Sobotka P A, Brottman M D, Weitz Z, Birnbaum A J, Skosey J L, Zarling E J
Department of Medicine, Loyola University of Chicago, Maywood, IL 60153.
Free Radic Biol Med. 1993 Jun;14(6):643-7. doi: 10.1016/0891-5849(93)90145-k.
Pentane, a product of lipid peroxidation, has been detected in situations involving ischemic injury. Such injury may be limited if lipid peroxidation can be controlled by antioxidants. The role of lipid peroxidation in chronic heart failure (CHF) was assessed by measuring breath pentane in patients with CHF vs. age matched controls. The effect of a free radical scavenger on pentane released during CHF was also measured. Pentane levels were correlated with the daily dose of captopril, a sulfhydril-containing drug used to treat CHF, which is an angiotensin converting enzyme inhibitor. To separate the scavenging effects of captopril from the pharmacologic effects of converting enzyme inhibitors, a crossover study using a nonsulfhydril inhibitor was used. Patients with CHF excreted (p < 0.005) high concentrations of pentane (5.7 +/- 2.1 vs. control 3.6 +/- 1.2 nmol/l). Patients treated with captopril also had significantly higher (p < 0.05) excretion of pentane than the control patients (4.7 +/- 1.3 vs. 3.6 +/- 1.2 nmol/l). The dose of captopril was inversely proportional to the concentration of pentane excreted (r = 0.55, p < 0.05). Pentane excretion during captopril therapy was significantly lower before (p < 0.01) and after (p < 0.02) nonsulfhydril inhibitor therapy.
breath pentane is elevated in CHF and it can be reduced by a free radical scavenger. This reduction of pentane excretion is not a converting enzyme inhibitor class effect.
戊烷是脂质过氧化的产物,在缺血性损伤的情况下已被检测到。如果脂质过氧化能被抗氧化剂控制,这种损伤可能会受到限制。通过测量慢性心力衰竭(CHF)患者与年龄匹配的对照组的呼出戊烷,评估脂质过氧化在慢性心力衰竭中的作用。还测量了自由基清除剂对CHF期间释放的戊烷的影响。戊烷水平与卡托普利(一种用于治疗CHF的含巯基药物,是一种血管紧张素转换酶抑制剂)的日剂量相关。为了将卡托普利的清除作用与转换酶抑制剂的药理作用区分开来,使用了一项使用非巯基抑制剂的交叉研究。CHF患者排出(p<0.005)高浓度的戊烷(5.7±2.1对对照组3.6±1.2 nmol/l)。接受卡托普利治疗的患者排出的戊烷也明显高于对照组患者(4.7±1.3对3.6±1.2 nmol/l,p<0.05)。卡托普利的剂量与排出的戊烷浓度成反比(r = 0.55,p<0.05)。在非巯基抑制剂治疗前(p<0.01)和治疗后(p<0.02),卡托普利治疗期间的戊烷排出量显著降低。
CHF患者呼出的戊烷升高,自由基清除剂可使其降低。戊烷排出量的这种降低不是转换酶抑制剂类的作用。