培哚普利及缬沙坦预防冠状动脉支架内再狭窄

目的 观察血管紧张素转化酶抑制药(angiotensin-converting enzyme inhibitor,ACEI)培哚普利和血管紧张素受体阻断药(angiotensin receptor blocker,ARB)缬沙坦预防冠状动脉支架植入术后支架内再狭窄的临床效果.方法 将126例成功接受支架治疗的冠心病病人随机分为ACEI组64例和ARB组62例,通过冠状动脉造影以支架内或支架临近血管管腔直径狭窄程度等于或大于50%为再狭窄的诊断标准,随访6～12个月,记录主要不良心脏事件(包括死亡、心绞痛及非致死性心肌梗死)的发生率、靶血管再次形成率和支架内再狭窄发生率.结果 两组病人的性别、年龄、既往疾病、超声心动图左心房直径和左心室内径、服用药物种类、血脂、操作因素、治疗时间差异无统计学意义(P＞0.05).ACEI组支架内再狭窄发生率(18.8%)高于ARB组支架内再狭窄发生率(4.8%),两组差异有统计学意义(P=0.03).ACEI组和ARB组主要不良心脏事件发生率分别为6.3%和1.6%,但差异无统计学意义(P=0.36).靶血管再次重建率ACEI组(15.6%)高于ARB组(3.2%),差异有统计学差异(P=0.04).结论 ARB可能比ACEI更有效预防冠状动脉支架内再狭窄.     

血管紧张素转换酶抑制剂和血管紧张素受体拮抗剂治疗糖尿病肾病的临床疗效分析

目的对血管紧张素转换酶抑制剂(ACEI)及血管紧张素受体拮抗剂(ARB)对于糖尿病肾病的治疗效果进行分析探讨。方法将该院2009年1月—2014年3月收治的153例糖尿病肾病患者随机分为ACEI组(采用ACEI治疗)、ARB组(采用ARB治疗)及联合组(采用ACEI联合ARB治疗),对比3组患者的治疗效果和血肌酐、24 h尿蛋白定量及血压等指标。结果 3组患者在血压下降幅度方面差异无统计学意义(P0.05),联合组的血肌酐及尿蛋白定量的下降幅度优于ACEI组及ARB组,差异有统计学意义(P0.05)。结论 ACEI联和ARB治疗糖尿病肾病能够有效缓解病情进展,保护肾功能,值得临床推广借鉴。     

血管紧张素转化酶抑制剂与血管紧张素受体拮抗剂临床疗效对比

肾素-血管紧张素-醛固酮系统（RAAS）激活与高血压及其他心血管不良事件密切相关。虽然血管紧张素转化酶抑制剂（ACEI）与血管紧张素受体拮抗剂（ARB）在高血压治疗中同样重要，但研究发现二者心血管系统保护作用差异明显。本文将综述评估上述药物临床疗效的相关研究。     

阻断肾素-血管紧张素系统对高血压患者心房颤动发生危险的影响

研究阻断肾素-血管紧张素系统(RAS)对高血压患者心房颤动(AF)发生危险的影响。将高血压患者分为AF组(n=216)和非AF组(n=216),对性别、年龄、既往病史、过敏史、高血压病程、血压控制水平、超声心动图左房直径和左室厚度、服用抗高血压药物种类和持续时间进行回顾性调查。结果:两组性别、年龄、病程、血压控制水平、超声心动图左房直径和左室厚度的差异无显著性意义,服用利尿剂、钙离子拮抗剂、α受体阻滞剂和β受体阻滞剂的情况无明显差别(P均>0.05)。AF组服用血管紧张素转换酶抑制剂/血管紧张素Ⅱ受体阻滞剂(ACEI/ARB)者有61例(28.2%),非AF组服用ACEI/ARB者有87例(40.3%),两组相比差异具有统计学意义(P<0.01),服用ACEI/ARB的患者发生AF的危险降低(OR=0.58)。多因素分析表明只有ACEI/ARB对AF发生起作用。结论:阻断RAS可能对高血压患者AF的防治有益。     

