Mouren S, Vicaut E, Charansonney O, Duvelleroy M
Laboratoire de Biophysique, Hôpital Fernand Widal, Paris, France.
Cardiovasc Res. 1994 Sep;28(9):1326-30. doi: 10.1093/cvr/28.9.1326.
The aim was to investigate the effect on the coronary network of the interaction between high arterial blood oxygen tension (PaO2) and stimulation by the alpha adrenergic agonist phenylephrine or by serotonin in an isolated, blood perfused rabbit heart preparation.
Fresh pig erythrocytes in Krebs-Henseleit buffer were oxygenated to reach normal PaO2 [19.4(SEM 0.7) kPa] or high PaO2 [53.2(5.5) kPa]. Blood oxygen content was kept constant despite the higher PaO2, by slightly reducing the haemoglobin concentration from 9.3(0.2) to 8.8(0.2) g.100 ml-1 (p < 0.01). Coronary blood flow was kept constant throughout the study, so that the oxygen supply would not vary with the rise in PaO2. Increases in coronary resistance were therefore reflected by increased perfusion pressure.
Switching from normal to high PaO2 induced coronary vasoconstriction, reflected by enhanced perfusion pressure of +21(5)%. After pretreatment with the alpha adrenergic agonist phenylephrine, perfusion of a high PaO2 solution increased coronary resistance by +35(7)% (p < 0.05), a value significantly higher than that found without phenylephrine. Oxygen consumption and myocardial performance did not vary throughout the study. To determine whether this amplification of the response was specifically due to alpha agonist stimulation or could be observed with other vasoactive agents, we applied the same protocol using serotonin instead of phenylephrine. Here again, coronary vasoconstriction rose in response to high PaO2 after serotonin infusion [+25(5)% versus +59(10)%].
The response of the coronary network to high PaO2 is amplified by pretreatment with the alpha adrenergic agonist phenylephrine or with serotonin, regardless of any changes in metabolic status.
旨在研究在离体血液灌注兔心标本中，高动脉血氧张力（PaO₂）与α肾上腺素能激动剂去氧肾上腺素或5-羟色胺刺激之间的相互作用对冠脉循环的影响。
用Krebs-Henseleit缓冲液将新鲜猪红细胞氧合，使其达到正常PaO₂[19.4（标准误0.7）kPa]或高PaO₂[53.2（5.5）kPa]。尽管PaO₂升高，但通过将血红蛋白浓度从9.3（0.2）g·100ml⁻¹略微降至8.8（0.2）g·100ml⁻¹（p<0.01），使血氧含量保持恒定。在整个研究过程中，冠脉血流量保持恒定，因此氧供应不会随PaO₂升高而变化。冠脉阻力增加因此通过灌注压升高来反映。
从正常PaO₂切换至高PaO₂会引起冠脉血管收缩，表现为灌注压升高21（5）%。用α肾上腺素能激动剂去氧肾上腺素预处理后，灌注高PaO₂溶液使冠脉阻力增加35（7）%（p<0.05），该值显著高于未用去氧肾上腺素时。在整个研究过程中，氧消耗和心肌功能没有变化。为了确定这种反应增强是否特定归因于α激动剂刺激，或者使用其他血管活性药物时是否也能观察到，我们采用相同方案，用5-羟色胺代替去氧肾上腺素。同样，输注5-羟色胺后，高PaO₂引起冠脉血管收缩增加[+25（5）%对+59（10）%]。
用α肾上腺素能激动剂去氧肾上腺素或5-羟色胺预处理可增强冠脉循环对高PaO₂的反应，而与代谢状态的任何变化无关。
