Publications by authors named "Ewing D"

Resting heart rates were measured lying, sitting, and standing in 61 diabetics with varying degrees of cardiovascular reflex abnormalities. Those with parasympathetic abnormalities alone had the highest heart rates, while those with both parasympathetic and sympathetic involvement had slightly less rapid heart rates, which were still faster than those in diabetics with normal cardiovascular reflexes. 38 other diabetics in whom autonomic function tests had been done at least three times had a similar pattern of resting heart rate.

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Autonomic mechanisms underlying the initial heart rate response to standing were analyzed in nine normal subjects. The normal pattern of response was altered by atropine to a small and gradual R-R interval shortening over 30 beats, with no rebound R-R interval lengthening. With additional propranolol, R-R interval shortening was even less and confined to the first 15-20 beats, whereas propranolol alone did not affect the normal response pattern, showing that this is under vagal control with increased cardiac sympathetic activity occurring only if the vagus is blocked.

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Although there are ambiguities about these results and their interpretations, this unambiguous experimental observation was made: the two kinds of experiments designed to measure deoxygenation times did not give the same answer, for a given N2 flushing rate, unless t-butanol was present. The addition of t-butanol caused large changes in the positions of the survival curve breakpoints, but only small changes in the 'times to anoxia' in the pre-irradiation glushing experiments. Although careful additional work is needed, these initial results suggest that in the spore, the survival curve breakpoint probably does not represent the dose at which anoxia is reached unless t-butanol is present.

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Cardiovascular effects of diabetic autonomic neuropathy include postural hypotension, resting tachycardia, and, possibly, painless myocardial infarction. Involvement of cardiovascular reflexes in diabetes can be assessed using simple noninvasive tests: the Valsalva maneuver, beat-to-beat heart rate variation, the heart rate response to standing, postural fall in blood pressure, and the sustained handgrip test. Tests of parasympathetic function appear to be abnormal more frequently and earlier in cardiac autonomic involvement, whereas sympathetic damage usually occurs later and is associated with clinical symptoms.

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Seventy-three diabetics (62 males and 11 females) who complained of symptoms suggestive of autonomic neuropathy were followed prospectively for up to five years. Thirty patients presented with impotence alone, while the other 43 presented with one or more of the following: postural hypotension, intermittent diarrhoea, hypoglycaemic unawareness, sweating abnormalities and gastric fullness. Most subjects with impotence alone had normal autonomic function tests (responses to the Valsalva manoeuvre and sustained handgrip) whereas the majority with other symptoms had abnormal tests.

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The effect of nitroglycerin on heart rate and systolic blood pressure was compared in 5 normal subjects, 12 diabetic subjects without autonomic neuropathy, and 5 diabetic subjects with autonomic neuropathy. The magnitude and time course of the increase in heart rate and the decrease in systolic blood pressure after nitroglycerin were similar in the normal and diabetic subjects without autonomic neuropathy, whereas a lesser increase in heart rate and a greater decrease in systolic blood pressure occurred in the diabetic subjects with autonomic neuropathy. It is therefore suggested that caution should be exercised when prescribing vasodilator drugs in diabetic patients, particularly those with autonomic neuropathy.

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Gastric emptying was studied in 12 diabetic patients, six with and six without objective evidence of autonomic neuropathy and in 20 nondiabetic controls, using a double isotope scintiscanning technique which differentiated between solid and liquid emptying. Three patients with autonomic neuropathy exhibited gastric stasis, although this was detected by conventional radiology in only one. Neither the patients with stasis nor those without exhibited abnormally rapid early gastric emptying.

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This review attempts to outline the present understanding of diabetic autonomic neuropathy. The clinical features have been increasinly recognised but knowledge of the localization and morphology of the lesions and their pathogenesis remains fragmentary. A metabolic causation as postulated in somatic nerves accords best with clinical observations.

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The left ventricular response to the Valsalva manoeuvre was studied in 5 normal subjects (group 1), 6 diabetics without autonomic neuropathy (group 2), and 5 diabetics with autonomic neuropathy (group 3), using the maximum amplitude of the praecordial accelerocardiogram (DE) as a noninvasive index of left ventricular performance. During the Valsalva manoeuvre DE decreased in all 3 groups. In groups 1 and 2, DE increased significantly above the control value after release of the manoveuvre (DE overshoot) but this did not occur in group 3.

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Fifty-one diabetic patients with mononeuropathies wereoneuropathy were studied to examine possible etiological factors, to determine the relationship with other diabetic complications, and to correlate with the presence and severity of background peripheral and autonomic neuropathy. The median, ulnar, and lateral popliteal nerves were most commonly affected and cranial neuropathy was relatively uncommon. When bilateral involvement of the same nerve was excluded, multiple mononeuropathies were found in only five patients.

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The family of mycobactins from Mycobacterium smegmatis were resolved into seven fractions by high-pressure liquid chromatography. This separation was by virtue of the differences in length and character of the long acyl substituents as shown by g.l.

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