双源CT对冠状动脉支架靶血管再狭窄的诊断价值

目的:探讨双源CT（DSCT）对冠状动脉支架置入靶血管再狭窄的诊断价值。方法:对我院69例冠状动脉支架置入患者（共111枚支架）进行DSCT,评价支架图像质量得分与靶血管级别的相关性;并对部分患者同期进行冠状动脉造影（CAG）检查,对比分析DSCT对冠状动脉支架置入靶血管病变的真实性。结果:DSCT支架图像质量得分与靶血管级别正相关;DSCT对支架靶血管再狭窄诊断的灵敏度82%、特异度98%、和准确度95%;DSCT与CAG对不同直径支架的靶血管再狭窄检出率差异无统计学意义,但DSCT对直径≥3.0 mm支架靶血管再狭窄检出的特异度和准确度明显高于直径＜3.0 mm支架靶血管的相应指标（均P＜0.05）,而灵敏度的差异未达到显著水平。结论:DSCT可清晰的显示冠状动脉支架靶血管的病变情况,能较准确地评价冠状动脉支架靶血管再狭窄的发生,具有临床应用价值。     

血管紧张素受体阻滞剂在冠状动脉支架置入术后再狭窄中的研究进展

随着冠状动脉支架置入术的深入开展,支架置入术后再狭窄受到更多关注。肾素-血管紧张素系统在支架内再狭窄的发生中具有重要作用。血管紧张素受体选择性的不同,直接参与支架内再狭窄的发展。通过对于血管紧张素受体的选择性阻断,可延缓支架置入术后冠状动脉再狭窄的程度,对预防冠状动脉支架置入术后再狭窄具有重要意义。     

血管紧张素Ⅱ受体拮抗剂和血管紧张素转换酶抑制剂的脑保护作用之差异

血管紧张素Ⅱ受体拮抗剂（ARB）和血管紧张素转换酶抑制剂（ACEI）均作用于。肾素血管紧张素系统（RAS），一般认为ARB和ACEI的靶器官保护作用雷同，仅ARB不具有咳嗽的不良反应，因此各种指南中的有关表述多将ARB定位在ACEI的替代用药，近年来有的指南也提到ARB和ACEI的联合应用。脑作为高血压的一个重要靶器官，脑卒中已成为高血压患致死的主要原因。目前公认，降低血压水平是降低脑卒中风险的首要措施，收缩压下降1—3mmHg（1mmHg=0．133kPa），脑卒中风险可降低20％-30％，降压药物是否有降压之外的脑保护作用是近年来争论的热点之一。本探讨ARB与ACEI在脑保护方面的不同作用，为临床合理用药提供参考。     

药物洗脱支架与金属裸支架对冠状动脉临界病变的远期疗效

目的:评估药物洗脱支架与金属裸支架对于治疗冠状动脉临界病变的远期疗效。方法:自身冠状动脉首次介入治疗病变(在线定量冠状动脉造影分析50%≤管腔狭窄直径≤70%)的患者入选本研究,共计151例患者分为药物洗脱支架组(n=102)和金属裸支架组(n=49),两组的基本临床特征和冠状动脉造影结果差异无统计学意义。术前、术后和随访6～12个月时进行定量冠状动脉造影分析,并在住院期间、30天和6～12个月时观察严重不良心脏事件的发生。结果:151例患者支架置入成功率均为100%。住院期间严重不良心脏事件发生率,在药物洗脱支架组和金属裸支架组差异无统计学意义(0%和2.0%,P=0.15)。在随访30天时,两组均无死亡和支架内血栓形成。6～12个月随访期间,药物洗脱支架组和金属裸支架组比较①严重不良心脏事件发生率(3.9%vs8.1%,P=0.97),②靶病变重复血管重建率(2.9%vs6.1%,P=0.39),③急性心肌梗死发生率(1.96%vs2.04%,P=0.95),差异均无统计学意义。12个月时药物洗脱支架组和金属裸支架组比较,支架内血栓发生率和病死率差异也无统计学意义(1.96%vs0%,P=0.34;0%vs4.08%,P0.05)。定量冠状动脉造影分析显示:远期管腔丢失药物洗脱支架组明显低于金属裸支架组[(0.23±0.73)mmvs(0.95±0.94)mm,P=0.01],两组比较差异有统计学意义;而支架内再狭窄率两组比较差异无统计学意义(12.9%vs25.0%,P=0.34)。结论:药物洗脱支架和金属裸支架对于治疗自身冠状动脉临界病变安全有效,两组远期严重不良心脏事件发生率差异无统计学意义。     

