Biro G P, Beresford-Kroeger D
Cardiovasc Res. 1979 Aug;13(8):459-68. doi: 10.1093/cvr/13.8.459.
The adequacy of oxygen-supply to the left ventricular myocardium was compared in anaesthetised dogs following: a) isovolaemic haemodilution with Dextran 70 (to haematocrit = 20 +/- 2%), b) the acute induction of methaemoglobinaemia (to methaemoglobin-concentration = 53 +/- 7%), bu subjecting them to an exchange-transfusion with methaemoglobin-containing erythrocytes in dextran) and c) a control exchange-transfusion with normal homologous erythrocytes in dextran. Myocardial oxygen-supply was assessed by the measurement of myocardial blood flow (using 15 +/- 5 micron microspheres) and of the PO2 in coronary sinus blood. In dextran-haemodiluted dogs, mean myocardial blood flow was 92% greater than in the control group, allowing the maintenance of normal coronary sinus PO2. In the methaemoglobinaemic group, flow was only 15% greater than in the control group; because oxygen-capacity was halved in this group, myocardial oxygen supply was impaired and coronary sinus PO2 fell. Infusions of isoproterenol (0.1 microgram . kg-1 . min-1) produced similar myocardial flow-increments in the haemodiluted and control groups with similar transmural distribution. In the methaemoglobinaemic group, however, the subendocardial flow-increment was reduced, in association with a further reduction in coronary sinus PO2 and an attenuated contractile response to the drug. These findings suggest that the rheological effects of haemodilution play an important role in the maintenance of myocardial oxygen-supply, but in significant methaemoglobinaemia, the oxygen supply of the myocardium may be severely curtailed.
在麻醉犬中比较了左心室心肌的氧供应情况,具体如下:a)用右旋糖酐70进行等容血液稀释(使血细胞比容=20±2%);b)急性诱导高铁血红蛋白血症(使高铁血红蛋白浓度=53±7%,方法是用含高铁血红蛋白的红细胞在右旋糖酐中对其进行换血);c)用正常同源红细胞在右旋糖酐中进行对照换血。通过测量心肌血流量(使用15±5微米的微球)和冠状窦血中的PO₂来评估心肌氧供应。在右旋糖酐血液稀释的犬中,平均心肌血流量比对照组大92%,从而能够维持正常的冠状窦PO₂。在高铁血红蛋白血症组中,血流量仅比对照组大15%;由于该组的氧容量减半,心肌氧供应受损,冠状窦PO₂下降。静脉输注异丙肾上腺素(0.1微克·kg⁻¹·min⁻¹)在血液稀释组和对照组中产生了相似的心肌血流增加,且跨壁分布相似。然而,在高铁血红蛋白血症组中,心内膜下血流增加减少,同时冠状窦PO₂进一步降低,对该药物的收缩反应减弱。这些发现表明,血液稀释的流变学效应在维持心肌氧供应中起重要作用,但在严重的高铁血红蛋白血症中,心肌的氧供应可能会严重减少。