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Biomedical subjects

K E Moore

Publications and source records attributed to K E Moore.

305 records · Page 17Linked to original sources
PubMedDate not supplied

Experimental analysis of fluid mechanical energy losses in aortic valve stenosis: importance of pressure recovery.

Current methods for assessing the severity of aortic stenosis depend primarily on measures of maximum systolic pressure drop at the aortic valve orifice and related calculations such as valve area. It is becoming increasingly obvious, however, that the impact of the obstruction on the left ventricle is equally important in assessing its severity and could potentially be influenced by geometric factors of the valve, causing variable degrees of downstream pressure recovery. The goal of this study was to develop a method for measuring fluid mechanical energy losses in aortic stenosis that could then be directly related to the hemodynamic load placed on the left ventricle. A control volume form of conservation of energy was theoretically analyzed and modified for application to aortic valve stenosis measurements. In vitro physiological pulsatile flow experiments were conducted with different types of aortic stenosis models, including a venturi meter, a nozzle, and 21-mm Medtronic-Hall tilting disc and St. Jude bileaflet mechanical valves. The energy loss created by each model was measured for a wide range of experimental conditions, simulating physiological variation. In all cases, there was more energy lost for the nozzle (mean = 0.27 J) than for any other model for a given stroke volume. The two prosthetic valves generated approximately the same energy losses (mean = 0.18 J), which were not statistically different, whereas the venturi meter had the lowest energy loss for all conditions (mean = 0.037 J). Energy loss correlated poorly with orifice pressure drop (r2 = 0.34) but correlated well with recovered pressure drop (r2 = 0.94). However, when the valves were considered separately, orifice and recovered pressure drop were both strongly correlated with energy loss (r2 = 0.99, 0.96). The results show that recovered pressure drop, not orifice pressure drop, is directly related to the energy loss that determines pump work and therefore is a more accurate measure of the hemodynamic significance of aortic stenosis.

Aortic Valve Stenosis↗
PubMedDate not supplied

Comparison of 2, 5-dimethoxy-4-methylamphetamine (DOM) and d-amphetamine for in vivo efflux of catecholamines from rat brain.

The neurochemical effects of DOM and d-amphetamine were compared under several conditions in unanesthetized rats implanted with chronic-indwelling push-pull cannulae in a cerebral lateral ventricle. Brain catecholamine storage sites were previously pulse-labelled with 14-C-norepinephrine administered intraventricularly. During the perfusion of the lateral ventricles with artificial cerebrospinal fluid, the animals were injected i.p. with 1.5 mg/kg of DOM, 2.0 mg/kg of d-amphetamine or 1.0 ml/kg of isotonic saline. Analysis of the perfusate in successive samples indicated an increased efflux of 14-C-radioactivity in rats administered DOM or d-amphetamine. Increased proportions of 14-C-norepinephrine and 14-C-normetanephrine were detected in samples of perfusate 15 to 30 min after drug injection. Pretreatment of other animals with 6-hydroxydopamine intraventricularly, which decreased brain levels of both norepinephrine and dopamine, blocked the increased efflux of 14-C-radioactivity induced by DOM or d-amphetamine. Pretreatment of rats with 6-hydroxydopa i.p., which depleted brain norepinephrine selectively, reduced to about half the d-amphetamine-induced efflux of 14-C-radioactivity for all samples during the time course of the effect. However, animals pretreated with 6-hydroxydopa and then tested for DOM effects showed a different pattern of 14-C-radioactivity efflux. The efflux for the initial samples was increased as with the DOM control, but the 6-hydroxydopa pretreatment attuated the DOM-induced efflux for the later samples. The results suggest DOM and d-amphetamine share qualitatively similar effects in releasing and/or blocking the reuptake of catecholamines at brain periventricular nerve terminals. Nevertheless, DOM appears to differ from d-amphetamine in the temporal pattern of net catecholamine release.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