血管紧张素转换酶抑制剂、血管紧张素Ⅱ受体拮抗剂治疗冠心病

比较血管紧张素转换酶抑制剂(ACEI)与血管紧张素Ⅱ受体拮抗剂(ARB)治疗冠心病的疗效:在全因死亡、心血管死亡、心肌梗死及心力衰竭治疗方面,ARB与ACEI无明显差异,但ARB因不良反应而停药方面优于ACEI。结论:ARB治疗冠心病在全因死亡、心血管死亡、心肌梗死及心力衰竭治疗方面,疗效与ACEI相似而耐受性更好。     

肾素血管紧张素系统阻断剂对冠状动脉介入治疗后对比剂肾病的影响

目的观察肾素血管紧张素系统(RAS)阻断剂(RASI)对冠状动脉介入术后对比剂急性肾损害(CI-AKI)的影响。方法根据介入术前RASI应用情况将401例患者分为3组:血管紧张素转换酶抑制剂(ACEI)组(n=204);血管紧张素受体拮抗剂(ARB)组(n=63);非RASI组(n=134)。同时根据估算的肾小球滤过率(eGFR),再将各组分为肾功能正常组[eGFR90mL/(min·1.73m~2)]和轻度肾功能不全组[eGFR 60~90mL/(min·1.73m~2)]两个亚组。所有患者围手术期均给予常规水化,测定冠状动脉介入术前及术后24、72h肾功能变化,观察CI-AKI的发生情况。结果与非RASI组相比,应用对比剂后72h,ARB组(14.3%比5.2%,P0.05)和ACEI组(11.3%比5.2%,P0.05)CI-AKI的发生率均升高。ACEI组介入前与介入后血肌酐、eGFR和血尿素氮水平与非RASI组差异无统计学意义,ARB组血肌酐高于ACEI组和非RASI组[24h:(98.0±46.8)比(86.0±33.0)、(84.4±24.9)μmol/L;72h:(102.5±49.2)比(91.1±38.9)、(87.2±26.0)μmol/L;均P0.05],eGFR低于ACEI组和非RASI组[24h:(74.3±23.0)比(84.4±29.0)、(84.2±24.7)mL/(min·1.73m~2);72h:(70.6±21.9)比(80.1±27.7)、(81.4±25.3)mL/(min·1.73m~2);均P0.05]。在肾功能正常人群,ARB组CI-AKI发生率显著高于非RASI组(17.1%比4.5%,P0.05);在轻度肾功能不全人群,ACEI组CI-AKI发生率较非RASI组升高(13.4%比6.7%,P0.05)。结论冠状动脉介入术前ARB治疗显著增加肾功能正常者CI-AKI发生,而对肾功能受损患者,ACEI显著增加CI-AKI发生。     

Limitations of angiotensin inhibition

Angiotensin-converting-enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs) have beneficial effects in patients with cardiovascular disease and in those with diabetes-related and diabetes-independent chronic kidney diseases. These beneficial effects are independent of the antihypertensive properties of these drugs. However, ACE inhibitors, ARBs, and combinations of agents in these two classes are limited in the extent to which they inhibit the activity of the renin-angiotensin-aldosterone system (RAAS). Angiotensin breakthrough and aldosterone breakthrough may be important mechanisms involved in limiting the effects of ACE inhibitors and ARBs. Whether direct renin inhibitors will overcome some of the limitations of ACE-inhibitor and ARB therapy by blocking the deleterious effects of the RAAS remains to be proven. This important area is, however, in need of further investigation.     

Modulating atherosclerosis through inhibition or blockade of angiotensin

Angiotensin-convertng enzyme (ACE) inhibitors are well recognized for their benefits in treating hypertension and congestive heart failure and preventing postmyocardial infarction heart failure or left ventricular (LV) dysfunction. Recently, blockade of the angiotensin II type 1 (AT1) receptor was shown to reduce cardiovascular events in hypertensive subjects with LV hypertrophy. Several lines of evidence are now converging to show that ACE inhibitors may affect the atherosclerotic process itself. Emerging clinical data indicate that angiotensin-receptor blockers (ARBs) may possibly modulate atherosclerosis as well. The antiatherogenic properties of ACE inhibitors and ARBs may derive from inhibition or blockade of angiotensin II, now recognized as an agent that increases oxidative stress.Angiotensin-converting enzyme inhibition and angiotensin-receptor blockade also increase endothelial nitric oxide formation, which improves endothelial function. In contrast to the effects of ARBs, the vascular effects of ACE inhibitors may, in part, be mediated by an increase in bradykinin. This article reviews some of the biologic mechanisms whereby ACE inhibitors and ARBs may modulate atherosclerosis.     

