Crystal G J, Salem M R
Department of Anesthesiology, Illinois Masonic Medical Center, Chicago 60657.
Anesth Analg. 1991 Feb;72(2):227-37. doi: 10.1213/00000539-199102000-00016.
Myocardial and systemic effects of isovolemic hemodilution alone and combined with controlled hypotension induced with sodium nitroprusside (SNP) were studied in halothane-anesthetized, open-chest dogs. Regional blood flow was measured with radioactive microspheres and used to compute regional oxygen (O2) supply. Values for regional blood flow in myocardium were used to compute myocardial O2 (MVO2) and lactate uptake (MVLAC) using the Fick equation. Hemodilution to hematocrit 50% of baseline increased aortic blood flow and decreased systemic vascular resistance, although other systemic hemodynamic values were not changed. Twofold increases in myocardial blood flow were accompanied by no change in MVO2, MVLAC, or coronary sinus PO2. Hemodilution increased regional blood flow sufficiently in the pancreas, liver, duodenum, skeletal muscle, skin, and brain to preserve O2 supply whereas unchanged blood flow in the spleen and kidney reduced O2 supply. Under hemodilution, 15 min of intravenous SNP sufficient to reduce mean arterial pressure by 50% caused parallel reductions in aortic blood flow, dP/dt max, and left ventricular end-diastolic pressure; systemic vascular resistance was unaffected. Myocardial blood flow and MVO2 decreased proportionally, whereas MVLAC and coronary sinus PO2 did not change. Regional blood flow and O2 supply decreased in the kidney, spleen, liver, and skin. Extending SNP infusion to 60 min increased myocardial blood flow and MVO2, but other hemodynamic values were unchanged. Comparing previous results with adenosine-induced hypotension inferred that coronary vasodilator reserve was greatly reduced at this time. In conclusion, although myocardial O2 supply versus demand balance was well maintained during SNP-induced hypotension under hemodiluted conditions, diminished coronary vasodilator reserve suggests increased vulnerability to ischemia if stresses of augmented cardiac work demand or impaired arterial oxygenation were superimposed. The decrease in O2 supply in the kidney during combined hemodilution and SNP-induced hypotension also warrants concern. These latter findings suggest the need for extensive clinical monitoring when SNP is used for controlled hypotension under hemodiluted conditions.
在氟烷麻醉、开胸的犬身上，研究了单纯等容血液稀释以及等容血液稀释联合硝普钠（SNP）诱导的控制性低血压对心肌和全身的影响。用放射性微球测量局部血流，并用于计算局部氧（O₂）供应。心肌局部血流值用于通过菲克方程计算心肌氧（MVO₂）和乳酸摄取量（MVLAC）。血液稀释至血细胞比容为基线的50%时，主动脉血流增加，全身血管阻力降低，尽管其他全身血流动力学值未改变。心肌血流增加两倍时，MVO₂、MVLAC或冠状窦PO₂没有变化。血液稀释使胰腺、肝脏、十二指肠、骨骼肌、皮肤和大脑的局部血流充分增加，以维持氧供应，而脾脏和肾脏血流未变，氧供应减少。在血液稀释状态下，静脉注射SNP 15分钟足以使平均动脉压降低50%，导致主动脉血流、最大dp/dt和左心室舒张末期压力平行降低；全身血管阻力未受影响。心肌血流和MVO₂成比例下降，而MVLAC和冠状窦PO₂没有变化。肾脏、脾脏、肝脏和皮肤的局部血流和氧供应减少。将SNP输注延长至60分钟，心肌血流和MVO₂增加，但其他血流动力学值未改变。将先前的结果与腺苷诱导的低血压进行比较推断，此时冠状动脉扩张储备大大降低。总之，尽管在血液稀释条件下SNP诱导的低血压期间心肌氧供应与需求平衡得到良好维持，但冠状动脉扩张储备减少表明，如果叠加心脏工作需求增加或动脉氧合受损的应激，缺血易感性增加。血液稀释联合SNP诱导的低血压期间肾脏氧供应减少也值得关注。这些结果表明，在血液稀释条件下使用SNP进行控制性低血压时，需要进行广泛的临床监测。
