Miyamoto Tadaomi-Alfonso, Ueno Takayuki, Iguro Yoshihumi, Yotsumoto Goichi, Fukumoto Yoshihiro, Nakamura Kazuo, Sakata Ryuzo
Kokura Memorial Hospital, Kitakyushu, Fukuoka, Japan.
Adv Exp Med Biol. 2009;643:27-36. doi: 10.1007/978-0-387-75681-3_3.
Taurine (TA) administered exogenously before the induction of myocardial ischemia decreases lactic acid production and increases pyruvic acid production during ischemia. It also preserves the activity of GOT, GPT, LDH and CPK during ischemia and enhances recovery of CKMB synthesis as early as 5 minutes after onset of reperfusion. The aim of the study was to determine the optimal conditions for administering TA in order to reduce myocardial ischemia-reperfusion injury. Left ventricular (LV) function, creatine kinase (CK) and lipid peroxide products (LPOP = oxidant stress), as well as the area at risk (AAR), and infarct size (IS) after reperfusion were studied in 3 groups of isolated rat hearts perfused with Krebs Henseleit Buffer (KHB)-stabilized isolated rat hearts that were subjected to 20 minutes(') of global ischemia at 37 degrees C followed by 60' of reperfusion with KHB: Hearts were perfused with TA containing KHB for 10' just prior to ischemia or during the first 10' of reperfusion.
Taurine before ischemia or during reperfusion was equally effective in preventing infarction; however, when administered at reperfusion, taurine reduced lipid peroxidation and myocardial injury more, thereby providing improved early recovery of function.
在诱导心肌缺血前外源性给予牛磺酸（TA）可减少缺血期间乳酸生成并增加丙酮酸生成。它还能在缺血期间保持谷草转氨酶（GOT）、谷丙转氨酶（GPT）、乳酸脱氢酶（LDH）和肌酸磷酸激酶（CPK）的活性，并在再灌注开始后5分钟就增强肌酸激酶同工酶MB（CKMB）合成的恢复。本研究的目的是确定给予TA的最佳条件以减少心肌缺血-再灌注损伤。在3组用Krebs Henseleit缓冲液（KHB）灌注的离体大鼠心脏中研究了左心室（LV）功能、肌酸激酶（CK）和脂质过氧化物产物（LPOP =氧化应激），以及再灌注后的危险区域（AAR）和梗死面积（IS）：这些稳定的离体大鼠心脏在37℃下进行20分钟全心缺血，然后用KHB再灌注60分钟：心脏在缺血前10分钟或再灌注的前10分钟用含TA的KHB灌注。
缺血前或再灌注期间给予牛磺酸在预防梗死方面同样有效；然而，在再灌注时给予牛磺酸能更有效地减少脂质过氧化和心肌损伤，从而使功能早期恢复更好。