Endothelin-converting enzyme inhibition ameliorates angiotensin II-induced cardiac damage

We tested the hypothesis that endothelin-converting enzyme (ECE) inhibition ameliorates end-organ damage in rats harboring both human renin and human angiotensinogen genes (dTGR). Hypertension develops in the animals, and they die by age 7 weeks of heart and kidney failure. Three groups were studied: dTGR (n=12) receiving vehicle, dTGR receiving ECE inhibitor (RO0687629; 30 mg/kg by gavage; n=10), and Sprague-Dawley control rats (SD; n=10) receiving vehicle, all after week 4, with euthanasia at week 7. Systolic blood pressure was not reduced by ECE inhibitor compared with dTGR (205+/-6 versus 206+/-6 mm Hg at week 7, respectively). In contrast, ECE inhibitor treatment significantly reduced mortality rate to 20% (2 of 10), whereas untreated dTGR had a 52% mortality rate (7 of 12). ECE inhibitor treatment ameliorated cardiac damage and reduced left ventricular ECE activity below SD levels. Echocardiography at week 7 showed reduced cardiac hypertrophy (4.8+/-0.2 versus 5.7+/-0.2 mg/g, P<0.01) and increased left ventricular cavity diameter (5.5+/-0.3 versus 3.1+/-0.1 mm, P<0.001) and filling volume (0.42+/-0.04 versus 0.16+/-0.06 mL, P<0.05) after ECE inhibitor compared with untreated dTGR. ECE inhibitor treatment also reduced cardiac fibrosis, tissue factor expression, left ventricular basic fibroblast growth factor mRNA levels, and immunostaining in the vessel wall, independent of high blood pressure. In contrast, the ECE inhibitor treatment showed no renoprotective effect. These data are the first to show that ECE inhibition reduces angiotensin II-induced cardiac damage.     

Determinants of angiotensin II generation during converting enzyme inhibition

The reaction of the renin-angiotensin system to acute angiotensin converting enzyme inhibition was investigated in a single-blind, crossover study in nine normal volunteers receiving two out of three regimens in random order: the new converting enzyme inhibitor benazepril (20 mg once or 5 mg four times at 6-hour intervals) or enalapril (20 mg). Plasma converting enzyme activity, drug levels, angiotensin I and angiotensin II, active renin, and aldosterone were measured before and 1-4 hours and 14-30 hours after drug intake. Baseline in vitro plasma converting enzyme activity was 97 +/- 15 nmol/ml/min (mean +/- SD) when Hip-Gly-Gly was used as substrate, but with carbobenzoxy-Phe-His-Leu (Z-Phe-His-Leu) or angiotensin I as substrate it was only 20 +/- 4 and 1.7 +/- 0.3 nmol/ml/min, respectively. Discriminating power at peak converting enzyme inhibition was enhanced with the two latter substrates. In vivo converting enzyme activity was estimated by the plasma angiotensin II/angiotensin I ratio, which correlated well with in vitro converting enzyme activity using Z-Phe-His-Leu as substrate (r = 0.76, n = 252). Angiotensin II levels returned to baseline less than 24 hours after drug administration, whereas in vitro and in vivo converting enzyme activity remained considerably inhibited and active renin together with angiotensin I levels were still elevated. A close linear relation was found between plasma angiotensin II and the angiotensin I/drug level ratio (r = 0.91 for benazeprilat and r = 0.88 for enalaprilat, p less than 0.001). Thus, plasma angiotensin II truly reflects the resetting of the renin-angiotensin system at any degree of converting enzyme inhibition. The ratio of plasma angiotensin II to angiotensin I represents converting enzyme inhibition more accurately than in vitro assays, which vary considerably depending on substrates and assay conditions used.     

Effect of chronic angiotensin converting enzyme inhibition on angiotensin I and bradykinin metabolism in rats

