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We studied the adaptive response of the arterial wall and intimal thickening under conditions of increased flow in an atherogenic model. Blood flow was increased by construction of an arteriovenous fistula between the right iliac artery and vein in six cynomolgus monkeys fed a diet containing 2% cholesterol and 25% peanut oil. The left iliac artery served as the control. Serum cholesterol increased from 135 +/- 22 mg/dl to 880 +/- 129 mg/dl during the experiment. After 6 months, blood flow in the right iliac artery (420 +/- 95 ml/min) was 10 times greater than in the left iliac artery (44 +/- 9 ml/min, p less than 0.005). Flow velocity in the right iliac artery (31 +/- 6 cm/sec) was more than twofold greater than in the left (12 +/- 1 cm/sec, p less than 0.05). Despite the marked difference in blood flow and flow velocity, calculated wall shear stress was the same in both the right (16 +/- 4 dynes/cm2) and left iliac vessels (15 +/- 2 dynes/cm2) because of a twofold increase in lumen diameter (p less than 0.001) of the right iliac artery. Shear stress in the aorta was also normal (12 +/- 2 dynes/cm2). There was no difference in plaque deposition or mean intimal thickness between the right and left iliac arteries. In the right iliac artery there was a twofold increase in media cross-sectional area (p less than 0.001) but no change in media thickness or total wall thickness. Tangential wall tension and tangential wall stress were two times greater on the right than on the left (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

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The biochemical effects of peripheral vascular disease on skeletal muscle have not been characterized precisely because of the lack of satisfactory noninvasive analytic methods. 31P nuclear magnetic resonance (NMR) spectroscopy was used to measure the high-energy phosphate compounds, phosphocreatine (PCr) and adenosine triphosphate, as well as metabolic byproducts, such as inorganic phosphates (Pi) and phosphate monoesters in calf muscles of 214 limbs with peripheral vascular disease. Intracellular pH was also measured. The NMR index (Pi[PCr + Pi]) was used to quantitate the impairment of oxidative phosphorylation as a result of ischemia. Studies done at rest documented the impairment of oxidative metabolism only in limbs with severe ischemia (ankle-brachial pressure index (API) less than 0.4). Exercise resulted in a significant elevation of the NMR index in all limbs and the rate of return of this value toward normal following exercise was prolonged even in limbs with moderate ischemia (0.4 less than or equal to API less than or equal to 0.9). Correlation of 31P NMR parameters with arteriograms showed that infrapopliteal occlusions resulted in prolonged recovery times only when the superficial femoral artery was occluded and emphasized the metabolic consequences of multisegmental disease. Accumulation of glycolytic pathway intermediates correlated with the decrease in muscle cell pH observed with exercise. Despite immediate improvement in symptoms and hemodynamic parameters following revascularization, return to normal biochemical function occurs over a prolonged period of time. This study demonstrates that 31P NMR spectroscopy can successfully measure noninvasively the important phosphorus-containing compounds involved in the bioenergetics of skeletal muscle in vivo rapidly enough to permit real-time determination during exercise and recovery.