The distribution of electrical current and the resultant Joule heating in tissues of the human upper extremity for a worst-case hand-to-hand high-voltage electrical shock was modelled by solving the Bioheat equation using the finite element method. The model of the upper extremity included skin, fat, skeletal muscle, and bone. The parameter sets for these tissues included specific thermal and electrical properties and their respective tissue blood flow rates. The extent of heat mediated cellular injury was estimated by using a damage rate equation based on a single energy barrier chemical reaction model. No cellular injury was assumed to occur for temperatures less than 42 degrees C. This model was solved for the duration of Joule heating required to produce membrane damage in cells, termed the lethal time (of contact) for injury. LT's were determined for contact voltages ranging from 5 to 20 kV. For a 10,000 volt electrical shock LT's for skeletal muscle are predicted to be: 0.5 second in the distal forearm, 1.1 second in the mid-forearm, 1.2 second in the proximal elbow, and 2.0 seconds in the mid-arm. This analysis of the electrical shock provides useful insight into the mechanisms of resultant tissue damage and provides important performance guidelines for the development of safety devices.

In the hypertensive region in the aorta proximal to the stenosis, monocyte adhesion and endothelial VCAM-1 expression were increased, with intimal thickening and accumulation of macrophages. These findings suggest that hypertension may promote atherosclerotic plaque formation by enhancing monocyte adhesion.

Abstract-Hypertension is a well-known risk factor for coronary artery disease and carotid and lower extremity occlusive disease. Surgically induced hypertension in hypercholesterolemic animals results in increased aortic wall motion and increased plaque formation. We tested the hypothesis that reduction in aortic wall motion, despite continued hypertension, could reduce plaque formation. New Zealand White rabbits (nϭ26) underwent thoracic aortic banding to induce hypertension and were fed an atherogenic diet for 3 weeks. In 13 rabbits, a segment of aorta proximal to an aortic band was externally wrapped to reduce wall motion. All animals were fed an atherogenic diet for 3 weeks. Four groups were studied: 1, coarctation control (no wrap, nϭ7); 2, coarctation with loose wrap (nϭ6); 3, coarctation with firm wrap (nϭ7); and 4, control (noncoarcted, nϭ6). Wall motion, blood pressure, and pulse pressure were measured at standard reference sites proximal and distal to the coarctation by use of intravascular ultrasound. Quantitative morphometry was used to measure intimal plaque. Mean arterial pressure and cyclic aortic wall motion were equally increased proximal to the aortic coarctation in all 3 coarcted rabbit groups compared with the control group (PϽ0.001). Wall motion in the segment of aorta under the loose and firm wraps was no different from the control value. The external wrap significantly reduced intimal thickening in the 4 groups by the following amounts: group 1, 0.30Ϯ0.03 mm 2 ; group 2, 0.06Ϯ0.02 mm 2 ; group 3, 0.04Ϯ0.02 mm 2 ; and group 4, 0.01Ϯ0.01 mm 2 (PϽ0.001). Localized inhibition of aortic wall motion in the lesion-prone hypertensive aorta resulted in significant reduction in intimal plaque formation. These data suggest that arterial wall cyclic motion may stimulate cellular proliferation and lipid uptake in experimental atherosclerosis. Key Words: wall motion Ⅲ hypertension Ⅲ atherosclerosis Ⅲ pulse pressure H ypertension is an independent risk factor for coronary artery disease 1,2 and for carotid 3,4 and lower extremity 5,6 occlusive disease. Other multivariate clinical studies have shown that pulse pressure is also an independent risk factor for atherosclerosis. 7,8 Previous experimental studies in our laboratory 9,10 and in others 11,12 have demonstrated that surgically created aortic coarctations increase blood pressure proximal to the coarctation and increase the rate of plaque deposition in hypercholesterolemic rabbits and monkeys.On the other hand, the aorta distal to a severe coarctation experiences reduced wall motion and is largely protected from plaque formation despite hypercholesterolemia in animals. 13 In a separate study, rigid external casts of lesion-prone arteries in normotensive hypercholesterolemic rabbits inhibited plaque formation, perhaps because of reduced wall motion. 14 In the present experiment, we reduced aortic wall motion in the hypertensive atherosclerosis-prone aorta proximal to a coarctation by externally wrapping a segment of aorta and studied the effect on plaq...

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