We determined the effect of chronic administration of the angiotensin converting enzyme (ACE) inhibitor, enalapril, on the in vivo pulmonary inactivation of bradykinin (BK) and conversion of angiotensin I (Ang I). In addition we assessed whether chronic ACE inhibition influenced the activity of prolylendopeptidase (PEP), which metabolizes Ang I to generate angiotensin-(1-7) (Ang-[1-7]) and inactivates BK. Male Wistar rats were treated orally with enalapril (10 mg/kg once a day) for 7 to 15 days (n = 20) and 21 to 30 days (n = 11). Vehicle-treated rats (7 to 30 days, n = 11) were used as controls. Pulmonary inactivation of BK and conversion of Ang I were determined in conscious enalapril- or vehicle-treated rats before and after intravenous administration of the ACE inhibitor enalaprilat (MK-422, 10 mg/kg). Pulmonary inactivation of BK (%) was determined by comparing equipotent doses of BK injected by the intravenous and intraaortic routes, and Ang I conversion (%) by comparing the pressor effect of Ang I and Ang II injected intravenously. PEP-like activity in plasma and lung homogenates was determined fluorometrically using the synthetic substrate Suc-Gly-Pro-MCA. In control rats, pulmonary BK inactivation averaged 97.6% ± 0.54%. Acute ACE inhibition with MK-422 reduced BK inactivation to 42.0% ± 2.7%. However, in rats treated chronically with enalapril, BK inactivation was increased as compared with acute ACE inhibition, averaging 58.8% ± 3.7% at 7 to 15 days and 58.8% ± 4.5% at 21 to 30 days of treatment. Intravenous administration of MK-422 to the enalapril-treated rats did not return the increased BK inactivation to the level observed during acute ACE inhibition. In contrast, Ang I conversion was significantly reduced from 46.7% ± 6.5% to 0.9% ± 0.2% by MK-422, and this inhibition remained essentially unchanged during chronic treatment. PEP-like activity in plasma and lung homogenates of control rats was 4.4 ± 0.3 nmol MCA/min/mL and 11.4 ± 0.9 nmol MCA/min/mg protein, respectively. After chronic treatment with enalapril there was a progressive increase of PEP-like activity in both plasma and lung, which after 21 to 30 days of treatment averaged 10.7 ± 1.7 nmol MCA/min/mL and 29.2 ± 2.8 nmol MCA/min/mg protein, respectively. These data indicate that chronic ACE blockade induces alternative BK-inactivating mechanisms and increases Ang-(1-7)-generating mechanisms.     

Intrarenal aminopeptidase N inhibition augments natriuretic responses to angiotensin III in angiotensin type 1 receptor-blocked rats

The renal angiotensin angiotensin type 2 receptor has been shown to mediate natriuresis, and angiotensin III, not angiotensin II, may be the preferential angiotensin type 2 receptor activator of this response. Angiotensin III is metabolized to angiotensin IV by aminopeptidase N. The present study hypothesizes that inhibition of aminopeptidase N will augment natriuretic responses to intrarenal angiotensin III in angiotension type 1 receptor-blocked rats. Rats received systemic candesartan for 24 hours before the experiment. After a 1-hour control, cumulative renal interstitial infusion of angiotensin III at 3.5, 7, 14, and 28 nmol/kg per minute (each dose for 30 minutes) or angiotensin III combined with aminopeptidase N inhibitor PC-18 was administered into 1 kidney. The contralateral control kidney received renal interstitial infusion of vehicle. In kidneys infused with angiotensin III alone, renal sodium excretion rate increased from 0.05+/-0.01 micromol/min in stepwise fashion to 0.11+/-0.01 micromol/min at 28 nmol/kg per minute of angiotensin III (overall ANOVA F=3.68; P<0.01). In angiotensin III combined with PC-18, the renal sodium excretion rate increased from 0.05+/-0.01 to 0.32+/-0.08 mumol/min at 28 nmol/kg per minute of angiotensin III (overall ANOVA F=6.2; P<0.001). The addition of intrarenal PD-123319, an angiotensin type 2 receptor antagonist, to renal interstitial angiotensin III plus PC-18 inhibited the natriuretic response. Mean arterial blood pressure and renal sodium excretion rate from control kidneys were unchanged by angiotensin III +/- PC-18 + PD-123319. Angiotensin III plus PC-18 induced a greater natriuretic response than Ang III alone (overall ANOVA F=16.9; P=0.0001). Aminopeptidase N inhibition augmented the natriuretic response to angiotensin III, suggesting that angiotensin III is a major agonist of angiotensin type 2 receptor-induced natriuresis.     

