟后再灌注90分钟（C组）。
B组和C组之间的危险区域无显著差异（50±2%和45±5%；p=无显著性差异），梗死面积相对于危险区域也无显著差异（42±7%和55±5%；p=无显著性差异）。在冠状动脉结扎期间，B组氢清除率在对照组区域的22±4%保持恒定，C组为32±4%，而在同一时间段A组为87±2%（方差分析=p<0.05，具有显著的非线性趋势）。虽然缺血持续时间和缺血期间溶质交换水平与心肌坏死程度没有单独相关性，但它们共同显示出显著相关性（方差分析；p<0.05）。冠状动脉闭塞后，缺血30分钟后氢清除率恢复到72±9%，但缺血40分钟后仅恢复到57±5%，对照组为95±2%（三组之间的方差分析p<0.05，具有显著的线性趋势）。冠状动脉结扎后，心尖区域的心肌水合作用在B组下降了27±5%，在C组下降了25±5%，再灌注时升高，但B组仅升至结扎前值的80±3%，C组为83±3%。
在侧支循环不足的心肌中，心肌坏死程度取决于缺血期间发生的溶质交换水平。再灌注期间溶质交换水平取决于缺血持续时间。
