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Biomedical subjects

F M Dolan

Publications and source records attributed to F M Dolan.

5 recordsLinked to original sources
PubMed2003

Peripheral retinal dysfunction in patients taking vigabatrin.

OBJECTIVE: To assess the wide-field multifocal electroretinogram (WF-mfERG) for assessment of retinal function in vigabatrin-treated patients. METHODS: Thirty-two adults who had taken vigabatrin for at least 3 years for localization-related epilepsy underwent WF-mfERG, ERG, logMar visual acuity and color vision evaluation, Humphrey visual field analysis (static perimetry), and funduscopy. The group was matched with a cohort of patients who had never received vigabatrin. Results were compared with a normative data set (120 drug-free controls) with respect to potential bilateral abnormalities in response timing. RESULTS: There were no significant differences between groups in visual acuity or color vision testing. Of the vigabatrin patients, 19 (59%) had bilateral visual field defects compared to none of the controls. Using WF-mfERG, all patients on vigabatrin with visual field defects showed abnormalities (100% sensitivity) and only 2 of the 13 patients without a field defect showed retinal abnormalities (86% specificity). CONCLUSIONS: WF-mfERG may be useful for detecting retinal pathology in patients taking vigabatrin. The majority of previous reports based on subjective testing may have underestimated the prevalence of peripheral retinal toxicity related to the drug.

Adult↗
PubMed1997

Evidence for Y1 and Y2 subtypes of neuropeptide Y receptors linked to opposing postjunctional effects observed in rat cardiac myocytes.

The aim of this study was to confirm the existence of and identify the receptor subtypes for neuropeptide Y that are present post-junctionally in myocardium. The effects of the selective agonists, [Leu31, Pro34] neuropeptide Y (neuropeptide Y Y1 receptors), neuropeptide Y-(13-36) and peptide YY-(3-36) (neuropeptide Y Y2 receptors), and neuropeptide Y and the related peptide YY, which have differential action at neuropeptide Y Y3 receptors, on amplitudes of contraction of adult rat ventricular cardiomyocytes were studied. Also, the effect of the neuropeptide Y Y1-selective antagonist, bis(31/31')[[Cys31, Trp32, Nva34] neuropeptide Y-(31-36)] on neuropeptide Y-mediated changes in myocyte contraction was investigated. Neuropeptide Y, peptide YY, neuropeptide Y-(13-36) and peptide YY-(3-36) attenuated the isoprenaline (10(-7) M)-stimulated contractile response, and the EC50 values were 9.0 x 10(-9), 4.3 x 10(-10), 3.1 x 10(-11) and 8.5 x 10(-11) M, respectively. [Leu31, Pro34] neuropeptide Y increased the contractile response of cardiomyocytes, and the EC50 values were 8.1 x 10(-9) and 1.5 x 10(-9) M, in the absence and presence of isoprenaline, respectively. Since [Leu31, Pro34] neuropeptide Y caused a positive effect on ventricular myocyte contraction and neuropeptide Y-(13-36) and peptide YY (3-36) produced the most potent negative effects, it is proposed that both neuropeptide Y Y1 and neuropeptide Y Y2 receptors, linked respectively to the positive and negative responses, are expressed in cardiomyocytes. The finding of receptors with neuropeptide Y Y2 characteristics on cardiomyocytes represents a further example of a postjunctional location for this subtype. As there was no significant discrepancy between the potencies of peptide YY and neuropeptide Y to attenuate the contractile response, it appears that neuropeptide Y Y3-like receptors are not linked principally to contractile function in rat cardiomyocytes. Bis(31/31')[[Cys31, Trp32, Nva34] neuropeptide Y-(31-36)] antagonised the neuropeptide Y-mediated stimulation of contractile activity through neuropeptide Y Y1 receptors, but the compound also inhibited the attenuation of isoprenaline-stimulated contraction, apparently by acting as a partial agonist at the neuropeptide Y Y2 receptors.

Animals↗