Gaugl J F, Williams A G, Downey H F
Department of Physiology, Texas College of Osteopathic Medicine, Fort Worth 76107.
Cardiovasc Res. 1993 May;27(5):748-52. doi: 10.1093/cvr/27.5.748.
Reports of autoregulation in the right coronary vasculature have varied from non-existent to almost perfect. At least some of this discrepancy may be due to failure to account for changes in myocardial metabolism secondary to the method used to vary perfusion pressure. The aim of this study was to determine if the potent autoregulation reported when right coronary perfusion pressure was lowered by opening a large arteriovenous shunt was due to increased right ventricular myocardial oxygen consumption (MVO2) induced by augmented preload and afterload.
Two protocols were used to produce right coronary perfusion pressures of 100, 80, and 60 mm Hg in anaesthetised dogs. In both protocols the right coronary artery was cannulated and supplied with blood from a pressurised chamber. In protocol 1, right coronary perfusion pressure was decreased independently of aortic pressure, and in protocol 2, aortic pressure was decreased in parallel with right coronary perfusion pressure by opening a large arteriovenous shunt. Right coronary blood flow, central venous pressure, and pulmonary arterial pressure were measured, and right ventricular oxygen extraction and MVO2. Central venous pressure (right ventricular preload) and pulmonary arterial pressure (right ventricular afterload) did not change. In protocol 2, opening the arteriovenous shunt increased venous return, as shown by increased central venous pressure and pulmonary arterial pressure. This increased right ventricular MVO2 at the lower right coronary perfusion pressures and maintained right coronary blood flow at the level recorded when right coronary perfusion pressure was 100 mm Hg.
This apparently potent autoregulation resulted from the shunt induced increase in oxygen consumption at low right coronary perfusion pressures, in contrast to the decreased right ventricular oxygen consumption and right coronary blood flow observed when right coronary perfusion pressure is selectively decreased.
关于右冠状动脉血管系统自身调节的报道各不相同,从不存在到近乎完美。这种差异至少部分可能是由于未能考虑到因改变灌注压力的方法而继发的心肌代谢变化。本研究的目的是确定当通过打开一个大的动静脉分流来降低右冠状动脉灌注压力时所报道的强大自身调节是否是由于前负荷和后负荷增加导致右心室心肌氧耗(MVO2)增加所致。
使用两种方案在麻醉犬中产生100、80和60 mmHg的右冠状动脉灌注压力。在两种方案中,右冠状动脉均插管并由一个加压腔室供血。在方案1中,右冠状动脉灌注压力独立于主动脉压力降低,在方案2中,通过打开一个大的动静脉分流使主动脉压力与右冠状动脉灌注压力平行降低。测量右冠状动脉血流量、中心静脉压和肺动脉压,以及右心室氧摄取和MVO2。中心静脉压(右心室前负荷)和肺动脉压(右心室后负荷)未改变。在方案2中,打开动静脉分流增加了静脉回流,表现为中心静脉压和肺动脉压升高。这在较低的右冠状动脉灌注压力下增加了右心室MVO2,并使右冠状动脉血流量维持在右冠状动脉灌注压力为100 mmHg时记录的水平。
这种明显强大的自身调节是由于分流在低右冠状动脉灌注压力下导致氧消耗增加所致,这与选择性降低右冠状动脉灌注压力时观察到的右心室氧消耗和右冠状动脉血流量减少形成对比。