[Hepato-cerebral degeneration, especially of the acquired non-Wilsonian type].
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Biomedical subjects
Publications and source records attributed to R D Adams.
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The purpose of this study was to investigate the effects of chronic ethanol consumption on blood pressure and vascular responses, specifically, the possible alterations in endothelium-dependent relaxation which are associated with ethanol-induced hypertension in the rat model. Male rats received ethanol in drinking water for 13 weeks. Systolic pressure was recorded weekly. Following treatment, segments of thoracic aorta with and without intact endothelium were used to generate relaxation-response curves to the endothelium-dependent agents, acetylcholine, ATP and bradykinin, as well as the endothelium-independent agents, adenosine and sodium nitroprusside. Mean systolic pressures at the end of the treatment period were: 127.8 +/- 1.2 and 151.1 +/- 1.3 mmHg for controls and ethanol-treated rats, respectively. Ethanol treatment did not affect the relaxation produced by either acetylcholine, ATP or sodium nitroprusside in aorta with or without endothelium. In contrast, ring segments with intact endothelium from ethanol-treated rats exhibited augmented relaxation in response to both adenosine and bradykinin compared to controls. Removal of the endothelium abolished the relaxation produced by bradykinin in both groups. Although removal of the endothelium had no effect on the relaxation produced by adenosine in the control group, it attenuated the adenosine-induced relaxation in the ethanol-treated group back to control levels. These data suggest that chronic ingestion of ethanol causes elevated blood pressure and augments the endothelium-dependent relaxation to bradykinin. These findings also suggest that chronic ethanol treatment can cause the appearance of an endothelium-dependent component in the relaxation produced by adenosine.(ABSTRACT TRUNCATED AT 250 WORDS)
Methods to reduce increased fluid volume, or swelling, were evaluated as short- and long-term interventions. Forearm and hand volumes were measured in 45 fit and healthy subjects using a water displacement device with previously established reliability. Volumes were measured before and after 2 hours of recumbency and before and after overnight sleep under different conditions of arm elevation or head-up tilt. No arms-at-side lying-down position, whether after 2 hours awake or after overnight sleep or with bed-head elevated or not, resulted in significant changes in forearm and hand volume. Only 2 hours in a supine lying-down position with 30 degrees of arm elevation caused a significant effect, with an average decrease of 51 ml in forearm and hand volume.
Swelling, or increased volume, secondary to venous congestion is thought to be a factor in some upper limb conditions. This study aimed to establish a safe, easily applied method of inducing a transitory increase in forearm and hand volume that could be used as a symptom provocation test for upper limb conditions. Using the principles of venous occlusion plethysmography, movement of blood volume into the forearm and hand of asymptomatic subjects was measured after occlusion with three different sphygmomanometer cuff pressures over four minutes. Increases of between 37 and 62 ml (2.5% and 4.1%) were achieved at pressures between diastolic pressure minus 30 mm Hg and diastolic pressure plus 5 mm Hg, with minimal reported side effects. These data demonstrate that a sphygmomanometer can be used to induce transitory fluid congestion of the forearm and hand.
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OBJECTIVE: One explanation for the poor reliability of manual judgments of posteroanterior (PA) stiffness may be that if manual therapists use different forces when testing, different stiffness is perceived. This study was conducted to examine measurements of lumbar PA stiffness obtained using a device programmed to generate different loading forces. SUBJECTS: Twenty-five subjects with no history of low back pain and a mean age of 23.5 yr were measured. METHODS: Measures of lumbar PA stiffness were obtained using a mechanical device that applied a testing force of 200 N to the skin overlying the L3 spinous process. Six stiffness coefficients were determined from the force/displacement curve obtained from each subject by performing linear regressions from 30-80 N, 30-150 N, 30-200 N, and from 30-83.3 N, 83.3-136.7 N, and 136.7-200 N. Intraclass correlation coefficients and repeated measures analysis of variance were used to analyze the data. RESULTS: Although moderate reliability [ICC 2,1 = 0.67] was found for stiffness measures arising from increasingly wide force-interval regressions (30-80 N, 30-150 N, 300-200 N), poor reliability [ICC (2,1) = 0.39] was found for stiffness measures arising from same-width, higher force regressions (30-83.3 N, 83-137 N, 137-200 N). In both cases there were significant differences between the obtained K stiffness values corresponding to different force intervals. CONCLUSION: These results show that if therapists push harder, different stiffnesses will be felt. Studies using instrumental measurement of spinal stiffness to obtain 'K' values should report the force intervals used. Also, revised protocols for manually judging PA stiffness should ensure that stiffness is assessed by sampling specified force intervals rather than the raters determining their own force limits.