201Tl perfusion scintigraphy of the legs was evaluated to define intermittent claudication quantitatively, based on Sapirstein's indicator fractionation principle. After intravenous injection of 201Tl with or without exercise, the distribution of the radiotracer throughout the body was obtained using the whole blood scanner. Regional blood flow of cardiac output for three segments of the leg was estimated as a regional fractional uptake (rFU) distributed in these segments compared with the whole body distribution. The validity of the principle was confirmed by a comparative study with 99mTc-MAA (r = 0.979). Normal rFUs (%) for each section at rest and after stress, respectively, were 5.49 +/- 0.69 and 19.40 +/- 2.04 (whole leg); 3.57 +/- 0.49 and 12.26 +/- 1.91 (thigh); 1.59 +/- 0.34 and 6.58 +/- 0.61 (calf). The rates of rFU change from the state of rest to stress (delta rFU) in normals were 3.41 +/- 0.45 (whole leg), 3.44 +/- 0.61 (thigh), and 4.30 +/- 1.03 (calf). Although rFU was within normal limits in patients with arteriosclerosis obliterans (ASO) and thromboangitis obliterans (TAO), delta rFU of the whole leg was significantly decreased from the normal value of 3.41 +/- 0.45 to 1.95 +/- 0.40 for ASO (P less than 0.001) and 1.82 +/- 0.47 for TAO (P less than 0.001). A defect or decreased activity on the stress scintigraph was well correlated with the angiographic findings.

We placed a Gianturco self-expanding metallic stent across the recurrent stricture of an esophagojejunostomy in a patient with gastric cancer. Though excellent passage of food resulted, intractable reflux occurred. Two months later the patient succumbed to recurrent tumor. At autopsy, the stent was patent and was partially covered by esophageal mucosa. There were narrow but deep ulcers around the stent hooks. The Gianturco metallic stent may provide an additional option for treating recurrent enteric strictures after other methods fail. Further refinements of the technique appear necessary.

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SUMMARY Studies to assess the role of blood pressure rise in the growth of the collateral arterial supply following renal artery stenosis were performed in 70 rats. Assessment of the proliferative response was made by coded reading of endothelial cell turnover following tritiated thymidine administration, 5 days after renal artery stenosis. Stenosis induced the anticipated brisk increase in endothelial cell turnover in arterial collaterals and in the ipsilateral renal vein, and ureteric epithelium. Blood pressure elevation did not appear to play the dominant role, as the proliferative response did not parallel blood pressure changes; moreover, neither bilateral renal artery stenosis, designed to enhance the hypertension, nor hydralazine administration, to reduce the blood pressure, influenced endothelial cell turnover. A contribution of elevated blood pressure to the vasoproliferative response, however, was not ruled out definitively in this study. Captopril, also administered to assess the same question, resulted in an enhanced endothelial cell proliferative response, both in frequency and in degree, an observation that became the central thrust of our study. The mechanism by which converting enzyme inhibitor modified endothelial cell turnover is not clear, but may well provide insight into the responsible factors. (Hypertension 5: 307-311, 1983) KEY WORDS • tritiated thymidine • hypertension • anglotensin converting enzyme inhibition W E have documented a hyperplastic response of the endothelium and smooth muscle elements of growing arterial collateral vessels in the rat 1 and dog 2 following renal artery stenosis. Because biophysical factors are thought to influence vascular proliferative responses, 3 and hypertension (a common feature in the models in our earlier studies) is known to promote an increase in arterial cell turnover, 4 we initiated a systematic assessment of the role of hypertension in the hyperplastic response. Maneuvers were designed either to promote increased hypertension, or to prevent the hypertension with antihypertensive drugs. A surprising finding that the converting enzyme inhibitor, captopril, increased the vascular proliferative response rather than reduced it represents the primary thrust of this report.