Measurement of aortic-wall thickness in living dogs.
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Biomedical subjects
Publications and source records attributed to A E Marble.
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This report presents the early results of a new technique, using a solid-state transducer intracompartmental (STIC) catheter, developed to measure dynamic pressure changes in the anterior compartment of the leg in patients with exercise-induced anterior compartment syndrome. Nine male volunteers (15 limbs) with a history of exercise-induced anterior compartment pain were studied and compared to eleven asymptomatic male controls matched for age, weight and height. After catheter insertion, anterior compartment pressures were recorded with the subjects walking and running on a treadmill and performing several static maneuvers before and after the exercise period. The most statistically significant value between the two groups was the difference in mean pressure during running (P less than 0.001). Presently, all mean running pressures greater than 85 mm Hg are considered abnormal. This new technique offers the investigator the opportunity to measure dynamic intracompartmental pressures in symptomatic patients and provides an objective measurement for selection of patients for fasciotomy.
Compliance mismatch between host artery and synthetic vascular substitutes has rarely been mentioned in the literature as a possible cause of suture line disruption and damage to endothelial and platelet cells. In this paper we have attempted to elucidate on how compliance mismatch can predispose: (1) anastomotic rupture, (2) flow induced shear stres and, (3) reduced distal perfusion. We have concluded that in order to minimize all three of these factors the compliance of the vascular substitute should be equivalent to the host artery to which it is to be anastomosed. It appears that the factor which is most seriously affected by the compliance mismatch is the flow regimen in that flow separation regions forms at the distal anastomosis. Shear stresses, due to eddies in these regions of flow separation, are of significant magnitude to destroy endothelial cells lining the vascular wall and platelets existing in the boundary layer.