Pieper G M, Todd G L, Wu S T, Salhany J M, Clayton F C, Eliot R S
Cardiovasc Res. 1980 Dec;14(11):646-53. doi: 10.1093/cvr/14.11.646.
31P nuclear magnetic resonance (NMR) spectroscopy was used to ascertain whether propranolol could reduce the development of myocardial acidosis during periods of ischaemic arrest and were studied. Cardiac pH progressively declined during ischaemia from a normal 6.97 +/- 0.02 (n = 23) to 6.09 +/- 0.04 or 5.96 +/- 0.04, respectively. Normalisation of pH following reperfusion occurred only in the 35 min ischaemic hearts. Propranolol (1 mg. litre-1) given prior to arrest significantly reduced the magnitude of developing acidosis regardless of the length of ischaemia. Furthermore, it aided in the normalisation of intramyocardial pH upon reperfusion in both groups. Propranolol significantly reduced the magnitude of phosphocreatine (PCr loss normally seen during ischaemic arrest alone, but it did not protect against depletion of ATP. Restoration of PCr reperfusion was virtually complete in all cases, while transient increases in ATP were seen only in those hearts protected by propranolol. In summary, this NMR study demonstrated the first direct evidence that a significant component of the myocardial acidosis caused by global ischaemia and arrest can be blocked by propranolol.
采用31P核磁共振（NMR）波谱法来确定普萘洛尔是否能减少缺血性停搏期间心肌酸中毒的发生，并进行了相关研究。在缺血期间，心脏pH值从正常的6.97±0.02（n = 23）逐渐下降至分别为6.09±0.04或5.96±0.04。再灌注后pH值恢复正常仅发生在缺血35分钟的心脏中。在停搏前给予普萘洛尔（1毫克·升-1），无论缺血时间长短，均能显著降低酸中毒的程度。此外，它有助于两组心肌再灌注时心肌内pH值恢复正常。普萘洛尔显著降低了单独缺血性停搏期间通常所见的磷酸肌酸（PCr）损失幅度，但它并不能防止ATP的消耗。在所有情况下，再灌注时PCr的恢复几乎是完全的，而仅在那些受普萘洛尔保护的心脏中观察到ATP的短暂增加。总之，这项NMR研究首次直接证明，普萘洛尔可以阻断由全心缺血和停搏引起的心肌酸中毒的一个重要组成部分。
