Melvin J. Schwartz

A general population sample of adult men and women was followed biennially over 14 years during which time 79 men and 46 women developed initial symptoms of intermittent claudication. A detailed examination of the incidence of this manifestation of atherothrombosis in comparison to that of coronary heart disease and atherothrombotic brain infarction was undertaken. As for coronary heart disease (CHD), the incidence of intermittent claudication increased with age. Women lagged behind men by 10 years in incidence. Atherothrombotic brain infarction in contrast exhibited no male predominance and after the early sixties the women actually surged ahead. Uncomplicated angina, surprisingly, resembled brain infarction more than intermittent claudication in the age-sex trend. A pronounced increase in risk of intermittent claudication was noted for persons with CHD in general and angina in particular, suggesting a common underlying basis for claudication and coronary disease. The principal hazard for subjects with claudication appeared to derive from an increased propensity to cardiovascular morbidity and mortality rather than from the consequences of impaired circulation to the limb. Risk of death was twofold for those with claudication as compared to those without.

The relationship of pressure in the superior mesenteric artery, mesenteric small artery, mesenteric small vein, and portal vein to the rate of blood flow in the superior mesenteric artery was studied in eight dogs. Total bed resistance to blood flow decreased as a function of flow over the range 20–60 ml/min but increased as a function of flow over the range 90–270 ml/min. The onset and cessation of the resistance increase were associated with pressures in the superior mesenteric artery of 64 and 205 mm Hg, respectively. These resistance changes resulted mainly from change of resistance to flow through vessels less than 0.5 mm diameter. The findings suggest that the intestinal vascular bed, like the renal vascular bed, has a local mechanism which antagonizes changes of flow rate produced by variation of arterial pressure.