Cigarette smoking increases the development of initial hyperplasia after vascular injury.

PURPOSE: Our purpose was to determine whether exposure to cigarette smoke increases the development of intimal hyperplasia (IH) after vascular injury. METHODS: Sixteen adult male Sprague-Dawley rats underwent standardized balloon catheter injury of the left common carotid artery. For 4 weeks before and 4 weeks after injury, animals in the experimental group (n=8) were exposed to cigarette smoke with an automated vacuum pump device. Animals in the control group (n=8) were restrained in the smoking device for an identical amount of time and underwent arterial injury at 4 vivo, prepared as histologic cross sections, and stained for elastin. IH was measured by planimetry and is reported both as the absolute area of IH and as the ratio (IH/IEL) of the absolute area of IH to the normalized area enclosed by the internal elastic lamina (expressed as a percent). RESULTS: The absolute area of IH was 2.09 +/- 0.34 for the experimental group compared with 0.94 +/- 0.25 for the control group; mean IH/IEL was 43% +/- 7.1% for the experimental group versus 17.7% +/- 4.7% for the control group (p < 0.05, two tailed unpaired t test. CONCLUSIONS: Inhalation of cigarette smoke increases the development of intimal hyperplasia in a rat model of a balloon catheter arterial injury.

Endarterectomy versus angioplasty in the treatment of localized stenosis of the abdominal aorta.

OBJECTIVE: To compare the outcome after aortoiliac endarterectomy and percutaneous transluminal angioplasty (PTA) of the aorta for localized stenosis of the lower abdominal aorta. DESIGN: Chart review of patients treated over a 5-year period. SETTING: A university centre. PATIENTS: Sixteen women, all of whom were smokers; 5 had hyperlipidemia, 4 had evidence of coronary artery disease, 3 were hypertensive, and 1 was diabetic. INTERVENTIONS: Aortoiliac endarterectomy (eight women) and PTA (eight women). MAIN OUTCOME MEASURES: Ankle-brachial pressure index (ABI), degree of claudication and clinical outcome. RESULTS: Angiography showed localized stenosis of the lower aorta in all patients, aortic hypoplasia in nine patients and associated common iliac disease in seven. None of the eight patients managed by aortoiliac endarterectomy had complications or died. All were free of claudication at a mean follow-up of 29 months and had durable improvement in their ABI: mean ABI preoperatively was 0.69 (standard deviation [SD] 0.1) and postoperatively was 1.06 (SD 0.07). Of the eight patients treated by PTA, only one had partial dilatation; another had a subintimal tear with worsening symptoms and a fall in ABI, requiring surgery within 18 months. The remaining six were symptom free after a mean follow-up of 13.4 months. Aortic PTA resulted in improvement of the ABI: mean ABI before PTA was 0.69 (SD 0.19) and after PTA was 1.06 (SD 0.15). CONCLUSIONS: Endarterectomy is a safe and effective method of treating occlusive disease limited to the distal aorta. PTA appears to be less reliable. However, it is recommended as the initial treatment of choice in patients with angiographically suitable lesions because it is less invasive.

Suppression of intimal hyperplasia in a rabbit model of arterial balloon injury by enalaprilat but not dimethyl sulfoxide.

Intimal hyperplasia appears to result from the deposition of collagen and matrix by medial myofibroblasts, which are stimulated in response to vascular injury. We hypothesized that pharmacologic inhibitors of fibroblast proliferation would suppress the development of intimal hyperplasia. We evaluated the effect of two agents known to inhibit fibroblast proliferation in vitro: enalaprilat, an angiotensin-converting enzyme (ACE) inhibitor, and dimethyl sulfoxide (DMSO), an organic solvent. Thirty-five New Zealand white rabbits underwent standardized balloon catheter injury of the left common carotid artery. Experimental groups received daily intramuscular injections of the following: group I (n = 15), saline solution; group II (n = 10), 0.07 mg/kg enalaprilat; and group III (n = 10), 2 ml/kg of a 25% by weight DMSO solution. Injections were started 1 day prior to injury and continued 5 days a week for 8 weeks. Carotid arteries were perfusion-fixed at 12 weeks and cross-sectioned for measurement by planimetry. Intimal hyperplasia was measured as the ratio of the absolute area of intimal hyperplasia to the normalized area enclosed by the internal elastic lamina (IH/IEL) and was expressed as a percent. Mean values for IH/IEL were as follows: group I (control), 20.6 +/- 2.3%; group II (enalaprilat), 9.5 +/- 0.7%; and group III (DMSO), 17.6 +/- 2.6%. Enalaprilat-treated animals demonstrated a statistically significant suppression of intimal hyperplasia compared with controls (p < 0.01, ANOVA, Student's t test), whereas the DMSO-treated group did not. We conclude that enalaprilat is effective in suppressing the development of intimal hyperplasia in this model of arterial injury.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of hypofibrinogenemia and fibrinolysis on skeletal muscle function after ischemia and reperfusion.

Isometric contraction to direct supramaximal tetanic stimulation of the anterior tibialis (AT) muscle was measured in 50 New Zealand White rabbits after ischemia and reperfusion. Ischemia was produced unilaterally by collateral ligation and temporary inflow control until AT muscle function decreased to < 5% of contralateral (control) AT muscle and the ischemic interval was recorded. Reperfusion was carried out in one of the following ways: group I (n = 20), release of vascular clamps (blood reperfusion [BR]); group II (n = 10), release of vascular clamps and simultaneous intraarterial administration of 50,000 units of urokinase (urokinase reperfusion [UR]); group III (n = 10), release of vascular clamps and simultaneous administration of 50,000 units of urokinase and 28 mg (5 units) of purified rabbit plasminogen (urokinase plasminogen reperfusion [UPR]); and group IV (n = 10), animals defibrinated to < 50 mg/dl with ancrod prior to ischemia and received BR (ancrod blood reperfusion [ABR]). During reperfusion, function was recorded every 60 min for 2 hr. Recovery of experimental muscle function is expressed as the percentage of contralateral control limb function. The mean ischemic interval (mean +/- SEM), to achieve < 5% of contralateral control limb function, was 206.7 +/- 9.9, 209.5 +/- 16.6, 221.7 +/- 12.5, and 272.0 +/- 14.2 min for animals in groups I-IV, respectively. The mean experimental muscle function (mean +/- SEM) following the ischemic interval was 3.2 +/- 0.8, 4.5 +/- 1.4, 4.4 +/- 1.2, and 3.3 +/- 1.0 for groups I-IV, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)