Indolfi C, Guth B D, Miura T, Miyazaki S, Schulz R, Ross J
Department of Medicine, University of California, San Diego, La Jolla 92093.
Circulation. 1989 Oct;80(4):983-93. doi: 10.1161/01.cir.80.4.983.
In anesthetized swine, the left anterior descending coronary artery was cannulated and perfused at constant blood flow levels during two grades of ischemia. In one group (n = 10), moderate ischemia reduced percent systolic wall thickening (by sonomicrometry) from 25 +/- 7% to 6 +/- 2%, whereas in the other group (n = 7), severe ischemia reduced percent wall thickening from 24 +/- 6% to -0.5 +/- 4%. Heart rate was paced in both groups at 91 beats/min. After reperfusion and complete return to control conditions, administration of the bradycardic agent UL-FS 49 (0.37 mg/kg i.v.) decreased the heart rate to 55 +/- 5 beats/min. During subsequent ischemia at the same coronary inflow as before bradycardia, percent wall thickening in the ischemic zone during moderate ischemia was increased from 6 +/- 2% to 25 +/- 6% (p less than 0.01) (not significantly different from control without ischemia), and during severe ischemia, percent wall thickening increased from -0.5 +/- 4% to 13 +/- 7% (p less than 0.01). During moderate ischemia, bradycardia caused an increase in the subendocardial blood flow from 0.24 +/- 0.60 to 0.42 +/- 0.17 (ml/min)/g (p less than 0.009) and during severe ischemia, bradycardia caused an increase from 0.14 +/- 0.08 to 0.2 +/- 0.1 (ml/min)/g (p less than 0.001). At each level of ischemia, a more marked improvement occurred in subendocardial blood flow per beat ([(ml/min)/g]/heart rate). The relation between myocardial blood flow and wall function at a heart rate of 55 beats/min (n = 14) was plotted and compared with that studied at a heart rate of 122 beats/min in another group of pigs (n = 14). The increase in subendocardial blood flow per minute during bradycardia was not sufficient to explain the striking increase in function; thus, an independent relation (p less than 0.05) between blood flow per minute and contractile function (percent wall thickening) was found for for each heart rate. In contrast, when myocardial blood flow was normalized for heart rate and expressed per beat, data from both heart rate groups could be described by a single relation. Thus, the subendocardial blood flow per beat predicted wall function independently of heart rate and accounted for changes in both oxygen supply and demand.
在麻醉的猪身上,在两种程度的缺血期间,将左冠状动脉前降支插管并以恒定血流水平灌注。在一组(n = 10)中,中度缺血使收缩期室壁增厚百分比(通过超声心动图测量)从25±7%降至6±2%,而在另一组(n = 7)中,重度缺血使室壁增厚百分比从24±6%降至-0.5±4%。两组的心率均起搏至91次/分钟。再灌注并完全恢复至对照状态后,给予减慢心率药物UL-FS 49(0.37 mg/kg静脉注射)使心率降至55±5次/分钟。在随后与心动过缓前相同冠状动脉血流量的缺血期间,中度缺血时缺血区的室壁增厚百分比从6±2%增加至25±6%(p<0.01)(与无缺血的对照无显著差异),重度缺血时,室壁增厚百分比从-0.5±4%增加至13±7%(p<0.01)。在中度缺血期间,心动过缓使心内膜下血流量从0.24±0.60增加至0.42±0.17(ml/分钟)/克(p<0.009),在重度缺血期间,心动过缓使血流量从0.14±0.08增加至0.2±0.1(ml/分钟)/克(p<0.001)。在每个缺血水平,每搏心内膜下血流量有更显著的改善([(ml/分钟)/克]/心率)。绘制了心率为55次/分钟(n = 14)时心肌血流量与室壁功能之间的关系,并与另一组猪(n = 14)心率为122次/分钟时的研究结果进行比较。心动过缓期间每分钟心内膜下血流量的增加不足以解释功能的显著增加;因此,发现每分钟血流量与收缩功能(室壁增厚百分比)之间存在独立关系(p<0.05)。相比之下,当心肌血流量按心率进行归一化并以每搏表示时,两个心率组的数据可用单一关系描述。因此,每搏心内膜下血流量可独立于心率预测室壁功能,并解释了氧供需的变化。