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Biomedical subjects

M V Moore

Publications and source records attributed to M V Moore.

7 recordsLinked to original sources

Autonomic neuropathy and the pathogenesis of glaucoma in diabetes mellitus.

In order to determine whether ocular hypertension and glaucoma may be a complication of autonomic neuropathy in diabetes mellitus, 30 asymptomatic diabetic patient volunteers were studied. A correlation was sought between reduced anterior chamber depth which is thought to predispose to the development of glaucoma, and two markers of autonomic dysfunction, loss of sinus arrhythmia and reduced diameter of dark adapted pupils. A significant correlation was found between reduced chamber depth and pupil diameter arrhythmia (r = 0.36, p = 0.025) and between chamber depth and pupil diameter (r = 0.45, p = 0.006). As expected, there was also a significant correlation between sinus arrhythmia and pupil diameter (r = 0.68, p less than 0.001). The correlation between pupil diameter and sinus arrhythmia, and between pupil diameter and chamber depth was preserved after the data were adjusted for age (r = 0.54, p less than 0.001 and r = 0.35, p = 0.03, respectively), while that between sinus arrhythmia and chamber depth was lost (r = 0.23, NS). No association was found between intraocular pressure and either marker of autonomic dysfunction, but intraocular pressure was not abnormal (less than 22 mmHg) in any individual case. These data suggest that autonomic denervation of the eye in diabetes may be associated with alteration of anterior chamber depth.

Adult

Apparent improvement in diabetic autonomic neuropathy induced by captopril.

Eight diabetic subjects with moderately elevated blood pressure (BP) (systolic (SBP) greater than 140 and/or diastolic (DBP) greater than 90 mmHg) were studied. Each had evidence of mild asymptomatic autonomic neuropathy (impairment of forced sinus arrhythmia). The effect of a single oral 25 mg dose of captopril on BP and some aspects of autonomic function was compared with matched placebo in a double-blind, cross-over study. Resting supine SBP and DBP fell significantly (P less than 0.01) over 90 minutes following captopril, indicating that the hypotensive effect of the drug was not dependent on intact autonomic function. There was no significant change in resting heart rate. The bradycardic response to apnoeic face immersion was significantly (P less than 0.01) enhanced following captopril. Sinus arrhythmia did not change. The BP responses to standing and to the cold pressor test were unaffected. There was no exacerbation of postural hypotension. The ingestion of a single dose of captopril appears to increase vagal function, without affecting sympathetic nervous function, in diabetics with evidence of mild vagal impairment.

Adult