Hoffman William E, Albrecht Ronald F, Jonjev Zivojin S
Departments of Anesthesiology and Physiology, University of Illinois at Chicago, Chicago, IL60612, USA.
J Cardiothorac Vasc Anesth. 2002 Jun;16(3):286-9. doi: 10.1053/jcan.2002.124134.
To compare sodium nitroprusside (SNP)-induced hypotension with desflurane-induced hypotension for the effects on myocardial blood flow and tissue oxygenation in dogs.
Prospective, randomized, crossover, nonblinded.
University teaching hospital.
Male nonpurpose-bred hounds (n = 8).
Dogs were anesthetized with 8% desflurane. Catheters were inserted into the femoral artery and coronary sinus. A flow probe was placed in the left anterior descending (LAD) branch of the coronary artery. A sensor that measured myocardial oxygen pressure (PmO(2)) was inserted into the myocardium of the left ventricle. Myocardial oxygen consumption (MVO(2)) was calculated as LAD flow x arterial - coronary sinus oxygen content.
Measurements were made at baseline blood pressure levels of 99 mmHg (measure 1), during hypotension to 62 to 66 mmHg using intravenous SNP or 14% desflurane (measure 2), and during SNP or 14% desflurane with blood pressure support using phenylephrine (measure 3). Each dog randomly received both hypotensive treatments, separated by 1 hour. Baseline measures were PmO(2) = 46 +/- 9 mmHg, LAD flow = 43 +/- 11 mL/min, and MVO(2) = 2.47 +/- 0.73 mL O(2)/min. During hypotension induced with SNP, PmO(2) decreased 30% (p < 0.05), LAD flow increased 40% (p < 0.05), and MVO(2) did not change. During hypotension induced with 14% desflurane, PmO(2) did not change, and LAD flow and MVO(2) decreased 25% and 40% (p < 0.05). Blood pressure support with phenylephrine increased LAD flow and MVO(2) but did not change PmO(2) during SNP or 14% desflurane treatment.
SNP-induced hypotension produced myocardial vasodilation, but tissue oxygenation was impaired. PmO(2) was maintained during desflurane-induced hypotension.
比较硝普钠(SNP)诱导的低血压与地氟醚诱导的低血压对犬心肌血流和组织氧合的影响。
前瞻性、随机、交叉、非盲法。
大学教学医院。
雄性非特定品种猎犬(n = 8)。
犬用8%地氟醚麻醉。将导管插入股动脉和冠状窦。在冠状动脉左前降支(LAD)分支处放置流量探头。将一个测量心肌氧分压(PmO₂)的传感器插入左心室心肌。心肌耗氧量(MVO₂)通过LAD血流量×动脉血 - 冠状窦血氧含量来计算。
在血压基线水平99 mmHg时进行测量(测量1),在使用静脉注射SNP或14%地氟醚使血压降至62至66 mmHg期间进行测量(测量2),以及在使用去氧肾上腺素进行血压支持的SNP或14%地氟醚治疗期间进行测量(测量3)。每只犬随机接受两种降压治疗,间隔1小时。基线测量值为PmO₂ = 46 ± 9 mmHg,LAD血流量 = 43 ± 11 mL/分钟,MVO₂ = 2.47 ± 0.73 mL O₂/分钟。在SNP诱导的低血压期间,PmO₂下降30%(p < 0.05),LAD血流量增加40%(p < 0.05),而MVO₂未改变。在14%地氟醚诱导的低血压期间,PmO₂未改变,LAD血流量和MVO₂分别下降25%和40%(p < 0.05)。在SNP或14%地氟醚治疗期间,用去氧肾上腺素进行血压支持可增加LAD血流量和MVO₂,但不改变PmO₂。
SNP诱导的低血压导致心肌血管舒张,但组织氧合受损。地氟醚诱导的低血压期间PmO₂得以维持。