From the Biomedical Imaging Research Institute, Department of Biomedical Sciences, Cedars-Sinai Medical Center, 8700 Beverly Blvd, PACT Building, Suite 800, Los Angeles, CA 90048 (H.J.Y., R.T., I.C., A.K., B.S., D.L., R.D.); Departments of Bioengineering (H.J.Y., A.K., D.L.), Anesthesiology (R.Y.), and Medicine (D.L., R.D.), University of California, Los Angeles, Calif; Department of Physiology (O.S., M.K., J.A.F.) and Department of Anesthesiology, University Health Network (J.A.F.), University of Toronto, Toronto, Ontario, Canada; IMT Institute for Advanced Studies Lucca, Lucca, Italy (S.A.T.); Siemens Medical Solutions USA, Chicago, Ill (X.B.); and Department of Anesthesiology (R.Y., J.T., A.H.C.) and Cedars-Sinai Heart Institute (R.D.), Cedars-Sinai Medical Center, Los Angeles, Calif.
Radiology. 2014 Aug;272(2):397-406. doi: 10.1148/radiol.14132549. Epub 2014 Apr 17.
To examine whether controlled and tolerable levels of hypercapnia may be an alternative to adenosine, a routinely used coronary vasodilator, in healthy human subjects and animals.
Human studies were approved by the institutional review board and were HIPAA compliant. Eighteen subjects had end-tidal partial pressure of carbon dioxide (PetCO2) increased by 10 mm Hg, and myocardial perfusion was monitored with myocardial blood oxygen level-dependent (BOLD) magnetic resonance (MR) imaging. Animal studies were approved by the institutional animal care and use committee. Anesthetized canines with (n = 7) and without (n = 7) induced stenosis of the left anterior descending artery (LAD) underwent vasodilator challenges with hypercapnia and adenosine. LAD coronary blood flow velocity and free-breathing myocardial BOLD MR responses were measured at each intervention. Appropriate statistical tests were performed to evaluate measured quantitative changes in all parameters of interest in response to changes in partial pressure of carbon dioxide.
Changes in myocardial BOLD MR signal were equivalent to reported changes with adenosine (11.2% ± 10.6 [hypercapnia, 10 mm Hg] vs 12% ± 12.3 [adenosine]; P = .75). In intact canines, there was a sigmoidal relationship between BOLD MR response and PetCO2 with most of the response occurring over a 10 mm Hg span. BOLD MR (17% ± 14 [hypercapnia] vs 14% ± 24 [adenosine]; P = .80) and coronary blood flow velocity (21% ± 16 [hypercapnia] vs 26% ± 27 [adenosine]; P > .99) responses were similar to that of adenosine infusion. BOLD MR signal changes in canines with LAD stenosis during hypercapnia and adenosine infusion were not different (1% ± 4 [hypercapnia] vs 6% ± 4 [adenosine]; P = .12).
Free-breathing T2-prepared myocardial BOLD MR imaging showed that hypercapnia of 10 mm Hg may provide a cardiac hyperemic stimulus similar to adenosine.
研究在健康人体和动物中，控制并耐受一定程度的高碳酸血症是否可以替代腺苷作为一种常规使用的冠状动脉扩张剂。
人体研究获得了机构审查委员会的批准并符合 HIPAA 规定。18 名受试者的呼气末二氧化碳分压（PetCO2）升高 10mmHg，并用心肌血氧水平依赖（BOLD）磁共振（MR）成像监测心肌灌注。动物研究获得了机构动物护理和使用委员会的批准。在接受麻醉的犬中，有（n=7）和没有（n=7）诱导的左前降支（LAD）狭窄，分别用高碳酸血症和腺苷进行血管扩张剂挑战。在每次干预时测量 LAD 冠状动脉血流速度和自由呼吸心肌 BOLD MR 反应。进行了适当的统计检验，以评估在二氧化碳分压变化时，所有感兴趣参数的测量定量变化。
心肌 BOLD MR 信号的变化与报告的腺苷变化相当（11.2%±10.6[高碳酸血症，10mmHg] vs 12%±12.3[腺苷]；P=.75）。在完整的犬中，BOLD MR 反应与 PetCO2 之间存在着一个 S 型关系，其中大部分反应发生在 10mmHg 的范围内。BOLD MR（17%±14[高碳酸血症] vs 14%±24[腺苷]；P=.80）和冠状动脉血流速度（21%±16[高碳酸血症] vs 26%±27[腺苷]；P>.99）的反应与腺苷输注相似。在 LAD 狭窄的犬中，高碳酸血症和腺苷输注期间的 BOLD MR 信号变化没有差异（1%±4[高碳酸血症] vs 6%±4[腺苷]；P=.12）。
自由呼吸 T2 准备的心肌 BOLD MR 成像显示，10mmHg 的高碳酸血症可能提供与腺苷相似的心脏充血刺激。