Effects of angiotensin converting enzyme and angiotensin II receptor inhibition on impaired fibrinolysis in systemic hypertension

Abnormalities in fibrinolysis have been reported in hypertension. Angiotensin converting enzyme (ACE) inhibitors have been shown to improve altered fibrinolytic balance in hypertensive patients. It has not been documented, however, whether this is due to a decrease in angiotensin II (Ang-II) generation or is a consequence of elevated local levels of bradykinin. Accordingly, the aim of this study was to determine the effects of an ACE inhibitor (perindopril) and an Ang-II receptor antagonist (losartan) on fibrinolytic kinetics.We have examined the serum levels of the plasminogen activator inhibitor type-1 (PAI-1) antigen and activity, tissue plasminogen activator (t-PA) antigen and activity, soluble thrombomodulin (sTM), and tissue factor pathway inhibitor (TFPI) before and after reaching the target blood pressure (< 140/90 mm Hg) in 13 hypertensive patients receiving perindopril (mean age 40 ± 11 years, 6 women, 7 men) and in 12 patients receiving losartan (mean age 38 ± 9 years, 6 women, 6 men). We also compared the baseline fibrinolytic activity of hypertensive patients with that of 12 normotensive control persons (mean age 40 ± 9 years, 6 women, 6 men). The mean basal plasma levels of PAI-1 antigen, PAI-1 activity, and sTM were significantly higher in the hypertensive patients than in normal controls (P < .005). The values of other analytes were similar in both groups. Increased plasma levels of PAI-1 antigen, PAI-1 activity, and sTM were reduced in patients after they were given perindopril and losartan (P < .005); the reductions in losartan-receiving group were more pronounced (P < .05). There were no significant effects on the plasma levels of t-PA antigen, t-PA activity, and TFPI in patients receiving the two therapeutic regimens (P > .05).In conclusion, chronic hypertension is associated with hypofibrinolysis. The beneficial effect of ACE inhibitors on fibrinolysis seems to be related to the blockade of Ang-II, and increased kinin activity does not appear to play a major role.     

Interaction of angiotensin converting enzyme inhibition and atrial natriuretic factor

The interaction of angiotensin converting enzyme (ACE) inhibition and atrial natriuretic factor (ANF) was investigated in six supine, sodium-replete, normal volunteers who received captopril (10 mg i.v. bolus followed by 10 mg/hr constant infusion) or vehicle superimposed on background 3-hour, constant, low-dose (1.5 pmol/kg/min) infusions of human ANF (99-126). Plasma converting enzyme activity was significantly inhibited but this had no effect on endogenous plasma ANF concentrations. ANF infusions, with or without captopril, caused similar increases in plasma ANF concentrations, and calculated metabolic clearance rates for ANF were unchanged. Similarly, blood pressure, heart rate, renal blood flow, glomerular filtration rate, and renal electrolyte excretion, including ANF-induced natriuresis, were unaffected by captopril. The combination of ANF plus captopril produced a significant increase in plasma aldosterone (79 +/- 8 vs. 60 +/- 6 pmol/l, p less than 0.05), cortisol (406 +/- 52 vs. 265 +/- 29 nmol/l, p less than 0.01), adrenaline (119 +/- 21 vs. 76 +/- 10 pg/ml, p less than 0.05), and noradrenaline (319 +/- 49 vs. 215 +/- 38 pg/ml, p less than 0.05) compared with time-matched placebo data. Converting enzyme inhibition, in the absence of major changes in blood pressure or renal blood flow, has little effect on ANF metabolism or renal bioactivity. However, ACE inhibition and ANF combined may interact to increase activity of the hypothalamo-pituitary-adrenal axis and sympathetic nervous system by unknown mechanisms.     

Targeting the angiotensin system in posttransplant airway obliteration: the antifibrotic effect of angiotensin converting enzyme inhibition

The angiotensin system plays a role in the pathogenesis of fibrotic diseases. We used a rat heterotopic tracheal transplant model of bronchiolitis obliterans (BO) to examine the role of angiotensin converting enzyme (ACE) in development of the fibroproliferative lesion of BO. Isograft and allograft tracheal transplants were performed. Allograft rats received either no treatment (control) or captopril (100 mg/kg/d) in their drinking water. The drug treatment given to the recipient rats was begun 5 days before transplantation, on postoperative Day 1, or on postoperative Day 5. The treatment was continued until postoperative Day 21, when tracheal specimens were harvested and subjected to histologic, immunohistologic, and morphometric analyses. We noted heavy staining for ACE in the obliterated portion of the tracheas of allograft control animals. This area was not present in nontransplanted or isograft tracheas. Captopril administration begun 5 d before transplantation and on postoperative Day 1 resulted in a significant attenuation in the percent airway obliteration (45% and 26%, respectively) as compared with that in control allografts (83%; p < 0.05). This study demonstrates the presence of ACE in the fibroproliferative lesion in a rat model of BO, and shows that inhibition of ACE can limit development of airway obliteration.