Valsson F, Lundin S, Kirnö K, Hedner T, Houltz E, Saito Y, Ricksten S E
Department of Anesthesia and Intensive Care, Sahlgrenska University Hospital, Göteborg, Sweden.
Anesth Analg. 1999 Feb;88(2):279-85. doi: 10.1097/00000539-199902000-00010.
Atrial natriuretic peptide (ANP) exerts a dilatory effect on coronary arteries in humans. We investigated the effects of ANP on pacing-induced myocardial ischemia during enflurane anesthesia in patients with coronary artery disease (CAD). In 20 patients with CAD, myocardial ischemia was induced by atrial pacing before and after an i.v. infusion of ANP (50 mg x kg(-1) min(-1), n = 10) or placebo (n = 10). We studied the effects of ANP or placebo on pacing-induced changes in central hemodynamics, myocardial blood flow and regional myocardial indices of lactate uptake (RMLU), and oxygen consumption (RMVO2) and extraction (RMO2E). ST-segment depression was less pronounced during pacing with ANP compared with control pacing (-0.09 +/- 0.01 vs -0.24 +/- 0.02 mV; P < 0.001). RMLU decreased to -11.1 micromol/min during control pacing compared with -0.7 micromol/min during pacing with ANP (P < 0.01). ANP did not affect pacing-induced changes in RMVO2, RMO2E, or the rate pressure product. Placebo did not affect pacing-induced changes in ST-segment depression or RMLU. In conclusion, ANP attenuates ischemic ST-segment depression and lactate release during pacing-induced myocardial ischemia in patients with CAD. The antiischemic effect of ANP was not accompanied by any improvement in the regional myocardial oxygen supply/demand relationship.
We evaluated the effects of i.v. atrial natriuretic peptide (50 ng x kg(-1) x min(-1)) on pacing-induced myocardial ischemia during general anesthesia in patients with coronary artery disease. In contrast to placebo, atrial natriuretic peptide attenuated ST-segment depression and myocardial lactate production and improved left ventricular function during pacing-induced ischemia.
心房利钠肽（ANP）对人体冠状动脉有扩张作用。我们研究了ANP对冠心病（CAD）患者在恩氟烷麻醉期间起搏诱导的心肌缺血的影响。在20例CAD患者中，在静脉输注ANP（50 μg·kg⁻¹·min⁻¹，n = 10）或安慰剂（n = 10）之前和之后，通过心房起搏诱导心肌缺血。我们研究了ANP或安慰剂对起搏诱导的中心血流动力学、心肌血流量以及乳酸摄取（RMLU）、氧消耗（RMVO2）和提取（RMO2E）的区域心肌指标变化的影响。与对照起搏相比，使用ANP起搏时ST段压低不那么明显（-0.09±0.01 vs -0.24±0.02 mV；P<0.001）。对照起搏期间RMLU降至-11.1 μmol/min，而使用ANP起搏时为-0.7 μmol/min（P<0.01）。ANP不影响起搏诱导的RMVO2、RMO2E或心率血压乘积的变化。安慰剂不影响起搏诱导的ST段压低或RMLU的变化。总之，ANP可减轻CAD患者起搏诱导的心肌缺血期间的缺血性ST段压低和乳酸释放。ANP的抗缺血作用并未伴随区域心肌氧供需关系的任何改善。
我们评估了静脉注射心房利钠肽（50 ng·kg⁻¹·min⁻¹）对冠心病患者全身麻醉期间起搏诱导的心肌缺血的影响。与安慰剂相比，心房利钠肽在起搏诱导的缺血期间减轻了ST段压低和心肌乳酸生成，并改善了左心室功能。
