Matsunaga T, Okumura K, Tsunoda R, Tayama S, Tabuchi T, Yasue H
Division of Cardiology, Kumamoto University School of Medicine, Japan.
Am J Physiol. 1996 Feb;270(2 Pt 2):H427-34. doi: 10.1152/ajpheart.1996.270.2.H427.
Endothelium-derived nitric oxide (NO) regulates coronary blood flow, but it is unclear how NO synthesis inhibition affects myocardial metabolism. In pentobarbital sodium-anesthetized dogs, myocardial oxygen metabolism, adenosine release, lactate extraction rate (LER), and systolic ventricular wall thickening (SWT) at baseline and during atrial pacing were estimated before and after intracoronary NG-nitro-L-arginine methyl ester (L-NAME) infusion. Coronary blood flow and PO2 in the anterior interventricular vein at baseline were both significantly decreased by L-NAME (3 x 10(-4) M in the coronary blood). Coronary flow was increased during pacing, which was not affected by L-NAME. Myocardial adenosine release remained unchanged during pacing before L-NAME, but it was significantly increased after L-NAME infusion. Neither LER nor SWT changed during pacing performed before and after L-NAME. The experiment was also performed in dogs pretreated with 8-phenyltheophyl-line. After L-NAME, pacing-induced increase in coronary flow was suppressed, and both LER and SWT were significantly decreased during pacing. In conclusion, when NO synthesis is inhibited, adenosine release is increased in response to the increase in myocardial oxygen demand. With this compensatory adenosine release, coronary flow is increased and ventricular function is unaffected.
内皮源性一氧化氮（NO）调节冠状动脉血流，但目前尚不清楚NO合成抑制如何影响心肌代谢。在戊巴比妥钠麻醉的犬中，在冠状动脉内注入NG-硝基-L-精氨酸甲酯（L-NAME）之前和之后，估计基础状态及心房起搏期间的心肌氧代谢、腺苷释放、乳酸摄取率（LER）和心室壁收缩期增厚（SWT）。基础状态下前室间静脉的冠状动脉血流和PO2均因L-NAME（冠状动脉内浓度为3×10⁻⁴ M）而显著降低。起搏期间冠状动脉血流增加，L-NAME对此无影响。在注入L-NAME之前，起搏期间心肌腺苷释放保持不变，但注入L-NAME后显著增加。在L-NAME前后进行的起搏过程中，LER和SWT均未改变。该实验也在预先用8-苯基茶碱处理的犬中进行。注入L-NAME后，起搏诱导的冠状动脉血流增加受到抑制，起搏期间LER和SWT均显著降低。总之，当NO合成受到抑制时，腺苷释放会因心肌氧需求增加而增加。通过这种代偿性腺苷释放，冠状动脉血流增加且心室功能不受影响。
