These data indicate that conduit artery distensibility is increased by acetylcholine and increased blood flow in healthy subjects but not in CHF patients, whereas the effects of adenosine and GTN on distensibility are preserved in CHF patients. This implies that EDRF-mediated increases in distensibility are impaired in CHF patients, thus adding to cardiac work.
Objectives: Controversy persists with regard to the atherogenic risk associated with adult growth hormone deficiency (GHD). Endothelial dysfunction and enhanced oxidative stress are early features of atherogenesis. Therefore, we have studied the effect of three months of low dose GH replacement therapy (0.03 IU/kg/day) on these parameters in GHD adults. Subjects and Methods: Eight hypopituitary GHD adults (4 male, 4 female), who were receiving conventional hormone replacement therapy, were studied before and after 3 months of GH replacement (0.03 IU/kg/day). All observations obtained were compared with similar measurements made in 8 matched control subjects. All study subjects were non-smokers, normotensive and gave no personal or family history of premature vascular disease. Endothelial function was assessed using a specialised vessel wall tracking system to measure endothelium-dependent, flow-mediated, brachial artery dilatation (FMD). Measurements were repeated following glyceryl-trinitrate (GTN) (endotheliumindependent dilatation). Oxidative stress was assessed by directly measuring lipid-derived free radicals in venous blood by electron paramagnetic resonance spectroscopy. Fasting lipids, insulin, plasma glucose and IGF-I were also measured at baseline and following GH replacement. Results: FMD, expressed as a percentage change from resting base-line diameter, was significantly impaired in the pre-treatment GHD patients compared with controls (3.1 Ϯ 2.1% vs 6.1 Ϯ 0.9%, P < 0.001; means Ϯ S.D.) indicating endothelial dysfunction. Significant increase in FMD was noted following GH therapy (3.1 Ϯ 2.1% vs 6.5 Ϯ 1.9%, P < 0.001). Free radicals (arbitrary units) were elevated in the pre-treatment GHD patients compared with controls (0.36 Ϯ 0.09 vs 0.11 Ϯ 0.12, P < 0.05) and fell significantly following GH therapy (0.23 Ϯ 0.03 vs 0.36 Ϯ 0.09, P < 0.05), although they remained elevated compared with controls. Fasting insulin was significantly higher (25.9 Ϯ 18.8 vs 13.9 Ϯ 6.7 mu/l, P < 0.05) and IGF-I concentrations lower (10.8 Ϯ 4.7 vs 20.2 Ϯ 6.3 nmol/l, P < 0.05) in the pre-treatment GHD subjects. After treatment there were no changes in insulin concentration, although IGF-I levels were normalised (10.8 Ϯ 2.3 vs 23.6 Ϯ 11.4 nmol/l, P < 0.05). Conclusions: Endothelial dysfunction and enhanced oxidative stress are features of adult GHD. This study suggests plausible mechanisms underlying any proatherogenic tendency in adult GHD and demonstrates improvement of these factors following GH replacement.
This qualitative study examined the medication-taking behaviors and attitudes of participants determined to be 100% adherers to antiretroviral therapy from a NIH-funded study testing a 12-week telephone adherence intervention. Using open-ended questions, interviewers collected data on a sample of 13 informants, whose medication adherence to a randomly selected antiretroviral medication was 100%, based on a 30-day data collection using electronic event monitoring (EEM). The analysis revealed 'successful medication management' as the core category or main theme. The participants achieved success with medication adherence through managing specific areas (regimen, self and environment). By adopting realistic expectations and pragmatic attitudes, adherence is fostered when medication taking is a priority, when patients believe in the efficacy of their medications and when there is a strong patient/provider relationship. Future research is needed to develop tailored interventions using strategies identified by this population. Further in-depth examination of medication-taking behaviors in 100% adherers may be useful in developing individualized programs to maximize adherence to antiretroviral therapy in the clinical setting.
In isolated myocytes and papillary muscles, both nitric oxide, acting through guanosine 3',5'-cyclic monophosphate (cGMP), and cGMP analogues exert a novel effect on myocardial contraction, influencing mainly the onset of relaxation. We studied the effect of the exogenous nitric oxide donor, sodium nitroprusside (0.1-10 microM), in isolated ejecting guinea pig hearts at constant filling pressure, afterload, and heart rate to identify its direct myocardial effects in the whole heart. Sodium nitroprusside induced concentration-dependent increases in coronary flow as well as premature and faster early left ventricular (LV) pressure decline, but did not change end-diastolic or peak LV pressure or peak rate of rise of LV pressure. There was no correlation between changes in coronary flow and LV pressure decline. Sodium nitroprusside effects were inhibited by hemoglobin, which inactivates nitric oxide. The cGMP-independent vasodilator nicardipine also increased coronary flow but did not influence early LV pressure fall. Thus exogenous nitric oxide exerts novel direct myocardial relaxant effects in the isolated ejecting heart, independent of its known vasodilator activity, and without compromising systolic function.
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